Abstract

and p<0.03 respectively) after SP treatment in UC-derivedmesenteric preadipocytes. Furthermore, SP induced activation of both p38MAPK and ERK1/2 in UC-derived preadipocytes, in contrast to control preadipocytes where activation of these kinases was either reduced (ERK) or unaffected (p38). Conclusions: Our data suggest a distinct disease-dependent proinflammatory effect of SP on preadipocytes, which may be due to the different expression levels of NK1R and/or altered state of downstream regulatory pathways. Our preliminary evidence suggests a potential role for p38 MAPK and ERK1/2 signaling pathways in the regulation of differential cytokine responses between control and UC-derived preadipocytes. Support: NIH RC1DK086150, RO1DK47343, and the Broad Medical Foundation (BMRP)

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