TNP-470 (a fungus-derived inhibitor of angiogenesis) reduces proliferation of cultured fibroblasts isolated from primary pterygia: a possible drug therapy for pterygia

Abstract

TNP-470 appears to have a marked inhibitory effect on PF proliferation, and it may be of considerable value in the prevention of pterygium growth and recurrence.

Treatment with sulfasalazine or sulfapyridine, but not 5-aminosalicylic acid, inhibits basic fibroblast growth factor-induced endothelial cell chemotaxis

“…The loss of inhibition of EC proliferation at higher concentrations of SSZ may be due to SSZ inducing HMVEC to release adenosine, a known inducer of EC proliferation (31). Both SSZ and SP also inhibited proliferation of the fibroblast cell line CLR1635, indicating that the inhibitory effects of SSZ and SP, like those of other angiogenesis inhibitors, are not specific to EC (32). Finally, 5-ASA significantly increases basal HMVEC proliferation in a concentration-dependent manner.…”

TNP-470, an angiogenesis inhibitor, suppresses the progression of peritoneal fibrosis in mouse experimental model

“…The efficacy of TNP-470 as an angiogenesis inhibitor has been demonstrated experimentally in the treatment of hemangiomas [17], corneal neovascularization [18], collagen-induced arthritis [19,20], primary tumors, and metastatic diseases [21][22][23][24]. While TNP-470 is known to exert its antiangiogenic effect through the preferential inhibition of endothelial cell proliferation [16,25], it has been recently demonstrated that this agent also inhibits proliferation of fibroblasts [16,26], vascular smooth muscle cells [27], hepatic stellate cells [28], and mesangial cells [29].…”

Stromelysin-1 expression is activated in vivo by Ets-1 through palindromic head-to-head Ets binding sites present in the promoter

“…However, their action is not restricted to endothelial cells (Rodriguez-Nieto et al, 2001) and some effects have been shown on fibroblasts (Kria et al, 1998). Interestingly, fumagillin was also reported to inhibit Ets-1 expression induced by vascular endothelial growth factor (VEGF) (Wernert et al, 1999).…”