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Complications
Author(s) -
Siberry USINTL
Publication year - 1999
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/dme.1999.16.s1.23
Subject(s) - medicine , citation , library science , information retrieval , computer science
The haemodynamic insult has been implicated in the pathogenesis of the exaggerated mcsangial matrix deposition seen in diabetic nephropathy. Exposure to mechanical stretch, mimicking the haemodynamic insult in vivo, enhances matrix production in rat mcsangial cells (MC), but the intracellular mechanisms underlying this response arc not yet defined. p38-MAPK (p38), a dualphosphorylated kinase, is activated by various stresses and active p38 levels arc enhanced in glomeruli from diabetic animals. We studied ~ stretch induces fibronec:tin protein production via p38 actlvabon m human MC. Serum and insulin-deprived human MC were exposed to stretch (10% elongation) for 33 hours. Control cells were seeded in non-deformable, but otherwise identical plates in parallel. Levels of p38 protein and activated phospbo-p38 were dctcnnined by immunoblotting. Fibroncctin protein levels in the supernatants were mcasun:d by ELISA (range O.OS.O.S ~w'ml intraassay:1.6%). Exposure to stretch induced a significant 3 fold increase in activated phospbo-p38 (p