Ets on the induction Peptidase-4 of BMP4 MSC adipogenic commitment and differentiation. In particular, we have shown that MSC adipogenesis cell eliminated by Extensible Application k Nnte in the processing step, before BMP4 adipogenic inducers were added. Our data suggest a new panel do Distinguish, U, that the mechanical stimulation of the cells are induced before the MSCs, can be used as a potent suppressor of obesity act. This is in contrast to other studies showing elongation of the cells may need during the differentiation phase can reduce adipogenesis adipocyte precursor cells of various shore. As an m Glicher mechanism of regulation, we observed that stretch-induced cell activation of ERK-tron in the repression Be part of BMP4 k Nnte is his destiny to mediate MSC adipogenesis. It is interesting that the BMPs that were originally on their R Called ability to induce bone formation, also instructive to commit signals for MSC to adipocytes. The data in FIG. 1B are consistent with these studies. The MSC-line commitment is defined judged by the activation of specific transcription factors in this line. MSC differentiation of adipocytes Pr Initiated by activation of C / EBPB of PPARC. PPARC and activated C / EBPa in the positive feedback of transcription, upregulation of co-ordinate others and the biology of adipocytes downstream development. The upregulation of PPARC and C / EBPa with BMP4 treatment and their down-regulation as evidence of BMP4 in stretch and stretch control of MSC fate to serve. Terminal adipogenesis to BMP4 followed this trend and extensible. Smad signaling pathway is important for the BMPs. Activated BMP receptors, type II, then I type that induces the phosphorylation of Smad1/5/8. Smad1/5/8 then form Smoothened heteromeric with Smad4 and translocates to the nucleus, tax The Transkriptionsaktivit t of target genes. In addition, there is evidence of BMP signaling by non-Smad as p38MAPK. BMP to foreign MSC adipocyte commitment sen, Both Smad and p38 was suggested to be involved. Huang et al. proposed for the modulation of BMP2 and 4 MSC to adipocytes, which may play a Smad dominant since the p38 surcharge smaller effect on the BMP-induced adipogenesis displayed. In our recent study reported by BMP4 and Smad1/5/8 in stimulating adipogenesis p38MAPK MSC, which were both significantly decreased by treatment with S Acid retino, That the cooperation. In the current study on the mechanical St Changes the function of BMP4, induced elongation of the cells no Ver Changes in the phosphorylation of Smad1/5/8 in BMP4 exposure and p38MAPK. Our data suggest that stretch-induced inhibitory effects of BMP4 is not the feature in BMP4 or BMP4-Smad signaling, p38, unlike S Acid retino St Be involved changes That of BMP4. Instead, we observed that cells induced by stretching the phosphorylation of ERK1 / 2 compared with BMP4 alone up-regulated cell processing. Furthermore, blocking ERK by PD98059 adversely Tron chtigt the distance We observed BMP4 induces MSC adipogenic commitment and differentiation. These data combined with the data of image. 2, suggest a Bergenin vorl INDICATIVE schlu Clusion, there the suppression of induction of adipogenesis of BMP4 MSC cell lines is reached, either by direct downregulation of Smad BMP4 or BMP4 p3.