Xiangjun He

FAM3A enhances adipogenesis of 3T3-L1 preadipocytes via activation of ATP-P2 receptor-Akt signaling pathway

FAM3A plays important roles in regulating hepatic glucose/lipid metabolism and the proliferation of VSMCs. This study determined the role and mechanism of FAM3A in the adipogenesis of 3T3-L1 preadipocytes. During the adipogenesis of 3T3-L1 preadipocytes, FAM3A expression was significantly increased. FAM3A overexpression enhanced 3T3-L1 preadipocyte adipogenesis with increased phosphorylated Akt (pAkt) level, whereas FAM3A silencing inhibited 3T3-L1 preadipocyte adipogenesis with reduced pAkt level. Moreover, FAM3A silencing reduced the expression and secretion of adipokines in 3T3-L1 cells. FAM3A protein is mainly located in mitochondrial fraction of 3T3-L1 cells and mouse adipose tissue. FAM3A overexpression increased, whereas FAM3A silencing decreased ATP production in 3T3-L1 preadipocytes. FAM3A-induced adipogenesis of 3T3-L1 preadipocytes was blunted by inhibitor of P2 receptor. In white adipose tissues of db/db and HFD-fed obese mice, FAM3A expression was reduced. One-month rosiglitazone administration upregulated FAM3A expression, and increased cellular ATP content and pAkt level in white adipose tissues of normal and obese mice. In conclusion, FAM3A enhances the adipogenesis of preadipocytes by activating ATP-P2 receptor-Akt pathway. Under obese condition, a decrease in FAM3A expression in adipose tissues plays important roles in the development of adipose dysfunction and type 2 diabetes.

Apoptin induces chromatin condensation in normal cells.

Apoptin, a chicken anemia virus protein, was reported to induce tumor specific apoptosis, which was correlated with the nuclear localization of the protein in tumor cells. While in normal human cells, Apoptin was detected mainly in the cytoplasm and did not induce apoptosis. Using a recombinant adenovirus expressing Apoptin, we have found that Apoptin induced G2-M cell cycle arrest and chromatin condensation in cancer cells. Here we report that adenovirus mediated Apoptin expression also induces G2-M arrest in normal cells. In normal cells Apoptin is localized mainly in the cytoplasm but is also found in the nucleus of a subset of cells. Apoptin induces chromatin condensation not only when it is expressed in the nucleus but also when it is expressed in the cytoplasm. Our results indicate that Apoptin-induced chromatin condensation in the normal cells may not correlate with its nuclear localization and the mechanism of regulating the G2-M transition might be a target for Apoptin.