C-type natriuretic peptide promotes adipogenic differentiation of goat adipose-derived stem cells via cGMP/PKG/ p38 MAPK signal pathway.

Abstract

C-type natriuretic peptide (CNP) is a member of natriuretic peptide family, which plays unique roles in cardiovascular system. Once CNP binds to natriuretic peptide receptor B (NPR-B), NPR-B induces the production of cGMP, thereby activating PKG and downstream targets. The expression of NPR-B in adipose tissue led to a hypothesis that CNP could have roles involving in regulation of adipogenesis. However, there are few studies on the relationship between CNP and adipogenesis in goat. In the present study, goat adipose-derived stem cells (ADSCs) were isolated and employed to investigate the effect of CNP on adipogenesis in goat. The results showed that CNP significantly promoted adipogenic differentiation of goat ADSCs and also up-regulated the expression of brown adipose genes including uncoupling protein 1 (UCP-1) and peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α). Furthermore, treatment with CNP increased the cGMP production and the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), MAPK activated protein kinase 2 (MK2), and activating transcription factor 2 (ATF2) during adipogenic differentiation. Conversely, PKG inhibitor Rp-8-CPT-cGMP or p38 MAPK specific inhibitor SB203580 abolished stimulative effect of CNP on adipogenic differentiation. Collectively, it is proved that CNP promoted adipogenic differentiation of goat ADSCs depending on the cGMP/PKG/p38 MAPK signal pathway.