TGF-β1-induced thrombospondin-1 expression through the p38 MAPK pathway is abolished by fluvastatin in human coronary artery smooth muscle cells

Stimulatory Effects of Low-Dose 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitor Fluvatatin on Hepatocyte Growth Factor–Induced Angiogenesis: Involvement of p38 Mitogen-Activated Protein Kinase

“…Moreover, it has also been reported to induce apoptosis in ECs (13). On the other hand, statins have been shown to decrease p38 MAPK phosphoryla- (26), myocardium (27), and macrophages (28). In the present study, we demonstrated that 1) low-dose fluvastatin decreased apoptosis in HUVECs in the presence of HGF, 2) low-dose fluvastatin suppressed p38 MAPK phosphorylation in HUVECs in the presence of HGF, and 3) SB203580 reduced the anisomycin-induced angiogenesis suppression in the presence of HGF (Fig.…”

Smad and p38 MAP Kinase-mediated Signaling of Proteoglycan Synthesis in Vascular Smooth Muscle

“…In VSMC TGF-␤-mediated activation of p38 MAP kinase has been shown to induce expression of thrombospondin (34), vascular endothelial growth factor (35) and is involved in induction of smooth muscle marker genes (36). Although TGF-␤ has been demonstrated to regulate biglycan expression via p38 MAP kinase in the pancreatic adenocarcinoma cell line PANC-1 (16,17), in the present study we have described an involvement of p38 MAP kinase in TGF-␤-mediated proteoglycan synthesis in VSMC and demonstrated that inhibition of this pathway results in proteoglycans with decreased LDL binding.…”

Laser Capture Microdissection-Microarray Analysis of Focal Segmental Glomerulosclerosis Glomeruli

“…The TGF-β-thrombospondin axis could play an important role in the fibrotic progression of FSGS. TGF-β can induce expression of the thrombospondin gene [39], and the thrombospondin protein can activate the TGF-β protein [40]. Sustained expression of thrombospondin has been associated with the development of glomerular fibrosis in the remnant kidney model [41].…”