Premium
Na/K‐ATPase in Bone‐Marrow Derived Stromal Cells
Author(s) -
Sayed Moustafa Helmy,
Liu Jiang,
Xie Zijian,
Shapiro Joseph I,
Tian Jiang
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.726.8
Subject(s) - adipogenesis , stromal cell , chemistry , bone marrow , microbiology and biotechnology , mesenchymal stem cell , endocrinology , rosiglitazone , cell , medicine , cell growth , signal transduction , biology , receptor , biochemistry
Bone‐marrow derived stromal cells (BMSCs) have the capacity to differentiate multi‐directionally. We have demonstrated that the signaling function of Na/K‐ATPase plays an important role in regulating cell survival and cell growth. This study is to test if Na/K‐ATPase and its signaling functions affect BMSCs survival and differentiation capacity. BMSCs isolated from Sprauge‐Dawley male rats were cultured in α‐MEM containing 15% FBS. The purified third generation of BMSCs was treated with 10nM or 1μM marinobufagenin (MBG, a cardiotonic steroid) for 72h then the cells were induced to differentiate into adipocytes or osteoblasts using 1μM Rosiglitazone or 10mM β‐glycerophosphate, respectively. The results illustrated that MBG treatment activates the Na/K‐ATPase signaling pathway and promoted Rosiglitazone‐induced adipogenesis. In addition, MBG treatment resulted in a trend of decreased osteogenesis induced by β‐glycerophosphate, but not in a statistically significant manner. To evaluate the mechanism behind this phenomenon, BMSCs were pretreated with 1μM PP2 (a Src inhibitor) for 30 minutes, then cells were treated with 10nM and 1μM MBG for 72 hours before the induction of adipogenesis. This combined treatment decreased adipogenesis when compared to cells treated with MBG alone. These results suggest Na/K‐ATPase and its signaling functions are involved in the regulation of BMSCs differentiation. Supported by NIH HL‐105649