Despite different etiologies, virtually identical changes in local bFGF, PDGF and VEGF levels in duodenal ulceration and ulcerative colitis indicate similarities in healing

Role of anti-angiogenic factor endostatin in the pathogenesis of experimental ulcerative colitis

“…Depletion of angiopoietin-2 attenuated leukocyte infiltration, inflammation as well as blood and lymphatic vessel density during experimental UC (Ganta et al, 2010). At the same time administration of bFGF, PDGF or HGF accelerated the healing of both experimental UC (Kojima et al, 2007;Szabo et al, 1999;Thatch et al, 2009) and chronic duodenal ulcers (Szabo et al, , 1998bSatoh et al, 1997b). Thus, we postulate that VEGF stimulates both normal angiogenesis (e.g., in duodenal ulceration) and excessive/ pathologic angiogenesis in IBD.…”

The Role of Capsaicin-Sensitive Afferent Nerves in Gastric Mucosal Protection Initiated Centrally or Peripherally under Experimental Conditions

“…It was shown that PDGF (and bFGF) accelerated the healing of cysteamine induced duodenal ulcers in rats by stimulating angiogenesis and granulation tissue formation [56]. Furthermore, in experimental duodenal ulcer and colitis in rats (after a transitory reduction) of the concentrations of bFGF and PDGF increased in the healing phases both experimental lesions [57]. Vascular endothelial growth factor (VEGF) has dual role; in acute gastric ulcer it induced gastroprotective effect surprisingly by enhancing vascular permeability and the consequent perivascular dilution barrier towards gastric mucosal irritants [58].…”