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Differential regulation of adipocyte and osteoblast differentiation of mesenchymal stem cells by Chemerin and CMKLR1
Author(s) -
Shanmugam Muruganandan,
Roman Alexandra,
Sinal Christopher
Publication year - 2009
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.23.1_supplement.700.3
Subject(s) - chemerin , mesenchymal stem cell , adipogenesis , osteoblast , microbiology and biotechnology , adipocyte , bone marrow , biology , stem cell , cellular differentiation , progenitor cell , endocrinology , medicine , adipokine , immunology , adipose tissue , leptin , genetics , gene , in vitro , obesity
Adipocytes and osteoblasts are derived from a common mesenchymal stem cell progenitor within the bone marrow. Previous studies have identified an inverse relationship between adipocyte and osteoblast differentiation of these cells in bone marrow. Work from our laboratory identified chemerin as a novel adipokine that together with its cognate receptor, CMKLR1 plays an indispensable role in regulating adipocyte differentiation of 3T3‐L1 preadipocytes. In the present study we hypothesized that chemerin and its cognate receptor, CMKLR1 is also essential for adipocyte differentiation of bone marrow‐derived mesenchymal stem cells and may simultaneously competitively suppress the alternate osteoblastogenic program. Knockdown of chemerin or CMKLR1 by short hairpin loop RNAs (shRNA) in murine bone marrow primary mesenchymal stem cells abrogated preadipocyte clonal expansion, adipogenic gene expression and lipid accumulation along with the promotion of mineralization and osteoblastogenic gene expression. Thus we conclude that chemerin is essential for bone marrow mesenchymal stem cell adipogenesis and may negatively impact osteoblastogenesis in these cells. Funding: 1. Canadian Institutes of Health Research 2. Nova Scotia Health Research Foundation