ArticleThe American journal of pathology1999
Type IV collagen and laminin regulate glomerular mesangial cell susceptibility to apoptosis via beta(1) integrin-mediated survival signals.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
11 citing papers in PubMed, 80 citations in OpenAlex.
- Article
- Extracellular matrix-mediated cellular communication in the heart.Journal of molecular and cellular cardiology · 2016Review
- Review
- Identification of nephropathy candidate genes by comparing sclerosis-prone and sclerosis-resistant mouse strain kidney transcriptomes.BMC nephrology · 2012Article
- The lysophosphatidic acid receptor LPA1 promotes epithelial cell apoptosis after lung injury.American journal of respiratory cell and molecular biology · 2012Article
- Molecular mechanisms of chronic kidney transplant rejection via large-scale proteogenomic analysis of tissue biopsies.Journal of the American Society of Nephrology : JASN · 2010Article
- Laminin-332-integrin interaction: a target for cancer therapy?Current medicinal chemistry · 2008Review
- N-Myc overexpression leads to decreased beta1 integrin expression and increased apoptosis in human neuroblastoma cells.Oncogene · 2003Article
- Apoptosis and myofibroblasts in the pathogenesis of systemic sclerosis.Current rheumatology reports · 2002Review
- Integrin-mediated survival signals regulate the apoptotic function of Bax through its conformation and subcellular localization.The Journal of cell biology · 2000Article
- Contribution of apoptotic cell death to renal injury.Journal of cellular and molecular medicineReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Postinflammatory scarring is characterized by changes in extracellular matrix (ECM) composition and progressive loss of normal resident cells. In glomerular inflammation there is now evidence that unscheduled apoptosis (programmed cell death) of mesangial and other resident cells may mediate progression to irreversible glomerulosclerosis. In the current study we examined the hypothesis that ECM components may differ in their capacity to support mesangial cell survival by suppression of apoptosis. Using a well-established in vitro model of mesangial cell apoptosis, we found that collagen IV and laminin, components of normal mesangial ECM, protected rat mesangial cells from apoptosis induced by serum starvation and DNA damage, by a beta(1) integrin-mediated, but arg-gly-asp (RGD)-independent mechanism. In contrast, collagen I, fibronectin, and osteonectin/SPARC, which are overexpressed in diseased glomeruli, failed to promote rat mesangial cell survival. However, the survival-promoting effect of collagen IV and laminin was not associated with changes in cellular levels of apoptosis regulatory proteins of the Bcl-2 family. These experiments demonstrate that glomerular mesangial cell survival is dependent on interactions with ECM and provide insights into potential mechanisms by which resident cell loss may occur during acute inflammation and postinflammatory scarring of the kidney and other organs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.