NDLI: Different activation forms of MMP-2 oppositely affect the fate of endothelial cells.

Please wait, while we are loading the content...

Stimulation of neuronal $K_{ATP}$ channels by cGMP-dependent protein kinase: involvement of ROS and 5-hydroxydecanoate-sensitive factors in signal transduction

American Journal of Physiology-Cell Physiology initiates a series of articles around a theme: autophagy is the first theme.

Passive mechanical forces upregulate the fast myosin heavy chain IId/x via integrin and p38 MAP kinase activation in a primary muscle cell culture.

Different activation forms of MMP-2 oppositely affect the fate of endothelial cells.

Role of purinergic signaling pathways in V-ATPase recruitment to apical membrane of acidifying epididymal clear cells

Regulation of gap junction coupling in bovine ciliary epithelium.

Mitochondria-produced superoxide mediates angiotensin II-induced inhibition of neuronal potassium current

Autophagy in health and disease. 1. Regulation and significance of autophagy: an overview.

Role of FAK phosphorylation in hypoxia-induced hMSCS migration: involvement of VEGF as well as MAPKS and eNOS pathways.

IL-7 is expressed and secreted by human skeletal muscle cells.

A preferential p110alpha/gamma PI3K inhibitor attenuates experimental inflammation by suppressing the production of proinflammatory mediators in a NF-kappaB-dependent manner.

Volume-sensitive outwardly rectifying chloride channel in white adipocytes from normal and diabetic mice.

Dysregulation of lipolysis and lipid metabolism in visceral and subcutaneous adipocytes by high-fat diet: role of ATGL, HSL, and AMPK.

Posttranscriptional regulation of sodium-iodide symporter mRNA expression in the rat thyroid gland by acute iodide administration.

ADP-ribosylation factor 6 modulates adrenergic stimulated lipolysis in adipocytes.

Year: 2010 Volume: 298 Issue: 3

Year: 2010 Volume: 298 Issue: 2

Year: 2010 Volume: 298 Issue: 1

Year: 2009 Volume: 297

Year: 2009 Volume: 296

Year: 2008 Volume: 295

Year: 2008 Volume: 294

Year: 2007 Volume: 293

Year: 2007 Volume: 292

Year: 2006 Volume: 291

Year: 2006 Volume: 290

Year: 2005 Volume: 289

Year: 2005 Volume: 288

Year: 2004 Volume: 286

Year: 2003 Volume: 284

Year: 2002 Volume: 283

Year: 2002 Volume: 282

Year: 2001 Volume: 281

Year: 2001 Volume: 280

Year: 2000 Volume: 279

Different activation forms of MMP-2 oppositely affect the fate of endothelial cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Shapiro, Sarah Khodalev, Olga Bitterman, Haim Auslender, Ron Lahat, Nitza
Description	Country affiliation: Israel Author Affiliation: Shapiro S ( Immunology Research Unit, Carmel Medical Center, 7 Michal St., Haifa 34362, Israel.)
Abstract	Detachment of endothelial cells (ECs) from the extracellular matrix (ECM) is required not only for angiogenesis, but also for EC apoptosis. Matrix metalloproteinase (MMP)-2 plays a major role in the degradation of the ECM, supporting an essential role for this enzyme in both survival (angiogenesis) and death of ECs. Our aim was to study these seemingly paradoxical effects of MMP-2. We rationalized that inhibiting apoptosis would drive MMP-2 toward a prosurvival activity, clarifying the mechanisms involved. By employing specific inhibitors to two major apoptotic pathways in ECs, caspases and p38 MAPK (p38), we demonstrated that they differently affected EC behavior as well as MMP-2 expression. The p38 pathway appears to enhance MMP-2 synthesis, its partial ('intermediate') and its full activation, probably via membrane type (MT)1-MMP, while caspases enhance MMP-2 synthesis and full activation but reduce MT1-MMP and MMP-2 intermediate form. Evaluation of the reciprocal influences of MMP-2 on ECs showed that the intermediate form supported survival and migration, and the fully active form led to cell death. In addition, a pro- and intermediate form-rich environment, even in the presence of the fully active form, exerted protective effects. Thus the seemingly conflicting effects of MMP-2 on EC survival may be explained by the ratio between the MMP-2 activation forms. A regulatory loop between active MMP-2 and p38 but not between MMP-2 and caspases was also observed, suggesting that MMP-2 is downstream to caspases where it serves as an 'exterminator' molecule. Altogether, modification of caspase and p38 pathways, via changes of local MMP-2, affect survival and angiogenic steps in ECs.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
Journal	American Journal of Physiology - Cell Physiology
Issue Number	4
Volume Number	298
Language	English
Publisher	American Physiological Society
Publisher Date	2010-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Apoptosis Physiology Endothelial Cells Matrix Metalloproteinase 2 Metabolism Amino Acid Chloromethyl Ketones Pharmacology Drug Effects Caspase 3 Genetics Caspase Inhibitors Cell Movement Cell Shape Cells, Cultured Cytology Enzyme Inhibitors Extracellular Matrix Imidazoles Pyridines Signal Transduction P38 Mitogen-activated Protein Kinases Antagonists & Inhibitors Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Pharmacologically activated migration of aortic endothelial cells is mediated through p38 SAPK.

Effect of phosphatidyl inositol 3-kinase, extracellular signal-regulated kinases 1/2, and p38 mitogen-activated protein kinase inhibition on osteogenic differentiation of muscle-derived stem cells.

Epigallocatechin3gallate inhibits the proliferation and migration of human ovarian carcinoma cells by modulating p38 kinase and matrix metalloproteinase2.

Protective effect of nicorandil on hypoxiainduced apoptosis in HPAECs through inhibition of p38 MAPK phosphorylation.

Fibroblasts and extracellular matrix differently modulate MMP activation by primary and metastatic head and neck cancer cells.

Roles of mitogen-activated protein kinases in the modulation of endothelial cell function following thermal injury.

A Role for the p38 Mitogen-activated Protein Kinase Pathway in Myocardial Cell Growth, Sarcomeric Organization, and Cardiac-specific Gene Expression

CTGF Is Increased in Basal Deposits and Regulates Matrix Production through the ERK $(p42/p44^{mapk})$ MAPK and the p38 MAPK Signaling Pathways

Malondialdehyde inhibits cardiac contractile function in ventricular myocytes via a p38 mitogen-activated protein kinase-dependent mechanism

Different activation forms of MMP-2 oppositely affect the fate of endothelial cells.

Similar Documents

Pharmacologically activated migration of aortic endothelial cells is mediated through p38 SAPK.

Effect of phosphatidyl inositol 3-kinase, extracellular signal-regulated kinases 1/2, and p38 mitogen-activated protein kinase inhibition on osteogenic differentiation of muscle-derived stem cells.

Epigallocatechin­3­gallate inhibits the proliferation and migration of human ovarian carcinoma cells by modulating p38 kinase and matrix metalloproteinase­2.

Protective effect of nicorandil on hypoxia­induced apoptosis in HPAECs through inhibition of p38 MAPK phosphorylation.

Fibroblasts and extracellular matrix differently modulate MMP activation by primary and metastatic head and neck cancer cells.

Roles of mitogen-activated protein kinases in the modulation of endothelial cell function following thermal injury.

A Role for the p38 Mitogen-activated Protein Kinase Pathway in Myocardial Cell Growth, Sarcomeric Organization, and Cardiac-specific Gene Expression

CTGF Is Increased in Basal Deposits and Regulates Matrix Production through the ERK $(p42/p44^{mapk})$ MAPK and the p38 MAPK Signaling Pathways

Malondialdehyde inhibits cardiac contractile function in ventricular myocytes via a p38 mitogen-activated protein kinase-dependent mechanism

Different activation forms of MMP-2 oppositely affect the fate of endothelial cells.

Epigallocatechin3gallate inhibits the proliferation and migration of human ovarian carcinoma cells by modulating p38 kinase and matrix metalloproteinase2.

Protective effect of nicorandil on hypoxiainduced apoptosis in HPAECs through inhibition of p38 MAPK phosphorylation.