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Thrombospondin-2 ELISA KIT

Thrombospondin-2 is an endogenous adipocyte inhibitor

The matricellular protein thrombospondin-2 (TSP2) inhibits proliferation and enhances osteoblastogenesis of multipotent mesenchymal progenitor cells (MPC). Osteoblastogenesis and adipogenesis are reciprocally regulated, thus we hypothesized that TSP2 could be an inhibitor of adipogenesis.TSP2 gene expression is up-regulated during MPC osteoblast differentiation and down-regulated during adipogenic differentiation through a cAMP-PKA pathway, relative to control cells. Next, the importance of TSP2 in adipogenesis was studied by comparing gene-targeted knockout mice that lack TSP2 protein (TSP2-null) and control wild-type mice. TSP2-null marrow-derived MPC show 25% increased adipocytes. Similarly, TSP2-null adipose-derived MPC show increased adipocytes (25-50%) and proliferation (2-fold) relative to wild-type cells. However, the increase in TSP2-null adipocytes is not due to an increase in MPC number, because the percentage of adipocytes relative to total MPC is still significantly increased. Surprisingly, there are only minor alterations in the adipogenic transcriptional program (PPARγ and C/EBPα expression). Weight gain over time was evaluated in TSP2-null and control wild-type mice fed normal and high-fat diets. Female TSP2-null mice are 30% heavier than wild-type controls due to an increase in non-visceral adipose tissue, measured by dual-energy X-ray absorptiometry (DEXA) and direct weighing of fat pads. These results show that TSP2 is an endogenous matricellular protein produced by MPC that in addition to enhancing osteoblastogenesis, inhibits adipocytes and decreases subcutaneous adiposity.
Shitaye HS, et al. Matrix Biol. 2010 Jul;29(6):549-56. Epub 2010 May 31.

Thrombospondin-2 and SPARC/osteonectin are critical regulators of bone remodelin

Thrombospondin-2 (TSP2) and osteonectin/BM-40/SPARC are matricellular proteins that are highly expressed by bone cells. Mice deficient in either of these proteins show phenotypic alterations in the skeleton, and these phenotypes are most pronounced under conditions of altered bone remodeling. For example, TSP2-null mice have higher cortical bone volume and are resistant to bone loss associated with ovariectomy, whereas SPARC-null mice have decreased trabecular bone volume and fail to demonstrate an increase in bone mineral density in response to a bone-anabolic parathyroid hormone treatment regimen. In vitro, marrow stromal cell (MSC) osteoprogenitors from TSP2-null mice have increased proliferation but delayed formation of mineralized matrix. Similarly, in cultures of SPARC-null MSCs, osteoblastic differentiation and mineralized matrix formation are decreased. Overall, both TSP2 and SPARC positively influence osteoblastic differentiation. Intriguingly, both of these matricellular proteins appear to impact MSC fate through mechanisms that could involve the Notch signaling system. This review provides an overview of the role of TSP2 and SPARC in regulating bone structure, function, and remodeling, as determined by both in vitro and in vivo studies.
Delany AM, Hankenson KD. J Cell Commun Signal. 2009 Dec;3(3-4):227-38. Epub 2009 Oct 28.
Human Thrombospondin-2 ELISA Kit
Code No.: SK00336-01
Size: 96 T
Price: $360.00 USD
Standard Range:156-10000 p g/mL
Sensitivity: 50-78 pg/ml
Sample Type: cell cultures, serum, plasma
Dilution Factor: 10
Sample require: 30 uL
Intra-CV: 4-8%
Inter-CV: 6-10
Protocol: PDF
Code No.
Price ($)
Thrombospondin-2 (Human) ELISA Kit
96 T