LIVIVO - Search results -

Search results

Result 1 - 10 of total 27

Search options

Article ; Online: Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions.

Mikosz, Andrew / Ni, Kevin / Gally, Fabienne / Pratte, Katherine A / Winfree, Seth / Lin, Qiong / Echelman, Isabelle / Wetmore, Brianna / Cao, Danting / Justice, Matthew J / Sandhaus, Robert A / Maier, Lisa / Strange, Charlie / Bowler, Russell P / Petrache, Irina / Serban, Karina A

American journal of physiology. Lung cellular and molecular physiology

2023 Volume 325, Issue 6, Page(s) L711–L725

Abstract: Chronic obstructive pulmonary disease (COPD) is characterized by nonresolving inflammation fueled by breach in the endothelial barrier and leukocyte recruitment into the airspaces. Among the ligand-receptor axes that control leukocyte recruitment, the ... ...

Abstract	Chronic obstructive pulmonary disease (COPD) is characterized by nonresolving inflammation fueled by breach in the endothelial barrier and leukocyte recruitment into the airspaces. Among the ligand-receptor axes that control leukocyte recruitment, the full-length fractalkine ligand (CX3CL1)-receptor (CX3CR1) ensures homeostatic endothelial-leukocyte interactions. Cigarette smoke (CS) exposure and respiratory pathogens increase expression of endothelial sheddases, such as a-disintegrin-and-metalloproteinase-domain 17 (ADAM17, TACE), inhibited by the anti-protease α-1 antitrypsin (AAT). In the systemic endothelium, TACE cleaves CX3CL1 to release soluble CX3CL1 (sCX3CL1). During CS exposure, it is not known whether AAT inhibits sCX3CL1 shedding and CX3CR1
MeSH term(s)	Animals ; Humans ; Mice ; alpha 1-Antitrypsin/pharmacology ; Cell Communication ; Chemokine CX3CL1 ; CX3C Chemokine Receptor 1/metabolism ; Endothelial Cells/metabolism ; Endothelium/metabolism ; Inflammation/metabolism ; Ligands ; Lipopolysaccharides/pharmacology ; Lipopolysaccharides/metabolism ; Lung/metabolism ; Monocytes ; Pulmonary Emphysema/metabolism
Chemical Substances	alpha 1-Antitrypsin ; Chemokine CX3CL1 ; CX3C Chemokine Receptor 1 ; Ligands ; Lipopolysaccharides ; CX3CL1 protein, human ; Cx3cl1 protein, mouse ; SERPINA1 protein, human
Language	English
Publishing date	2023-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00023.2023
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: Subcutaneous administration of neutralizing antibodies to endothelial monocyte-activating protein II attenuates cigarette smoke-induced lung injury in mice.

Koike, Kengo / Beatman, Erica L / Schweitzer, Kelly S / Justice, Matthew J / Mikosz, Andrew M / Ni, Kevin / Clauss, Matthias A / Petrache, Irina

American journal of physiology. Lung cellular and molecular physiology

2019 Volume 316, Issue 3, Page(s) L558–L566

Abstract: Proapoptotic and monocyte chemotactic endothelial monocyte-activating protein 2 (EMAPII) is released extracellularly during cigarette smoke (CS) exposure. We have previously demonstrated that, when administered intratracheally during chronic CS exposures, ...

Abstract	Proapoptotic and monocyte chemotactic endothelial monocyte-activating protein 2 (EMAPII) is released extracellularly during cigarette smoke (CS) exposure. We have previously demonstrated that, when administered intratracheally during chronic CS exposures, neutralizing rat antibodies to EMAPII inhibited endothelial cell apoptosis and lung inflammation and reduced airspace enlargement in mice (DBA/2J strain). Here we report further preclinical evaluation of EMAPII targeting using rat anti-EMAPII antibodies via either nebulization or subcutaneous injection. Both treatment modalities efficiently ameliorated emphysema-like disease in two different strains of CS-exposed mice, DBA/2J and C57BL/6. Of relevance for clinical applicability, this treatment showed therapeutic and even curative potential when administered either during or following CS-induced emphysema development, respectively. In addition, a fully humanized neutralizing anti-EMAPII antibody administered subcutaneously to mice during CS exposure retained anti-apoptotic and anti-inflammatory effects similar to that of the parent rat antibody. Furthermore, humanized anti-EMAPII antibody treatment attenuated CS-induced autophagy and restored mammalian target of rapamycin signaling in the lungs of mice, despite ongoing CS exposure. Together, our results demonstrate that EMAPII secretion is involved in CS-induced lung inflammation and cell injury, including apoptosis and autophagy, and that a humanized EMAPII neutralizing antibody may have therapeutic potential in emphysema.
MeSH term(s)	Animals ; Antibodies, Neutralizing/pharmacology ; Autophagy/drug effects ; Cytokines/drug effects ; Lung Injury/drug therapy ; Lung Injury/metabolism ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Monocytes/drug effects ; Monocytes/metabolism ; Neoplasm Proteins/drug effects ; Pneumonia/metabolism ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Emphysema/drug therapy ; Pulmonary Emphysema/metabolism ; RNA-Binding Proteins/drug effects ; Smoking/adverse effects
Chemical Substances	Antibodies, Neutralizing ; Cytokines ; Neoplasm Proteins ; RNA-Binding Proteins ; small inducible cytokine subfamily E, member 1
Language	English
Publishing date	2019-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00409.2018
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Inhibition of acid sphingomyelinase disrupts LYNUS signaling and triggers autophagy.

Justice, Matthew J / Bronova, Irina / Schweitzer, Kelly S / Poirier, Christophe / Blum, Janice S / Berdyshev, Evgeny V / Petrache, Irina

Journal of lipid research

2018 Volume 59, Issue 4, Page(s) 596–606

Abstract: Activation of the lysosomal ceramide-producing enzyme, acid sphingomyelinase (ASM), by various stresses is centrally involved in cell death and has been implicated in autophagy. We set out to investigate the role of the baseline ASM activity in ... ...

Abstract	Activation of the lysosomal ceramide-producing enzyme, acid sphingomyelinase (ASM), by various stresses is centrally involved in cell death and has been implicated in autophagy. We set out to investigate the role of the baseline ASM activity in maintaining physiological functions of lysosomes, focusing on the lysosomal nutrient-sensing complex (LYNUS), a lysosomal membrane-anchored multiprotein complex that includes mammalian target of rapamycin (mTOR) and transcription factor EB (TFEB). ASM inhibition with imipramine or sphingomyelin phosphodiesterase 1 (
MeSH term(s)	Animals ; Autophagy/drug effects ; Cells, Cultured ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/pharmacology ; Humans ; Imipramine/chemistry ; Imipramine/pharmacology ; Lysosomes/drug effects ; Lysosomes/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Multiprotein Complexes/antagonists & inhibitors ; Multiprotein Complexes/metabolism ; RNA, Small Interfering/chemistry ; RNA, Small Interfering/pharmacology ; Signal Transduction/drug effects ; Sphingomyelin Phosphodiesterase/antagonists & inhibitors ; Sphingomyelin Phosphodiesterase/deficiency ; Sphingomyelin Phosphodiesterase/metabolism
Chemical Substances	Enzyme Inhibitors ; Multiprotein Complexes ; RNA, Small Interfering ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12) ; Imipramine (OGG85SX4E4)
Language	English
Publishing date	2018-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.M080242
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 175: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Xeroderma Pigmentosum Group C Deficiency Alters Cigarette Smoke DNA Damage Cell Fate and Accelerates Emphysema Development.

Sears, Catherine R / Zhou, Huaxin / Justice, Matthew J / Fisher, Amanda J / Saliba, Jacob / Lamb, Isaac / Wicker, Jessica / Schweitzer, Kelly S / Petrache, Irina

American journal of respiratory cell and molecular biology

2017 Volume 58, Issue 3, Page(s) 402–411

Abstract: Cigarette smoke (CS) exposure is a major risk factor for the development of emphysema, a common disease characterized by loss of cells comprising the lung parenchyma. The mechanisms of cell injury leading to emphysema are not completely understood but ... ...

Abstract	Cigarette smoke (CS) exposure is a major risk factor for the development of emphysema, a common disease characterized by loss of cells comprising the lung parenchyma. The mechanisms of cell injury leading to emphysema are not completely understood but are thought to involve persistent cytotoxic or mutagenic DNA damage induced by CS. Using complementary cell culture and mouse models of CS exposure, we investigated the role of the DNA repair protein, xeroderma pigmentosum group C (XPC), on CS-induced DNA damage repair and emphysema. Expression of XPC was decreased in mouse lungs after chronic CS exposure and XPC knockdown in cultured human lung epithelial cells decreased their survival after CS exposure due to activation of the intrinsic apoptosis pathway. Similarly, cell autophagy and apoptosis were increased in XPC-deficient mouse lungs and were further increased by CS exposure. XPC deficiency was associated with structural and functional changes characteristic of emphysema, which were worsened by age, similar to levels observed with chronic CS exposure. Taken together, these findings suggest that repair of DNA damage by XPC plays an important and previously unrecognized role in the maintenance of alveolar structures. These findings support that loss of XPC, possibly due to chronic CS exposure, promotes emphysema development and further supports a link between DNA damage, impaired DNA repair, and development of emphysema.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; Cell Line, Transformed ; DNA Damage/genetics ; DNA Repair/genetics ; Female ; Genetic Predisposition to Disease/genetics ; Humans ; Lung/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Parenchymal Tissue/pathology ; Pulmonary Emphysema/genetics ; Pulmonary Emphysema/pathology ; Smoke/adverse effects ; Smoking/adverse effects ; Xeroderma Pigmentosum/genetics
Chemical Substances	Smoke
Language	English
Publishing date	2017-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2017-0251OC
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2851: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Sphingolipid regulation of lung epithelial cell mitophagy and necroptosis during cigarette smoke exposure.

Mizumura, Kenji / Justice, Matthew J / Schweitzer, Kelly S / Krishnan, Sheila / Bronova, Irina / Berdyshev, Evgeny V / Hubbard, Walter C / Pewzner-Jung, Yael / Futerman, Anthony H / Choi, Augustine M K / Petrache, Irina

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2018 Volume 32, Issue 4, Page(s) 1880–1890

Abstract: The mechanisms by which lung structural cells survive toxic exposures to cigarette smoke (CS) are not well defined but may involve proper disposal of damaged mitochondria by macro-autophagy (mitophagy), processes that may be influenced by pro-apoptotic ... ...

Abstract	The mechanisms by which lung structural cells survive toxic exposures to cigarette smoke (CS) are not well defined but may involve proper disposal of damaged mitochondria by macro-autophagy (mitophagy), processes that may be influenced by pro-apoptotic ceramide (Cer) or its precursor dihydroceramide (DHC). Human lung epithelial and endothelial cells exposed to CS exhibited mitochondrial damage, signaled by phosphatase and tensin homolog-induced putative kinase 1 (PINK1) phosphorylation, autophagy, and necroptosis. Although cells responded to CS by rapid inhibition of DHC desaturase, which elevated DHC levels, palmitoyl (C16)-Cer also increased in CS-exposed cells. Whereas DHC augmentation triggered autophagy without cell death, the exogenous administration of C16-Cer was sufficient to trigger necroptosis. Inhibition of Cer-generating acid sphingomyelinase reduced both CS-induced PINK1 phosphorylation and necroptosis. When exposed to CS, Pink1-deficient ( Pink1
MeSH term(s)	Alveolar Epithelial Cells/drug effects ; Alveolar Epithelial Cells/metabolism ; Cell Death ; Cells, Cultured ; Cigarette Smoking/adverse effects ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Humans ; Mitochondrial Degradation ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Sphingolipids/metabolism ; Sphingosine N-Acyltransferase/genetics ; Sphingosine N-Acyltransferase/metabolism ; Tobacco Smoke Pollution/adverse effects
Chemical Substances	Sphingolipids ; Tobacco Smoke Pollution ; Cers2 protein, mouse (EC 2.3.1.24) ; Sphingosine N-Acyltransferase (EC 2.3.1.24) ; Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1)
Language	English
Publishing date	2018-01-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201700571R
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 296: Show issues

Order via subito

Details ▾

Article ; Online: AMD3100 ameliorates cigarette smoke-induced emphysema-like manifestations in mice.

Barwinska, Daria / Oueini, Houssam / Poirier, Christophe / Albrecht, Marjorie E / Bogatcheva, Natalia V / Justice, Matthew J / Saliba, Jacob / Schweitzer, Kelly S / Broxmeyer, Hal E / March, Keith L / Petrache, Irina

American journal of physiology. Lung cellular and molecular physiology

2018 Volume 315, Issue 3, Page(s) L382–L386

Abstract: We have shown that cigarette smoke (CS)-induced pulmonary emphysema-like manifestations are preceded by marked suppression of the number and function of bone marrow hematopoietic progenitor cells (HPCs). To investigate whether a limited availability of ... ...

Abstract	We have shown that cigarette smoke (CS)-induced pulmonary emphysema-like manifestations are preceded by marked suppression of the number and function of bone marrow hematopoietic progenitor cells (HPCs). To investigate whether a limited availability of HPCs may contribute to CS-induced lung injury, we used a Food and Drug Administration-approved antagonist of the interactions of stromal cell-derived factor 1 (SDF-1) with its chemokine receptor CXCR4 to promote intermittent HPC mobilization and tested its ability to limit emphysema-like injury following chronic CS. We administered AMD3100 (5mg/kg) to mice during a chronic CS exposure protocol of up to 24 wk. AMD3100 treatment did not affect either lung SDF-1 levels, which were reduced by CS, or lung inflammatory cell counts. However, AMD3100 markedly improved CS-induced bone marrow HPC suppression and significantly ameliorated emphysema-like end points, such as alveolar airspace size, lung volumes, and lung static compliance. These results suggest that antagonism of SDF-1 binding to CXCR4 is associated with protection of both bone marrow and lungs during chronic CS exposure, thus encouraging future studies of potential therapeutic benefit of AMD3100 in emphysema.
MeSH term(s)	Animals ; Bone Marrow/metabolism ; Bone Marrow/pathology ; Chemokine CXCL12/antagonists & inhibitors ; Chemokine CXCL12/metabolism ; Female ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; Heterocyclic Compounds/pharmacology ; Lung Injury/etiology ; Lung Injury/metabolism ; Lung Injury/pathology ; Lung Injury/prevention & control ; Mice ; Pulmonary Alveoli/metabolism ; Pulmonary Alveoli/pathology ; Pulmonary Emphysema/etiology ; Pulmonary Emphysema/metabolism ; Pulmonary Emphysema/pathology ; Pulmonary Emphysema/prevention & control ; Receptors, CXCR4/metabolism ; Smoking/adverse effects ; Smoking/metabolism ; Smoking/pathology
Chemical Substances	CXCR4 protein, mouse ; Chemokine CXCL12 ; Cxcl12 protein, mouse ; Heterocyclic Compounds ; Receptors, CXCR4 ; plerixafor (S915P5499N)
Language	English
Publishing date	2018-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00185.2018
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: In vivo knockdown of intersectin-1s alters endothelial cell phenotype and causes microvascular remodeling in the mouse lungs.

Bardita, Cristina / Predescu, Dan / Justice, Matthew J / Petrache, Irina / Predescu, Sanda

Apoptosis : an international journal on programmed cell death

2012 Volume 18, Issue 1, Page(s) 57–76

Abstract: Intersectin-1s (ITSN-1s) is a general endocytic protein involved in regulating lung vascular permeability and endothelial cells (ECs) survival, via MEK/Erk1/2(MAPK) signaling. To investigate the in vivo effects of ITSN-1s deficiency and the resulting ECs ...

Abstract	Intersectin-1s (ITSN-1s) is a general endocytic protein involved in regulating lung vascular permeability and endothelial cells (ECs) survival, via MEK/Erk1/2(MAPK) signaling. To investigate the in vivo effects of ITSN-1s deficiency and the resulting ECs apoptosis on pulmonary vasculature and lung homeostasis, we used an ITSN-1s knocked-down (KD(ITSN)) mouse generated by repeated delivery of a specific siRNA targeting ITSN-1 gene (siRNA(ITSN)). Biochemical and histological analyses as well as electron microscopy (EM) revealed that acute KD(ITSN) [3-days (3d) post-siRNA(ITSN) treatment] inhibited Erk1/2(MAPK) pro-survival signaling, causing significant ECs apoptosis and lung injury; at 10d of KD(ITSN), caspase-3 activation was at peak, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive ECs showed 3.4-fold increase, the mean linear intercept (MLI) showed 48 % augment and pulmonary microvessel density as revealed by aquaporin-1 staining (AQP-1) decreased by 30 %, all compared to controls; pulmonary function was altered. Concomitantly, expression of several growth factors known to activate Erk1/2(MAPK) and suppress Bad pro-apoptotic activity increased. KD(ITSN) altered Smads activity, downstream of the transforming growth factor beta-receptor-1 (TβR1), as shown by subcellular fractionation and immunoblot analyses. Moreover, 24d post-siRNA(ITSN), surviving ECs became hyper-proliferative and apoptotic-resistant against ITSN-1s deficiency, as demonstrated by EM imaging, 5-bromo-deoxyuridine (BrdU) incorporation and Bad-Ser(112/155) phosphorylation, respectively, leading to increased microvessel density and repair of the injured lungs, as well as matrix deposition. In sum, ECs endocytic dysfunction and apoptotic death caused by KD(ITSN) contribute to the initial lung injury and microvascular loss, followed by endothelial phenotypic changes and microvascular remodeling in the remaining murine pulmonary microvascular bed.
MeSH term(s)	Adaptor Proteins, Vesicular Transport/deficiency ; Adaptor Proteins, Vesicular Transport/genetics ; Animals ; Apoptosis/drug effects ; Capillary Permeability/drug effects ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Gene Knockdown Techniques ; Lung/blood supply ; Lung/pathology ; Lung/physiology ; Lung Injury/pathology ; Mice ; Phenotype
Chemical Substances	Adaptor Proteins, Vesicular Transport ; intersectin 1
Language	English
Publishing date	2012-10-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1452360-7
ISSN	1573-675X ; 1360-8185
ISSN (online)	1573-675X
ISSN	1360-8185
DOI	10.1007/s10495-012-0762-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5178: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Effects of lipid interactions on model vesicle engulfment by alveolar macrophages.

Justice, Matthew J / Petrusca, Daniela N / Rogozea, Adriana L / Williams, Justin A / Schweitzer, Kelly S / Petrache, Irina / Wassall, Stephen R / Petrache, Horia I

Biophysical journal

2014 Volume 106, Issue 3, Page(s) 598–609

Abstract: The engulfment function of macrophages relies on complex molecular interactions involving both lipids and proteins. In particular, the clearance of apoptotic bodies (efferocytosis) is enabled by externalization on the cell target of phosphatidylserine ... ...

Abstract	The engulfment function of macrophages relies on complex molecular interactions involving both lipids and proteins. In particular, the clearance of apoptotic bodies (efferocytosis) is enabled by externalization on the cell target of phosphatidylserine lipids, which activate receptors on macrophages, suggesting that (local) specific lipid-protein interactions are required at least for the initiation of efferocytosis. However, in addition to apoptotic cells, macrophages can engulf foreign bodies that vary substantially in size from a few nanometers to microns, suggesting that nonspecific interactions over a wide range of length scales could be relevant. Here, we use model lipid membranes (made of phosphatidylcholine, phosphatidylserine, and ceramide) and rat alveolar macrophages to show how lipid bilayer properties probed by small-angle x-ray scattering and solid-state (2)H NMR correlate with engulfment rates measured by flow cytometry. We find that engulfment of protein-free model lipid vesicles is promoted by the presence of phosphatidylserine lipids but inhibited by ceramide, in accord with a previous study of apoptotic cells. We conclude that the roles of phosphatidylserine and ceramide in phagocytosis is based, at least in part, on lipid-mediated modification of membrane physical properties, including interactions at large length scales as well as local lipid ordering and possible domain formation.
MeSH term(s)	Animals ; Cell Line ; Ceramides/chemistry ; Ceramides/metabolism ; Lipid Bilayers/chemistry ; Lipid Bilayers/metabolism ; Liposomes/chemistry ; Liposomes/metabolism ; Macrophages/metabolism ; Phagocytosis ; Phosphatidylcholines/chemistry ; Phosphatidylcholines/metabolism ; Phosphatidylserines/chemistry ; Phosphatidylserines/metabolism ; Protein Binding ; Pulmonary Alveoli/cytology ; Rats
Chemical Substances	Ceramides ; Lipid Bilayers ; Liposomes ; Phosphatidylcholines ; Phosphatidylserines
Language	English
Publishing date	2014-02-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2013.12.036
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 235: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 2: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Alpha-1 antitrypsin supplementation improves alveolar macrophages efferocytosis and phagocytosis following cigarette smoke exposure.

Serban, Karina A / Petrusca, Daniela N / Mikosz, Andrew / Poirier, Christophe / Lockett, Angelia D / Saint, Lauren / Justice, Matthew J / Twigg, Homer L / Campos, Michael A / Petrache, Irina

PloS one

2017 Volume 12, Issue 4, Page(s) e0176073

Abstract: Cigarette smoking (CS), the main risk factor for COPD (chronic obstructive pulmonary disease) in developed countries, decreases alveolar macrophages (AM) clearance of both apoptotic cells and bacterial pathogens. This global deficit of AM engulfment may ... ...

Abstract	Cigarette smoking (CS), the main risk factor for COPD (chronic obstructive pulmonary disease) in developed countries, decreases alveolar macrophages (AM) clearance of both apoptotic cells and bacterial pathogens. This global deficit of AM engulfment may explain why active smokers have worse outcomes of COPD exacerbations, episodes characterized by airway infection and inflammation that carry high morbidity and healthcare cost. When administered as intravenous supplementation, the acute phase-reactant alpha-1 antitrypsin (A1AT) reduces the severity of COPD exacerbations in A1AT deficient (AATD) individuals and of bacterial pneumonia in murine models, but the effect of A1AT on AM scavenging functions has not been reported. Apoptotic cell clearance (efferocytosis) was measured in human AM isolated from patients with COPD, in primary rat AM or differentiated monocytes exposed to CS ex vivo, and in AM recovered from mice exposed to CS. A1AT (100 μg/mL, 16 h) significantly ameliorated efferocytosis (by ~50%) in AM of active smokers or AM exposed ex vivo to CS. A1AT significantly improved AM global engulfment, including phagocytosis, even when cells were simultaneously challenged with apoptotic and Fc-coated (bacteria-like) targets. The improved efferocytosis in A1AT-treated macrophages was associated with inhibition of tumor necrosis factor-α converting enzyme (TACE) activity, decreased mannose receptor shedding, and markedly increased abundance of efferocytosis receptors (mannose- and phosphatidyl serine receptors and the scavenger receptor B2) on AM plasma membrane. Directed airway A1AT treatment (via inhalation of a nebulized solution) restored in situ airway AM efferocytosis after CS exposure in mice. The amelioration of CS-exposed AM global engulfment may render A1AT as a potential therapy for COPD exacerbations.
MeSH term(s)	ADAM17 Protein/metabolism ; Adult ; Animals ; Bronchoalveolar Lavage Fluid/cytology ; Case-Control Studies ; Cells, Cultured ; Female ; Humans ; Macrophages, Alveolar/drug effects ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/metabolism ; Male ; Mice, Inbred C57BL ; Middle Aged ; Phagocytosis/drug effects ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/immunology ; Pulmonary Disease, Chronic Obstructive/pathology ; Rats ; Rats, Sprague-Dawley ; Smoke/adverse effects ; Nicotiana/chemistry ; Nicotiana/metabolism ; alpha 1-Antitrypsin/analysis ; alpha 1-Antitrypsin/metabolism ; alpha 1-Antitrypsin/pharmacology
Chemical Substances	Smoke ; alpha 1-Antitrypsin ; ADAM17 Protein (EC 3.4.24.86)
Language	English
Publishing date	2017-04-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0176073
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Oncostatin M and TNF-α Induce Alpha-1 Antitrypsin Production in Undifferentiated Adipose Stromal Cells.

Ni, Kevin / Umair Mukhtar Mian, Muhammad / Meador, Catherine / Gill, Amar / Barwinska, Daria / Cao, Danting / Justice, Matthew J / Jiang, Di / Schaefer, Niccolette / Schweitzer, Kelly S / Chu, Hong Wei / March, Keith L / Petrache, Irina

Stem cells and development

2017 Volume 26, Issue 20, Page(s) 1468–1476

Abstract: Alpha-1 antitrypsin (A1AT), a circulating acute-phase reactant antiprotease, is produced and secreted by cells of endodermal epithelial origin, primarily hepatocytes, and by immune cells. Deficiency of A1AT is associated with increased risk of excessive ... ...

Abstract	Alpha-1 antitrypsin (A1AT), a circulating acute-phase reactant antiprotease, is produced and secreted by cells of endodermal epithelial origin, primarily hepatocytes, and by immune cells. Deficiency of A1AT is associated with increased risk of excessive lung inflammation and injury, especially following chronic cigarette smoke (CS) exposure. Exogenous administration of mesenchymal progenitor cells, including adipose tissue-derived stromal/stem cells (ASC), alleviates CS-induced lung injury through paracrine effectors such as growth factors. It is unknown, however, if mesodermal ASC can secrete functional A1AT and if CS exposure affects their A1AT production. Human ASC collected via liposuction from nonsmoking or smoking donors were stimulated by inflammatory cytokines tumor necrosis alpha (TNFα), oncostatin M (OSM), and/or dexamethasone (DEX) or were exposed to sublethal concentrations of ambient air control or CS extract (0.5%-2%). We detected minimal expression and secretion of A1AT by cultured ASC during unstimulated conditions, which significantly increased following stimulation with TNFα or OSM. Furthermore, TNFα and OSM synergistically enhanced A1AT expression and secretion, which were further increased by DEX. The A1AT transcript variant produced by stimulated ASC resembled that produced by bronchial epithelial cells rather than the variant produced by monocytes/macrophages. While the cigarette smoking status of the ASC donor had no measurable effect on the ability of ASC to induce A1AT expression, active exposure to CS extract markedly reduced A1AT expression and secretion by cultured ASC, as well as human tracheobronchial epithelial cells. ASC-secreted A1AT covalently complexed with neutrophil elastase in control ASC, but not in cells transfected with A1AT siRNA. Undifferentiated ASC may require priming to secrete functional A1AT, a potent antiprotease that may be relevant to stem cell therapeutic effects.
MeSH term(s)	Adipose Tissue/cytology ; Bronchi/cytology ; Cell Differentiation/drug effects ; Cell Line ; Cigarette Smoking ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Humans ; Leukocyte Elastase/metabolism ; Macrophages/drug effects ; Macrophages/metabolism ; Oncostatin M/pharmacology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Stromal Cells/drug effects ; Stromal Cells/metabolism ; Tumor Necrosis Factor-alpha/pharmacology ; alpha 1-Antitrypsin/genetics ; alpha 1-Antitrypsin/metabolism
Chemical Substances	RNA, Messenger ; Tumor Necrosis Factor-alpha ; alpha 1-Antitrypsin ; Oncostatin M (106956-32-5) ; Leukocyte Elastase (EC 3.4.21.37)
Language	English
Publishing date	2017-09-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2142214-X
ISSN	1557-8534 ; 1547-3287
ISSN (online)	1557-8534
ISSN	1547-3287
DOI	10.1089/scd.2017.0099
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 3616: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito