Premium
Adiponectin mediates cellular plasticity of osteoblasts towards adipocytes
Author(s) -
Abbott Marcia J,
O'Carroll Dylan,
Nissenson Robert A
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.713.11
Subject(s) - adiponectin , endocrinology , medicine , osteocalcin , osteoblast , runx2 , chemistry , adipocyte , adipogenesis , alkaline phosphatase , biology , in vitro , adipose tissue , obesity , biochemistry , insulin resistance , enzyme
Adiponectin has been implicated in regulating skeletal homeostasis. Studies show that adiponectin is inversely related to bone mineral density (BMD) and positively related to fracture risk in adults. We sought to identify the role of adiponectin on differentiating osteoblasts in vitro . Mouse bone marrow stromal cells were treated with adiponectin (2.5 μg/ml) acutely for 24 hrs at various stages (day 7, 14, 21 & 28) or chronically (day 14–28) of osteoblastic differentiation. Osteoblast properties were observed in all experiments by day 21 of differentiation. Acute adiponectin decreased osteoblast markers, osterix (OSX) and runx2, mRNA at day 14 (35–29%, respectively) and day 21 (34–53%, respectively). At day 21 with acute adiponectin, osteocalcin (OC) and collagen type 1 (Col1) mRNA decreased (56–59%, respectively). Chronic adiponectin reduced colony formation, decreased mineralized nodules and decreased mRNA of OSX, runx2, alkaline phosphatase, Col1 and OC (53–82%). Adipocyte factors PPARγ and C/EBPα mRNA increased with acute and chronic adiponectin (39–64% & 39–64%, respectively). Chronic adiponectin increased lipid colonies and lipid droplet size as visualized by Oil Red O. Here we show that adiponectin mediates cellular plasticity by exerting negative osteoblastic effects in favor of adipogenesis in mature osteoblasts. These data may explain the negative association between adiponectin and BMD in humans.