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Title 

Regulation of adipogenic differentiation by LAR tyrosine phosphatase in human mesenchymal stem cells and 3T3-L1 preadipocytes

Authors 

Won Kon KimHyeyun JungDo-Hyung KimEun Young KimJ W ChungYeesook ChoSung Goo ParkByoung Chul ParkY KoKwang-Hee BaeSang Chul Lee

Publisher 

Company of Biologists

Issue Date 

2009

Citation 

Journal of Cell Science, vol. 122, no. 22, pp. 4160-4167

Keywords 

AdipocyteAdipogenesisLeukocyte common antigenrelatedMesenchymal stem cellsOsteoblastProtein tyrosine phosphatase

Abstract 

Mesenchymal stem cells (MSCs) are multipotent adult stem cells that can differentiate into a variety of mesodermal-lineage cells. MSCs have significant potential in tissue engineering and therapeutic applications; however, the low differentiation and proliferation efficiencies of these cells in the laboratory are fundamental obstacles to their therapeutic use, mainly owing to the lack of information on the detailed signal-transduction mechanisms of differentiation into distinct lineages. With the aid of protein-tyrosine-phosphatase profiling studies, we show that the expression of leukocyte common antigen related (LAR) tyrosine phosphatase is significantly decreased during the early adipogenic stages of MSCs. Knockdown of endogenous LAR induced a dramatic increase in adipogenic differentiation, whereas its overexpression led to decreased adipogenic differentiation in both 3T3-L1 preadipocytes and MSCs. LAR reduces tyrosine phosphorylation of the insulin receptor, in turn leading to decreased phosphorylation of the adaptor protein IRS-1 and its downstream molecule Akt (also known as PKB). We propose that LAR functions as a negative regulator of adipogenesis. Furthermore, our data support the possibility that LAR controls the balance between osteoblast and adipocyte differentiation. Overall, our findings contribute to the clarification of the mechanisms underlying LAR activity in the differentiation of MSCs and suggest that LAR is a candidate target protein for the control of stem-cell differentiation.

ISSN 

0021-9533

Link 

http://dx.doi.org/10.1242/jcs.053009

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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