LIVIVO - Search results -

Search results

Result 1 - 10 of total 85

Search options

Article ; Online: Cellular Mechanisms of FGF-Stimulated Tissue Repair.

Prudovsky, Igor

2021 Volume 10, Issue 7

Abstract: Growth factors belonging to the FGF family play important roles in tissue and organ repair after trauma. In this review, I discuss the regulation by FGFs of the aspects of cellular behavior important for reparative processes. In particular, I focus on ... ...

Abstract	Growth factors belonging to the FGF family play important roles in tissue and organ repair after trauma. In this review, I discuss the regulation by FGFs of the aspects of cellular behavior important for reparative processes. In particular, I focus on the FGF-dependent regulation of cell proliferation, cell stemness, de-differentiation, inflammation, angiogenesis, cell senescence, cell death, and the production of proteases. In addition, I review the available literature on the enhancement of FGF expression and secretion in damaged tissues resulting in the increased FGF supply required for tissue repair.
MeSH term(s)	Animals ; Cell Death/genetics ; Cell Dedifferentiation/genetics ; Cell Differentiation/genetics ; Cell Proliferation/genetics ; Cellular Senescence/genetics ; Eukaryotic Cells/cytology ; Eukaryotic Cells/metabolism ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Gene Expression Regulation ; Humans ; Inflammation ; Multigene Family ; Neovascularization, Physiologic/genetics ; Peptide Hydrolases/genetics ; Peptide Hydrolases/metabolism ; Receptors, Fibroblast Growth Factor/genetics ; Receptors, Fibroblast Growth Factor/metabolism ; Regeneration/genetics ; Signal Transduction ; Stem Cells/cytology ; Stem Cells/metabolism
Chemical Substances	Receptors, Fibroblast Growth Factor ; Fibroblast Growth Factors (62031-54-3) ; Peptide Hydrolases (EC 3.4.-)
Language	English
Publishing date	2021-07-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10071830
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Article ; Online: Cellular Mechanisms of FGF-Stimulated Tissue Repair

Igor Prudovsky

Cells, Vol 10, Iss 1830, p

2021 Volume 1830

Abstract	Growth factors belonging to the FGF family play important roles in tissue and organ repair after trauma. In this review, I discuss the regulation by FGFs of the aspects of cellular behavior important for reparative processes. In particular, I focus on the FGF-dependent regulation of cell proliferation, cell stemness, de-differentiation, inflammation, angiogenesis, cell senescence, cell death, and the production of proteases. In addition, I review the available literature on the enhancement of FGF expression and secretion in damaged tissues resulting in the increased FGF supply required for tissue repair.
Keywords	FGF ; repair ; regeneration ; proliferation ; stemness ; de-differentiation ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Tranexamic acid reduces inflammation, edema and burn wound conversion in a rodent model.

Prudovsky, Igor / Kacer, Doreen / Lindner, Volkhard / Rappold, Joseph / Carter, Damien Wilson

Burns : journal of the International Society for Burn Injuries

2024 Volume 50, Issue 4, Page(s) 947–956

Abstract: Burn wound conversion is the observed process where superficial partial thickness burns convert into deep partial or full thickness burn injuries. This conversion process often involves surgical excision to achieve timely wound healing. Unfortunately, ... ...

Abstract	Burn wound conversion is the observed process where superficial partial thickness burns convert into deep partial or full thickness burn injuries. This conversion process often involves surgical excision to achieve timely wound healing. Unfortunately, the pathophysiology of this phenomenon is multifactorial and poorly understood. Thus, a therapeutic intervention that may prevent secondary progression and cell death in burn-injured tissue is desirable. Recent work by our group and others has established that tranexamic acid (TXA) has significant anti-inflammatory properties in addition to its well-known anti-fibrinolytic effects. This study investigates TXA as a novel therapeutic treatment to mitigate burn wound conversion and reduce systemic inflammation. Sprague-Dawley rats were subjected to a hot comb burn contact injury. A subset of animals underwent a similar comb burn with an adjacent 30%TBSA contact injury. The interspaces represent the ischemic zones simulating the zone of stasis. The treatment group received injections of TXA (100 mg/kg) immediately after injury and once daily until euthanasia. Animals were harvested for analyses at 6 h and 7 days after injury. Full-thickness biopsies from the ischemic zones and lung tissue were assessed with established histological techniques. Plasma was collected for measurement of damage associated molecular patterns (DAMPs), and liver samples were used to study inflammatory cytokines expression. Treatment with TXA was associated with reduced burn wound conversion and decreased burn-induced systemic inflammatory response syndrome (SIRS). Lung inflammation and capillary leak were also significantly reduced in TXA treated animals. Future research will elucidate the underlying anti-inflammatory properties of TXA responsible for these findings.
MeSH term(s)	Animals ; Tranexamic Acid/pharmacology ; Tranexamic Acid/therapeutic use ; Burns/drug therapy ; Burns/complications ; Burns/pathology ; Rats, Sprague-Dawley ; Rats ; Antifibrinolytic Agents/pharmacology ; Antifibrinolytic Agents/therapeutic use ; Inflammation/drug therapy ; Disease Models, Animal ; Edema/drug therapy ; Male ; Wound Healing/drug effects ; Skin/drug effects ; Skin/pathology ; Skin/injuries ; Liver/drug effects ; Liver/pathology ; Lung/pathology ; Lung/drug effects ; Lung/metabolism
Chemical Substances	Tranexamic Acid (6T84R30KC1) ; Antifibrinolytic Agents
Language	English
Publishing date	2024-02-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	197308-3
ISSN	1879-1409 ; 0305-4179
ISSN (online)	1879-1409
ISSN	0305-4179
DOI	10.1016/j.burns.2024.01.024
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1250: 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: Nonclassically Secreted Regulators of Angiogenesis.

Prudovsky, Igor

Angiology: open access

2014 Volume 1, Issue 1, Page(s) 1000101

Abstract: Many secreted polypeptide regulators of angiogenesis are devoid of signal peptides. These proteins are released through nonclassical pathways independent of endoplasmic reticulum and Golgi. In most cases, the nonclassical protein export is induced by ... ...

Abstract	Many secreted polypeptide regulators of angiogenesis are devoid of signal peptides. These proteins are released through nonclassical pathways independent of endoplasmic reticulum and Golgi. In most cases, the nonclassical protein export is induced by stress. It usually serves to stimulate repair or inflammation in damaged tissues. We review the secreted signal peptide-less regulators of angiogenesis and discuss the mechanisms and biological significance of their unconventional export.
Language	English
Publishing date	2014-01-05
Publishing country	United States
Document type	Journal Article
ISSN	2329-9495
ISSN	2329-9495
DOI	10.4172/2329-9495.1000101
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Endothelial IL17RD promotes Western diet-induced aortic myeloid cell infiltration.

Pande, Shivangi / Vary, Calvin / Yang, Xuehui / Liaw, Lucy / Gower, Lindsey / Friesel, Robert / Prudovsky, Igor / Ryzhov, Sergey

Biochemical and biophysical research communications

2024 Volume 701, Page(s) 149552

Abstract: The Interleukin-17 (IL17) family is a group of cytokines implicated in the etiology of several inflammatory diseases. Interleukin-17 receptor D (IL17RD), also known as Sef (similar expression to fibroblast growth factor) belonging to the family of IL17 ... ...

Abstract	The Interleukin-17 (IL17) family is a group of cytokines implicated in the etiology of several inflammatory diseases. Interleukin-17 receptor D (IL17RD), also known as Sef (similar expression to fibroblast growth factor) belonging to the family of IL17 receptors, has been shown to modulate IL17A-associated inflammatory phenotypes. The objective of this study was to test the hypothesis that IL17RD promotes endothelial cell activation and consequent leukocyte adhesion. We utilized primary human aortic endothelial cells and demonstrated that RNAi targeting of IL17RD suppressed transcript levels by 83 % compared to non-targeted controls. Further, RNAi knockdown of IL17RD decreased the adhesion of THP-1 monocytic cells onto a monolayer of aortic endothelial cells in response to IL17A. Additionally, we determined that IL17A did not significantly enhance the activation of canonical MAPK and NFκB pathways in endothelial cells, and further did not significantly affect the expression of VCAM-1 and ICAM-1 in aortic endothelial cells, which is contrary to previous findings. We also determined the functional relevance of our findings in vivo by comparing the expression of endothelial VCAM-1 and ICAM-1 and leukocyte infiltration in the aorta in Western diet-fed Il17rd null versus wild-type mice. Our results showed that although Il17rd null mice do not have significant alteration in aortic expression of VCAM-1 and ICAM-1 in endothelial cells, they exhibit decreased accumulation of proinflammatory monocytes and neutrophils, suggesting that endothelial IL17RD induced in vivo myeloid cell accumulation is not dependent on upregulation of VCAM-1 and ICAM-1 expression. We further performed proteomics analysis to identify potential molecular mediators of the IL17A/IL17RD signaling axis. Collectively, our results underscore a critical role for Il17rd in the regulation of aortic myeloid cell infiltration in the context of Western diet feeding.
MeSH term(s)	Humans ; Animals ; Mice ; Intercellular Adhesion Molecule-1/metabolism ; Endothelial Cells/metabolism ; Vascular Cell Adhesion Molecule-1/metabolism ; Receptors, Interleukin-17/genetics ; Receptors, Interleukin-17/metabolism ; Diet, Western ; Aorta/metabolism ; Myeloid Cells/metabolism ; Monocytes/metabolism ; Cell Adhesion ; Receptors, Interleukin/metabolism
Chemical Substances	Intercellular Adhesion Molecule-1 (126547-89-5) ; Vascular Cell Adhesion Molecule-1 ; Receptors, Interleukin-17 ; IL17RD protein, human ; Receptors, Interleukin
Language	English
Publishing date	2024-01-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2024.149552
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 116: 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: Anti-fibrinolytic agent tranexamic acid suppresses the endotoxin-induced expression of Tnfα and Il1α genes in a plasmin-independent manner.

Kacer, Doreen / Machnitzky, Eva / Fung, Angus / Greene, Autumn / Carter, Damien / Rappold, Joseph / Prudovsky, Igor

Transfusion

2023 Volume 63 Suppl 3, Page(s) S168–S176

Abstract: Introduction: Tranexamic acid (TXA) is widely used as an antifibrinolytic agent in hemorrhagic trauma patients. The beneficial effects of TXA exceed the suppression of blood loss and include the ability to decrease inflammation and edema. We found that ... ...

Abstract	Introduction: Tranexamic acid (TXA) is widely used as an antifibrinolytic agent in hemorrhagic trauma patients. The beneficial effects of TXA exceed the suppression of blood loss and include the ability to decrease inflammation and edema. We found that TXA suppresses the release of mitochondrial DNA and enhances mitochondrial respiration. These results allude that TXA could operate through plasmin-independent mechanisms. To address this hypothesis, we compared the effects of TXA on lipopolysaccharide (LPS)-induced expression of proinflammatory cytokines in plasminogen (Plg) null and Plg heterozygous mice. Methods: Plg null and Plg heterozygous mice were injected with LPS and TXA or LPS only. Four hours later, mice were sacrificed and total RNA was prepared from livers and hearts. Real time quantitative polymerase chain reaction with specific primers was used to assess the effects of LPS and TXA on the expression of pro-inflammatory cytokines. Results: LPS enhanced the expression of Tnfα in the livers and hearts of recipient mice. The co-injection of TXA significantly decreased the effect of LPS both in Plg null and heterozygous mice. A similar trend was observed with LPS-induced Il1α expression in hearts and livers. Conclusions: The effects of TXA on the endotoxin-stimulated expression of Tnfα and Il1α in mice do not depend on the inhibition of plasmin generation. These results indicate that TXA has other biologically important target(s) besides plasminogen/plasmin. Fully understanding the molecular mechanisms behind the extensive beneficial effects of TXA and future identification of its targets may lead to improvement in the use of TXA in trauma, cardiac, and orthopedic surgical patients.
MeSH term(s)	Mice ; Animals ; Tranexamic Acid/pharmacology ; Fibrinolysin ; Fibrinolytic Agents ; Endotoxins ; Tumor Necrosis Factor-alpha/genetics ; Lipopolysaccharides/pharmacology ; Antifibrinolytic Agents/pharmacology ; Plasminogen/genetics ; Plasminogen/metabolism ; Hemorrhage
Chemical Substances	Tranexamic Acid (6T84R30KC1) ; Fibrinolysin (EC 3.4.21.7) ; Fibrinolytic Agents ; Endotoxins ; Tumor Necrosis Factor-alpha ; Lipopolysaccharides ; Antifibrinolytic Agents ; Plasminogen (9001-91-6)
Language	English
Publishing date	2023-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	208417-x
ISSN	1537-2995 ; 0041-1132
ISSN (online)	1537-2995
ISSN	0041-1132
DOI	10.1111/trf.17353
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 284: 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: Activated CTHRC1 promotes glycolysis in endothelial cells: Implications for metabolism and angiogenesis.

Toomey, Barbara H / Mitrovic, Sarah A / Lindner-Liaw, Maia / Leon Vazquez, Ruth G / Kacer, Doreen / Ryzhov, Sergey / Prudovsky, Igor / Lindner, Volkhard

Vascular pharmacology

2023 Volume 153, Page(s) 107246

Abstract: CTHRC1 is transiently expressed by activated fibroblasts during tissue repair and in certain cancers, and CTHRC1 derived from osteocytes is detectable in circulation. Because its biological activity is poorly understood, we investigated whether the N ... ...

Abstract	CTHRC1 is transiently expressed by activated fibroblasts during tissue repair and in certain cancers, and CTHRC1 derived from osteocytes is detectable in circulation. Because its biological activity is poorly understood, we investigated whether the N terminus of CTHRC1 encodes a propeptide requiring cleavage to become activated. The effects of full-length versus cleaved recombinant CTHRC1 on endothelial cell metabolism and gene expression were examined in vitro. Respirometry was performed on Cthrc1 null and wildtype mice to obtain evidence for biological activity of CTHRC1 in vivo. Cleavage of the propeptide observed in vitro was attenuated in the presence of protease inhibitors, and cleaved CTHRC1 significantly promoted glycolysis whereas full-length CTHRC1 was less effective. The respiratory exchange ratio was significantly higher in wildtype mice compared to Cthrc1 null mice, supporting the findings of CTHRC1 promoting glycolysis in vivo. Key enzymes involved in glycolysis were significantly upregulated in endothelial cells in response to treatment with CTHRC1. In healthy human subjects, 58% of the cohort had detectable levels of circulating full-length CTHRC1, whereas all subjects with undetectable levels of full-length CTHRC1 (with one exception) had measurable levels of truncated CTHRC1 (88 pg/ml to >400 ng/ml). Our findings support a concept where CTHRC1 induction in activated fibroblasts at sites of ischemia such as tissue injury or cancer functions to increase glycolysis for ATP production under hypoxic conditions, thereby promoting cell survival and tissue repair. By promoting glycolysis under normoxic conditions, CTHRC1 may also be a contributor to the Warburg effect characteristically observed in many cancers.
MeSH term(s)	Animals ; Humans ; Mice ; Angiogenesis ; Endothelial Cells/metabolism ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Mice, Knockout ; Neoplasms
Chemical Substances	CTHRC1 protein, human ; Extracellular Matrix Proteins ; Cthrc1 protein, mouse
Language	English
Publishing date	2023-11-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2082846-9
ISSN	1879-3649 ; 1537-1891 ; 1879-3649
ISSN (online)	1879-3649 ; 1537-1891
ISSN	1879-3649
DOI	10.1016/j.vph.2023.107246
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 591: 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: Tranexamic acid: Beyond antifibrinolysis.

Prudovsky, Igor / Kacer, Doreen / Zucco, Victoria Vieira / Palmeri, Monica / Falank, Carolyne / Kramer, Robert / Carter, Damien / Rappold, Joseph

Transfusion

2022 Volume 62 Suppl 1, Page(s) S301–S312

Abstract: Tranexamic acid (TXA) is a popular antifibrinolytic drug widely used in hemorrhagic trauma patients and cardiovascular, orthopedic, and gynecological surgical patients. TXA binds plasminogen and prevents its maturation to the fibrinolytic enzyme plasmin. ...

Abstract	Tranexamic acid (TXA) is a popular antifibrinolytic drug widely used in hemorrhagic trauma patients and cardiovascular, orthopedic, and gynecological surgical patients. TXA binds plasminogen and prevents its maturation to the fibrinolytic enzyme plasmin. A number of studies have demonstrated the broad life-saving effects of TXA in trauma, superior to those of other antifibrinolytic agents. Besides preventing fibrinolysis and blood loss, TXA has been reported to suppress posttraumatic inflammation and edema. Although the efficiency of TXA transcends simple inhibition of fibrinolysis, little is known about its mechanisms of action besides the suppression of plasmin maturation. Understanding the broader effects of TXA at the cell, organ, and organism levels are required to elucidate its potential mechanisms of action transcending antifibrinolytic activity. In this article, we provide a brief review of the current clinical use of TXA and then focus on the effects of TXA beyond antifibrinolytics such as its anti-inflammatory activity, protection of the endothelial and epithelial monolayers, stimulation of mitochondrial respiration, and suppression of melanogenesis.
MeSH term(s)	Antifibrinolytic Agents/pharmacology ; Antifibrinolytic Agents/therapeutic use ; Blood Coagulation Disorders ; Fibrinolysin/pharmacology ; Fibrinolysin/therapeutic use ; Fibrinolysis ; Hemorrhage ; Humans ; Tranexamic Acid/pharmacology ; Tranexamic Acid/therapeutic use
Chemical Substances	Antifibrinolytic Agents ; Tranexamic Acid (6T84R30KC1) ; Fibrinolysin (EC 3.4.21.7)
Language	English
Publishing date	2022-07-14
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	208417-x
ISSN	1537-2995 ; 0041-1132
ISSN (online)	1537-2995
ISSN	0041-1132
DOI	10.1111/trf.16976
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 284: 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 ▾

Article ; Online: Sustained Inhibition of Proliferative Response After Transient FGF Stimulation Is Mediated by Interleukin 1 Signaling.

Poole, Ashleigh / Kacer, Doreen / Cooper, Emily / Tarantini, Francesca / Prudovsky, Igor

Journal of cellular physiology

2016 Volume 231, Issue 3, Page(s) 650–658

Abstract: Transient FGF stimulation of various cell types results in FGF memory--a sustained blockage of efficient proliferative response to FGF and other growth factors. FGF memory establishment requires HDAC activity, indicating its epigenetic character. FGF ... ...

Abstract	Transient FGF stimulation of various cell types results in FGF memory--a sustained blockage of efficient proliferative response to FGF and other growth factors. FGF memory establishment requires HDAC activity, indicating its epigenetic character. FGF treatment stimulates proinflammatory NFκB signaling, which is also critical for FGF memory formation. The search for FGF-induced mediators of FGF memory revealed that FGF stimulates HDAC-dependent expression of the inflammatory cytokine IL1α. Similarly to FGF, transient cell treatment with recombinant IL1α inhibits the proliferative response to further FGF and EGF stimulation, but does not prevent FGF receptor-mediated signaling. Interestingly, like cells pretreated with FGF1, cells pretreated with IL1α exhibit enhanced restructuring of actin cytoskeleton and increased migration in response to FGF stimulation. IRAP, a specific inhibitor of IL 1 receptor, and a neutralizing anti-IL1α antibody prevent the formation of FGF memory and rescue an efficient proliferative response to FGF restimulation. A similar effect results following treatment with the anti-inflammatory agents aspirin and dexamethasone. Thus, FGF memory is mediated by proinflammatory IL1 signaling. It may play a role in the limitation of proliferative response to tissue damage and prevention of wound-induced hyperplasia.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Cell Proliferation/drug effects ; Cells, Cultured ; Fibroblast Growth Factors/metabolism ; Fibroblast Growth Factors/pharmacology ; Interleukin-1/metabolism ; Mice ; NF-kappa B/metabolism ; Signal Transduction/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Interleukin-1 ; NF-kappa B ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.25111
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.212: 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)

Order via subito

Details ▾

Article ; Online: Protective role of ErbB3 signaling in myeloid cells during adaptation to cardiac pressure overload.

Yin, Haifeng / Favreau-Lessard, Amanda J / deKay, Joanne T / Herrmann, Yodit R / Robich, Michael P / Koza, Robert A / Prudovsky, Igor / Sawyer, Douglas B / Ryzhov, Sergey

Journal of molecular and cellular cardiology

2020 Volume 152, Page(s) 1–16

Abstract: Background: Myeloid cells play an important role in a wide variety of cardiovascular disorders, including both ischemic and non-ischemic cardiomyopathies. Neuregulin-1 (NRG-1)/ErbB signaling has recently emerged as an important factor contributing to ... ...

Abstract	Background: Myeloid cells play an important role in a wide variety of cardiovascular disorders, including both ischemic and non-ischemic cardiomyopathies. Neuregulin-1 (NRG-1)/ErbB signaling has recently emerged as an important factor contributing to the control of inflammatory activation of myeloid cells after an ischemic injury. However, the role of ErbB signaling in myeloid cells in non-ischemic cardiomyopathy is not fully understood. This study investigated the role of ErbB3 receptors in the regulation of early adaptive response using a mouse model of transverse aortic constriction (TAC) for non-ischemic cardiomyopathy. Methods and results: TAC surgery was performed in groups of age- and sex-matched myeloid cell-specific ErbB3-deficient mice (ErbB3 Conclusion: Our data demonstrate the crucial role of myeloid cell-specific ErbB3 signaling in the cardiac accumulation of myeloid cells, which contributes to the activation of cardiac endothelial cells and fibroblasts and development of an early adaptive response to cardiac pressure overload in male mice.
MeSH term(s)	Adaptation, Physiological ; Animals ; Cardiomegaly/etiology ; Cardiomegaly/metabolism ; Cardiomegaly/pathology ; Cardiomegaly/prevention & control ; Disease Models, Animal ; Female ; Hypertrophy, Left Ventricular/etiology ; Hypertrophy, Left Ventricular/metabolism ; Hypertrophy, Left Ventricular/pathology ; Hypertrophy, Left Ventricular/prevention & control ; Male ; Mice ; Mice, Knockout ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Receptor, ErbB-3/physiology
Chemical Substances	ErbB3 protein, mouse (EC 2.7.10.1) ; Receptor, ErbB-3 (EC 2.7.10.1)
Language	English
Publishing date	2020-11-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2020.11.009
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 426: 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

To top

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

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

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito