Key result
In cultured rat peritoneal mesothelial cells, Angiotensin II induced a 1.5-2-fold increase in profibrotic molecules through AT1-mediated ERK1/2 phosphorylation.
Why the study?
Does Angiotensin II activate fibrotic pathways through ERK1/2 in rat peritoneal mesothelial cells?
Population
Rat peritoneal mesothelial cells (RPMCs) obtained by enzymatic digestion from the colic omentum
Comparison
Angiotensin II incubation, with or without… vs Untreated control cells
Design
Preclinical
Authors
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May implicate AT1-ERK1/2 signaling in peritoneal fibrosis; leaves open relevance to human dialysis outcomes.
Does Angiotensin II activate fibrotic pathways through ERK1/2 in rat peritoneal mesothelial cells?
Effect estimate: 1.5-2-fold increase
Angiotensin II promotes profibrotic signaling in rat peritoneal mesothelial cells via AT1-mediated ERK1/2 phosphorylation, suggesting a potential mechanism for peritoneal fibrosis in dialysis.
Xie et al. (2010) studied Peritoneal fibrosis. Angiotensin II was evaluated on mRNA and protein levels of TGF-beta1, FN, TIMP-1, and PAI-1 (1.5-2-fold increase). In cultured rat peritoneal mesothelial cells, Angiotensin II induced a 1.5-2-fold increase in profibrotic molecules through AT1-mediated ERK1/2 phosphorylation.
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