Nephrology Dialysis Transplantation, Vol 12, Issue 3 438-442, Copyright © 1997 by Oxford University Press
H Yamabe, H Osawa, H Inuma, M Kaizuka, N Tamura, S Tsunoda, Y Baba, K Shirato and K Onodera
Fibrin formation within the glomeruli occurs in various forms of human and
experimental glomerulonephritis and it may play an important role in
progressive glomerular injury. Transforming growth factor-beta (TGF- beta)
has been shown to participate in the glomerular accumulation of
extracellular matrix in glomerulonephritis. We investigated whether
thrombin, an important coagulation factor, could modulate the production of
TGF-beta by cultured human mesangial cells (HMC). TGF- beta levels in the
culture supernatants were measured by ELISA using a specific antibody. The
TGF-beta concentration was significantly increased by incubation of HMC
with thrombin in a time-dependent manner. The stimulating effect of
thrombin on TGF-beta was inhibited by addition of hirudin (a natural
thrombin inhibitor) and argatroban (a synthetic thrombin inhibitor). In
addition DFP-inactivated thrombin, which has no enzymatic activity, did not
stimulate TGF-beta production. A protein kinase C inhibitor (H7) and a
tyrosine kinase inhibitor (herbimycin A) also inhibited thrombin induced
TGF-beta production. These findings suggested that thrombin may modulate
the synthesis of TGF-beta via protein kinase C- and tyrosine
kinase-dependent mechanisms in cultured HMC. Thus thrombin may participate
in the accumulation of extracellular matrix in glomeruli through the
augmentation of TGF-beta production.
ORIGINAL ARTICLES
Thrombin stimulates production of transforming growth factor-beta by cultured human mesangial cells
Second Department of Internal Medicine, Hirosaki University School of Medicine, Japan.
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