Formononetin accelerates wound repair by the regulation of early growth response factor-1 transcription factor through the phosphorylation of the ERK and p38 MAPK pathways

Lipin1 Regulates Skeletal Muscle Differentiation through Extracellular Signal-regulated Kinase (ERK) Activation and Cyclin D Complex-regulated Cell Cycle Withdrawal

“…Consistent with what we observed, ERK1/2 is required for myoblast terminal differentiation and multinucleated muscle fiber formation (30). Activation of ERK signaling occurs at early stages of muscle regeneration (42,43) and in wound repair (43,44), suggesting that ERK phosphorylation has some beneficial effects. Phosphatidic acid accumulation in peripheral nerves of lipin1-deficient fld mice increases ERK1/2 activation, mediating Schwann cell dedifferentiation and proliferation (45).…”

Acidic preconditioning improves the proangiogenic responses of endothelial colony forming cells

“…However, pretreatment with the p38 inhibitor SB203580, had no effect on ECFC proliferation. In this sense, although the role of p38 on the proliferation of EPC is still controversial, most of the studies using SB203580, in vitro and in vivo, have described a negative effect of this drug not only on cell growth and survival but also on tubulogenesis [41][42][43][44]. Interestingly, we also found that p38 blockade increased tubulogenesis in vitro at pH 7.4, suggesting that p38 pathway is a negative regulator of ECFC tubule formation and the fact that this molecule was completely suppressed in preconditioned ECFC explained, at least in part, the positive regulation of acidic preconditioning on microvessel formation.…”

Reactive oxygen species-mediated p38 MAPK regulates carbon nanotube-induced fibrogenic and angiogenic responses

“…These results suggest that although VEGF could be a key mediator of the fibrogenic effect of SWCNTs, other mediators or other mechanisms of fibroblast activation are also involved. Several growth factors under the regulation of p38 MAPK including platelet-derived growth factor (PDGF) and TGF-β1 have been reported (Huh et al 2011; Kolosova et al 2011; Roos et al 2011). These growth factors along with several others including basic fibroblast growth factor and VEGF have also been reported to regulate p38 MAPK (Goldberg et al 2002; Sorensen et al 2008; Xiong et al 2001; Zhang et al 2011).…”