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Article ; Online: A Non-canonical Pathway with Potential for Safer Modulation of Transforming Growth Factor-β1 in Steroid-Resistant Airway Diseases.

Li, Meina / Keenan, Christine R / Lopez-Campos, Guillermo / Mangum, Jonathan E / Chen, Qianyu / Prodanovic, Danica / Xia, Yuxiu C / Langenbach, Shenna Y / Harris, Trudi / Hofferek, Vinzenz / Reid, Gavin E / Stewart, Alastair G

iScience

2019 Volume 12, Page(s) 232–246

Abstract: Impaired therapeutic responses to anti-inflammatory glucocorticoids (GC) in chronic respiratory diseases are partly attributable to interleukins and transforming growth factor β1 (TGF-β1). However, previous efforts to prevent induction of GC ... ...

Abstract	Impaired therapeutic responses to anti-inflammatory glucocorticoids (GC) in chronic respiratory diseases are partly attributable to interleukins and transforming growth factor β1 (TGF-β1). However, previous efforts to prevent induction of GC insensitivity by targeting established canonical and non-canonical TGF-β1 pathways have been unsuccessful. Here we elucidate a TGF-β1 signaling pathway modulating GC activity that involves LIM domain kinase 2-mediated phosphorylation of cofilin1. Severe, steroid-resistant asthmatic airway epithelium showed increased levels of immunoreactive phospho-cofilin1. Phospho-cofilin1 was implicated in the activation of phospholipase D (PLD) to generate the effector(s) (lyso)phosphatidic acid, which mimics the TGF-β1-induced GC insensitivity. TGF-β1 induction of the nuclear hormone receptor corepressor, SMRT (NCOR2), was dependent on cofilin1 and PLD activities. Depletion of SMRT prevented GC insensitivity. This pathway for GC insensitivity offers several promising drug targets that potentially enable a safer approach to the modulation of TGF-β1 in chronic inflammatory diseases than is afforded by global TGF-β1 inhibition.
Language	English
Publishing date	2019-01-21
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2019.01.023
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Article ; Online: Integrin α7 expression is increased in asthmatic patients and its inhibition reduces Kras protein abundance in airway smooth muscle cells.

Teoh, Chun Ming / Tan, Sheryl S L / Langenbach, Shenna Y / Wong, Amanda H / Cheong, Dorothy H J / Tam, John K C / New, Chih Sheng / Tran, Thai

Scientific reports

2019 Volume 9, Issue 1, Page(s) 9892

Abstract: Airway smooth muscle (ASM) cells exhibit plastic phenotypic behavior marked by reversible modulation and maturation between contractile and proliferative phenotypic states. Integrins are a class of transmembrane proteins that have been implicated as ... ...

Abstract	Airway smooth muscle (ASM) cells exhibit plastic phenotypic behavior marked by reversible modulation and maturation between contractile and proliferative phenotypic states. Integrins are a class of transmembrane proteins that have been implicated as novel therapeutic targets for asthma treatment. We previously showed that integrin α7 is a novel marker of the contractile ASM phenotype suggesting that targeting this protein may offer new avenues to counter the increase in ASM cell mass that underlies airways hyperresponsiveness (AHR) in asthma. We now determine whether inhibition of integrin α7 expression would revert ASM cells back to a proliferative phenotype to cause an increase in ASM cell mass. This would be detrimental to asthmatic patients who already exhibit increased ASM mass in their airways. Using immunohistochemical analysis of the Melbourne Epidemiological Study of Childhood Asthma (MESCA) cohort, we show for the first time that integrin α7 expression in patients with severe asthma is increased, supporting a clinically relevant role for this protein in asthma pathophysiology. Moreover, inhibition of the laminin-integrin α7 signaling axis results in a reduction in smooth muscle-alpha actin abundance and does not revert ASM cells back to a proliferative phenotype. We determined that integrin α7-induced Kras isoform of p21 Ras acts as a point of convergence between contractile and proliferative ASM phenotypic states. Our study provides further support for targeting integrin α7 for the development of novel anti-asthma therapies.
MeSH term(s)	Antigens, CD/genetics ; Antigens, CD/metabolism ; Asthma/genetics ; Asthma/metabolism ; Asthma/pathology ; Biomarkers/metabolism ; Humans ; Integrin alpha Chains/genetics ; Integrin alpha Chains/metabolism ; Muscle, Smooth/metabolism ; Muscle, Smooth/pathology ; Mutation ; Phenotype ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Respiratory System/metabolism ; Respiratory System/pathology ; Signal Transduction
Chemical Substances	Antigens, CD ; Biomarkers ; Integrin alpha Chains ; KRAS protein, human ; integrin alpha7 ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2019-07-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-46260-2
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Article ; Online: Glucocorticoid Insensitivity in Virally Infected Airway Epithelial Cells Is Dependent on Transforming Growth Factor-β Activity.

Xia, Yuxiu C / Radwan, Asmaa / Keenan, Christine R / Langenbach, Shenna Y / Li, Meina / Radojicic, Danica / Londrigan, Sarah L / Gualano, Rosa C / Stewart, Alastair G

PLoS pathogens

2017 Volume 13, Issue 1, Page(s) e1006138

Abstract: Asthma and chronic obstructive pulmonary disease (COPD) exacerbations are commonly associated with respiratory syncytial virus (RSV), rhinovirus (RV) and influenza A virus (IAV) infection. The ensuing airway inflammation is resistant to the anti- ... ...

Abstract	Asthma and chronic obstructive pulmonary disease (COPD) exacerbations are commonly associated with respiratory syncytial virus (RSV), rhinovirus (RV) and influenza A virus (IAV) infection. The ensuing airway inflammation is resistant to the anti-inflammatory actions of glucocorticoids (GCs). Viral infection elicits transforming growth factor-β (TGF-β) activity, a growth factor we have previously shown to impair GC action in human airway epithelial cells through the activation of activin-like kinase 5 (ALK5), the type 1 receptor of TGF-β. In the current study, we examine the contribution of TGF-β activity to the GC-resistance caused by viral infection. We demonstrate that viral infection of human bronchial epithelial cells with RSV, RV or IAV impairs GC anti-inflammatory action. Poly(I:C), a synthetic analog of double-stranded RNA, also impairs GC activity. Both viral infection and poly(I:C) increase TGF-β expression and activity. Importantly, the GC impairment was attenuated by the selective ALK5 (TGFβRI) inhibitor, SB431542 and prevented by the therapeutic agent, tranilast, which reduced TGF-β activity associated with viral infection. This study shows for the first time that viral-induced glucocorticoid-insensitivity is partially mediated by activation of endogenous TGF-β.
MeSH term(s)	Anti-Inflammatory Agents/pharmacology ; Antiviral Agents/pharmacology ; Asthma/pathology ; Asthma/virology ; Benzamides/pharmacology ; Cell Line ; Dioxoles/pharmacology ; Drug Resistance, Viral/physiology ; Enzyme Activation ; Epithelial Cells/virology ; Glucocorticoids/pharmacology ; Humans ; Influenza A virus ; Influenza, Human/virology ; Picornaviridae Infections/virology ; Poly I-C/pharmacology ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Protein-Serine-Threonine Kinases/metabolism ; Pulmonary Disease, Chronic Obstructive/pathology ; Pulmonary Disease, Chronic Obstructive/virology ; Receptor, Transforming Growth Factor-beta Type I ; Receptors, Transforming Growth Factor beta/antagonists & inhibitors ; Receptors, Transforming Growth Factor beta/metabolism ; Respiratory Mucosa/virology ; Respiratory Syncytial Virus Infections/virology ; Respiratory Syncytial Viruses ; Rhinovirus ; Transforming Growth Factor beta/metabolism ; ortho-Aminobenzoates/pharmacology
Chemical Substances	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide ; Anti-Inflammatory Agents ; Antiviral Agents ; Benzamides ; Dioxoles ; Glucocorticoids ; Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta ; ortho-Aminobenzoates ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; TGFBR1 protein, human (EC 2.7.11.30) ; tranilast (HVF50SMY6E) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2017-01-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1006138
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Article: Annexin-1 signals mitogen-stimulated breast tumor cell proliferation by activation of the formyl peptide receptors (FPRs) 1 and 2

Khau, Thippadey / Langenbach, Shenna Y / Schuliga, Michael / Harris, Trudi / Johnstone, Cameron N / Anderson, Robin L / Stewart, Alastair G

FASEB journal. 2011 Feb., v. 25, no. 2

2011

Abstract: The role of the calcium- and phospholipid-binding protein annexin I (ANXA1) in cell cycle regulation has been investigated in estrogen receptor (ER)-positive MCF-7 and ER-negative MDA-MB-231 breast tumor cell lines. In MCF-7 cells, ANXA1-targeting small ... ...

Abstract	The role of the calcium- and phospholipid-binding protein annexin I (ANXA1) in cell cycle regulation has been investigated in estrogen receptor (ER)-positive MCF-7 and ER-negative MDA-MB-231 breast tumor cell lines. In MCF-7 cells, ANXA1-targeting small interfering RNA (siRNA) reduced ANXA1 mRNA and protein levels and attenuated cell proliferation induced by FCS, estradiol, or epidermal growth factor. Well-characterized agonists for the known ANXA1 receptor, FPR2, including the ANXA1 N-terminal proteolytic product ANXA1₂₋₂₆, lipoxin A₄ (LXA₄), and the synthetic peptide, Trp-Lys-Tyr-Met-Val-D-Met (WKYMVm), stimulated proliferation of MCF-7 and MDA-MB-231 cells that was attenuated by incubation with FPR2 antagonists WRW₄ (1 μM) or Boc2 (100 nM) or by siRNA against FPR2. FCS-induced mitogenic responses were attenuated by each of the FPR antagonists and by siRNA against FPR2 and, to a lesser extent, FPR1. LXA₄ increased phosphorylation of Akt, p70S⁶K but not ERK1/2. Increases in cyclin D1 protein induced by FCS or LXA₄ were blocked by the PI3 kinase inhibitor, LY294002, and attenuated by FPR2 antagonism using Boc2. In invasive breast cancer, immunohistochemistry revealed the presence of ANXA1 and its receptor, FPR2, in both tumor epithelium and stromal cells. These observations suggest a novel signaling role for ANXA1 in mitogen-activated proliferation of breast tumor epithelial cells that is mediated via activation of FPR1 and FPR2.--Khau, T., Langenbach, S. Y., Schuliga, M., Harris, T., Johnstone, C. N., Anderson, R. L., Stewart, A. G. Annexin-1 signals mitogen-stimulated breast tumor cell proliferation by activation of the formyl peptide receptors (FPRs) 1 and 2.
Language	English
Dates of publication	2011-02
Size	p. 483-496.
Publishing place	The Federation of American Societies for Experimental Biology
Document type	Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
Database	NAL-Catalogue (AGRICOLA)

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Article: Casein Kinase 1δ/ε Inhibitor, PF670462 Attenuates the Fibrogenic Effects of Transforming Growth Factor-β in Pulmonary Fibrosis.

Keenan, Christine R / Langenbach, Shenna Y / Jativa, Fernando / Harris, Trudi / Li, Meina / Chen, Qianyu / Xia, Yuxiu / Gao, Bryan / Schuliga, Michael J / Jaffar, Jade / Prodanovic, Danica / Tu, Yan / Berhan, Asres / Lee, Peter V S / Westall, Glen P / Stewart, Alastair G

Frontiers in pharmacology

2018 Volume 9, Page(s) 738

Abstract: Transforming growth factor-beta (TGF-β) is a major mediator of fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). However, therapeutic global inhibition of TGF-β is limited by unwanted immunosuppression and mitral valve defects. We ... ...

Abstract	Transforming growth factor-beta (TGF-β) is a major mediator of fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). However, therapeutic global inhibition of TGF-β is limited by unwanted immunosuppression and mitral valve defects. We performed an extensive literature search to uncover a little-known connection between TGF-β signaling and casein kinase (CK) activity. We have examined the abundance of CK1 delta and epsilon (CK1δ/ε) in lung tissue from IPF patients and non-diseased controls, and investigated whether inhibition of CK1δ/ε with PF670462 inhibits pulmonary fibrosis. CK1δ/ε levels in lung tissue from IPF patients and non-diseased controls were assessed by immunohistochemistry. Anti-fibrotic effects of the CK1δ/ε inhibitor PF670462 were assessed in pre-clinical models, including acute and chronic bleomycin mouse models and
Language	English
Publishing date	2018-07-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2018.00738
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Article ; Online: The lung inflammation and skeletal muscle wasting induced by subchronic cigarette smoke exposure are not altered by a high-fat diet in mice.

Hansen, Michelle J / Chen, Hui / Jones, Jessica E / Langenbach, Shenna Y / Vlahos, Ross / Gualano, Rosa C / Morris, Margaret J / Anderson, Gary P

PloS one

2013 Volume 8, Issue 11, Page(s) e80471

Abstract: Obesity and cigarette smoking independently constitute major preventable causes of morbidity and mortality and obesity is known to worsen lung inflammation in asthma. Paradoxically, higher body mass index (BMI) is associated with reduced mortality in ... ...

Abstract	Obesity and cigarette smoking independently constitute major preventable causes of morbidity and mortality and obesity is known to worsen lung inflammation in asthma. Paradoxically, higher body mass index (BMI) is associated with reduced mortality in smoking induced COPD whereas low BMI increases mortality risk. To date, no study has investigated the effect of a dietary-induced obesity and cigarette smoke exposure on the lung inflammation and loss of skeletal muscle mass in mice. Male BALB/c mice were exposed to 4 cigarettes/day, 6 days/week for 7 weeks, or sham handled. Mice consumed either standard laboratory chow (3.5 kcal/g, 12% fat) or a high fat diet (HFD, 4.3 kcal/g, 32% fat). Mice exposed to cigarette smoke for 7 weeks had significantly more inflammatory cells in the BALF (P<0.05) and the mRNA expression of pro-inflammatory cytokines and chemokines was significantly increased (P<0.05); HFD had no effect on these parameters. Sham- and smoke-exposed mice consuming the HFD were significantly heavier than chow fed animals (12 and 13%, respectively; P<0.05). Conversely, chow and HFD fed mice exposed to cigarette smoke weighed 16 and 15% less, respectively, compared to sham animals (P<0.05). The skeletal muscles (soleus, tibialis anterior and gastrocnemius) of cigarette smoke-exposed mice weighed significantly less than sham-exposed mice (P<0.05) and the HFD had no protective effect. For the first time we report that cigarette smoke exposure significantly decreased insulin-like growth factor-1 (IGF-1) mRNA expression in the gastrocnemius and tibialis anterior and IGF-1 protein in the gastrocnemius (P<0.05). We have also shown that cigarette smoke exposure reduced circulating IGF-1 levels. IL-6 mRNA expression was significantly elevated in all three skeletal muscles of chow fed smoke-exposed mice (P<0.05). In conclusion, these findings suggest that a down-regulation in local IGF-1 may be responsible for the loss of skeletal muscle mass following cigarette smoke exposure in mice.
MeSH term(s)	Animals ; Body Weight ; Bronchoalveolar Lavage Fluid/chemistry ; Bronchoalveolar Lavage Fluid/cytology ; Chemokines/genetics ; Chemokines/metabolism ; Cytokines/genetics ; Cytokines/metabolism ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Gene Expression ; Insulin-Like Growth Factor I/metabolism ; Lung/metabolism ; Lung/pathology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Atrophy/etiology ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; Organ Size ; Pneumonia/etiology ; Pneumonia/metabolism ; Pneumonia/pathology ; Smoking/adverse effects
Chemical Substances	Chemokines ; Cytokines ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2013-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0080471
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Article ; Online: CD151, a laminin receptor showing increased expression in asthmatic patients, contributes to airway hyperresponsiveness through calcium signaling.

Qiao, Yongkang / Tam, John Kit Chung / Tan, Sheryl S L / Tai, Yee Kit / Chin, Chin Yein / Stewart, Alastair G / Ashman, Leonie / Sekiguchi, Kiyotoshi / Langenbach, Shenna Y / Stelmack, Gerald / Halayko, Andrew J / Tran, Thai

The Journal of allergy and clinical immunology

2016 Volume 139, Issue 1, Page(s) 82–92.e5

Abstract: Background: Airway smooth muscle (ASM) contraction underpins airway constriction; however, underlying mechanisms for airway hyperresponsiveness (AHR) remain incompletely defined. CD151, a 4-transmembrane glycoprotein that associates with laminin-binding ...

Abstract	Background: Airway smooth muscle (ASM) contraction underpins airway constriction; however, underlying mechanisms for airway hyperresponsiveness (AHR) remain incompletely defined. CD151, a 4-transmembrane glycoprotein that associates with laminin-binding integrins, is highly expressed in the human lung. The role of CD151 in ASM function and its relationship to asthma have yet to be elucidated. Objective: We sought to ascertain whether CD151 expression is clinically relevant to asthma and whether CD151 expression affects AHR. Methods: Using immunohistochemical analysis, we determined the expression of CD151 in human bronchial biopsy specimens from patients with varying asthma severities and studied the mechanism of action of CD151 in the regulation of ASM contraction and bronchial caliber in vitro, ex vivo, and in vivo. Results: The number of CD151 Conclusions: We identify a role for CD151 in human ASM contraction. We implicate CD151 as a determinant of AHR in vivo, likely through regulation of GPCR-induced calcium and PKC signaling. These observations have significant implications in understanding the mechanism for AHR and the efficacy of new and emerging therapeutics.
MeSH term(s)	Adult ; Animals ; Asthma/metabolism ; Asthma/physiopathology ; Bronchoalveolar Lavage Fluid ; Calcium Signaling ; Cell Line ; Cells, Cultured ; Female ; Humans ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Protein Kinase C/metabolism ; Respiratory System/cytology ; Respiratory System/metabolism ; Respiratory System/physiopathology ; Tetraspanin 24/genetics ; Tetraspanin 24/metabolism
Chemical Substances	CD151 protein, human ; Tetraspanin 24 ; Protein Kinase C (EC 2.7.11.13)
Language	English
Publishing date	2016-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2016.03.029
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Article ; Online: IL-17A and serum amyloid A are elevated in a cigarette smoke cessation model associated with the persistence of pigmented macrophages, neutrophils and activated NK cells.

Hansen, Michelle J / Chan, Sheau Pyng J / Langenbach, Shenna Y / Dousha, Lovisa F / Jones, Jessica E / Yatmaz, Selcuk / Seow, Huei Jiunn / Vlahos, Ross / Anderson, Gary P / Bozinovski, Steven

PloS one

2014 Volume 9, Issue 11, Page(s) e113180

Abstract: While global success in cessation advocacy has seen smoking rates fall in many developed countries, persistent lung inflammation in ex-smokers is an increasingly important clinical problem whose mechanistic basis remains poorly understood. In this study, ...

Abstract	While global success in cessation advocacy has seen smoking rates fall in many developed countries, persistent lung inflammation in ex-smokers is an increasingly important clinical problem whose mechanistic basis remains poorly understood. In this study, candidate effector mechanisms were assessed in mice exposed to cigarette smoke (CS) for 4 months following cessation from long term CS exposure. BALF neutrophils, CD4+ and CD8+ T cells and lung innate NK cells remained significantly elevated following smoking cessation. Analysis of neutrophil mobilization markers showed a transition from acute mediators (MIP-2α, KC and G-CSF) to sustained drivers of neutrophil and macrophage recruitment and activation (IL-17A and Serum Amyoid A (SAA)). Follicle-like lymphoid aggregates formed with CS exposure and persisted with cessation, where they were in close anatomical proximity to pigmented macrophages, whose number actually increased 3-fold following CS cessation. This was associated with the elastolytic protease, MMP-12 (macrophage metallo-elastase) which remained significantly elevated post-cessation. Both GM-CSF and CSF-1 were significantly increased in the CS cessation group relative to the control group. In conclusion, we show that smoking cessation mediates a transition to accumulation of pigmented macrophages, which may contribute to the expanded macrophage population observed in COPD. These macrophages together with IL-17A, SAA and innate NK cells are identified here as candidate persistence determinants and, we suggest, may represent specific targets for therapies directed towards the amelioration of chronic airway inflammation.
MeSH term(s)	Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Bronchoalveolar Lavage Fluid/cytology ; Flow Cytometry ; Interleukin-17/blood ; Killer Cells, Natural/pathology ; Killer Cells, Natural/physiology ; Macrophages, Alveolar/pathology ; Macrophages, Alveolar/physiology ; Male ; Matrix Metalloproteinase 12/metabolism ; Mice ; Mice, Inbred BALB C ; Models, Animal ; Neutrophils/pathology ; Neutrophils/physiology ; Real-Time Polymerase Chain Reaction ; Serum Amyloid A Protein/metabolism ; Smoking Cessation ; Tobacco Smoke Pollution/adverse effects
Chemical Substances	Interleukin-17 ; Serum Amyloid A Protein ; Tobacco Smoke Pollution ; Matrix Metalloproteinase 12 (EC 3.4.24.65)
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0113180
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Article ; Online: Annexin-1 signals mitogen-stimulated breast tumor cell proliferation by activation of the formyl peptide receptors (FPRs) 1 and 2.

Khau, Thippadey / Langenbach, Shenna Y / Schuliga, Michael / Harris, Trudi / Johnstone, Cameron N / Anderson, Robin L / Stewart, Alastair G

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

2010 Volume 25, Issue 2, Page(s) 483–496

Abstract	The role of the calcium- and phospholipid-binding protein annexin I (ANXA1) in cell cycle regulation has been investigated in estrogen receptor (ER)-positive MCF-7 and ER-negative MDA-MB-231 breast tumor cell lines. In MCF-7 cells, ANXA1-targeting small interfering RNA (siRNA) reduced ANXA1 mRNA and protein levels and attenuated cell proliferation induced by FCS, estradiol, or epidermal growth factor. Well-characterized agonists for the known ANXA1 receptor, FPR2, including the ANXA1 N-terminal proteolytic product ANXA1(2-26), lipoxin A(4) (LXA(4)), and the synthetic peptide, Trp-Lys-Tyr-Met-Val-D-Met (WKYMVm), stimulated proliferation of MCF-7 and MDA-MB-231 cells that was attenuated by incubation with FPR2 antagonists WRW(4) (1 μM) or Boc2 (100 nM) or by siRNA against FPR2. FCS-induced mitogenic responses were attenuated by each of the FPR antagonists and by siRNA against FPR2 and, to a lesser extent, FPR1. LXA(4) increased phosphorylation of Akt, p70(S6K) but not ERK1/2. Increases in cyclin D1 protein induced by FCS or LXA(4) were blocked by the PI3 kinase inhibitor, LY294002, and attenuated by FPR2 antagonism using Boc2. In invasive breast cancer, immunohistochemistry revealed the presence of ANXA1 and its receptor, FPR2, in both tumor epithelium and stromal cells. These observations suggest a novel signaling role for ANXA1 in mitogen-activated proliferation of breast tumor epithelial cells that is mediated via activation of FPR1 and FPR2.
MeSH term(s)	Annexin A1/genetics ; Annexin A1/metabolism ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation ; Chromones/pharmacology ; Enzyme Inhibitors/pharmacology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lipoxins/metabolism ; Mitogens/metabolism ; Mitogens/pharmacology ; Morpholines/pharmacology ; Phosphoinositide-3 Kinase Inhibitors ; RNA Interference ; RNA, Small Interfering ; Receptors, Formyl Peptide/antagonists & inhibitors ; Receptors, Formyl Peptide/genetics ; Receptors, Formyl Peptide/metabolism ; Receptors, Lipoxin/antagonists & inhibitors ; Receptors, Lipoxin/genetics ; Receptors, Lipoxin/metabolism ; Signal Transduction
Chemical Substances	Annexin A1 ; Chromones ; Enzyme Inhibitors ; FPR1 protein, human ; FPR2 protein, human ; Lipoxins ; Mitogens ; Morpholines ; Phosphoinositide-3 Kinase Inhibitors ; RNA, Small Interfering ; Receptors, Formyl Peptide ; Receptors, Lipoxin ; lipoxin A4 ; 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (31M2U1DVID)
Language	English
Publishing date	2010-10-07
Publishing country	United States
Document type	Journal Article ; 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.09-154096
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Article ; Online: Functional expression of IgG-Fc receptors in human airway smooth muscle cells.

Xia, YuXiu C / Schuliga, Michael / Shepherd, Malcolm / Powell, Maree / Harris, Trudi / Langenbach, Shenna Y / Tan, Peck Szee / Gerthoffer, William T / Hogarth, P Mark / Stewart, Alastair G / Mackay, Graham A

American journal of respiratory cell and molecular biology

2010 Volume 44, Issue 5, Page(s) 665–672

Abstract: IgE-Fc receptors and IgG-Fc receptors are expressed on hematopoietic cells, but some evidence suggests that these receptors are also found on nonhematopoietic cells, including human airway smooth muscle (hASM) cells. Our study characterizes the ... ...

Abstract	IgE-Fc receptors and IgG-Fc receptors are expressed on hematopoietic cells, but some evidence suggests that these receptors are also found on nonhematopoietic cells, including human airway smooth muscle (hASM) cells. Our study characterizes the expression of IgE-Fc receptors (FcεRI/CD23) and IgG-Fc receptors (FcγRs-I, -II, and -III) in cultured hASM cells by flow cytometry and Western blotting, and the functional activity of receptors was determined through quantification of cell proliferation and released cytokines. Expression of Fc receptor-linked intracellular signaling proteins and phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase 1/2 and p38(MAPK) in hASM cells was examined by Western blotting. Expression of FcεRI and CD23 was not detectable in hASM cells. However, FcγRI and FcγRII were shown to be expressed on these cells. Specific antibodies, validated using transfected cell lines, revealed that the inhibitory IgG receptor, FcγRIIb, was the most abundant Fc receptor subtype expressed. Although cross-linking FcγR with heat-aggregated γ globulin (HAGG) did not induce detectable cell stimulation, pretreating hASM cells with HAGG significantly inhibited IL-1α-induced increases in cytokine levels and basic fibroblast growth factor-induced cell proliferation. This inhibitory effect of HAGG was abrogated by preincubation of cells with an anti-FcγRIIb antigen-binding fragment (Fab). Expression of proteins involved in the canonical FcγRIIb inhibitory signaling pathway was established in hASM cells. Pretreatment of hASM cells with HAGG significantly inhibited IL-1α- and basic fibroblast growth factor-induced extracellular signal-regulated kinase 1/2 and p38(MAPK) phosphorylation. This study identifies functional expression of FcγRIIb in hASM cells, with the potential to suppress their remodeling and immunomodulatory roles.
MeSH term(s)	Animals ; Bronchi/metabolism ; Cell Proliferation ; Cell Separation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Flow Cytometry ; Gene Expression Regulation, Enzymologic ; Humans ; Immune System ; Immunoglobulin G/chemistry ; MAP Kinase Signaling System ; Mast Cells/cytology ; Mice ; Muscle, Smooth/enzymology ; Myocytes, Smooth Muscle/cytology ; Receptors, Fc/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Immunoglobulin G ; Receptors, Fc ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2010-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2009-0371OC
Database	MEDical Literature Analysis and Retrieval System OnLINE

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