Thromb Haemost 2010; 104(06): 1124-1132
DOI: 10.1160/TH10-02-0101
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Urokinase-type plasminogen activator receptor is associated with the development of adipose tissue

Yosuke Kanno
1   Department of Clinical Pathological Biochemistry, Faculty of Pharmaceutical Science, Doshisha Women’s Collage of Liberal Arts, Kyoto, Japan
,
Hiroyuki Matsuno
1   Department of Clinical Pathological Biochemistry, Faculty of Pharmaceutical Science, Doshisha Women’s Collage of Liberal Arts, Kyoto, Japan
,
Eri Kawashita
1   Department of Clinical Pathological Biochemistry, Faculty of Pharmaceutical Science, Doshisha Women’s Collage of Liberal Arts, Kyoto, Japan
,
Kiyotaka Okada
2   Department of Physiology, Kinki University School of Medicine, Osaka, Japan
,
Hidetaka Suga
3   Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya, Japan
,
Shigeru Ueshima
2   Department of Physiology, Kinki University School of Medicine, Osaka, Japan
4   Department of Food Science and Nutrition, Kinki University School of Agriculture, Nara, Japan
,
Osamu Matsuo
2   Department of Physiology, Kinki University School of Medicine, Osaka, Japan
› Author Affiliations
Further Information

Publication History

Received: 08 February 2010

Accepted after major revision: 28 July 2010

Publication Date:
24 November 2017 (online)

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Summary

Urokinase-type plasminogen activator receptor (uPAR) plays a role in cellular responses which include cellular adhesion, differentiation, proliferation and migration. The aim of this study was to clarify the role of uPAR on the development of adipose tissue. To clarify the role of uPAR on adipogenesis, we examined the effect of uPAR overexpression and uPAR deficiency on the adipocyte differentiation. Adipocyte differentiation was induced by incubation of 3T3-L1 cells with differentiation media containing insulin, dexamethasone, and 1-methyl-3-isobutylxanthin. uPAR overexpression by transfection of uPAR expression vector induced adipocyte differentiation. In addition, we examined the difference in adipocyte differentiation of mesenchymal stem cells from wild-type mice and uPAR knockout (uPAR-/-) mice. The uPAR deficiency attenuated differentiation media-induced adipocyte differentiation. Moreover, we found that the inhibition of phosphatidylinositol 3-kinase (PI3K) pathway attenuated uPAR overexpression-induced adipocyte differentiation, and uPAR overexpression induced the activation of Akt. We also found that an increase of the adipose tissue mass in uPAR-/- mice was less than that observed in wild-type mice. The present results suggest that uPAR plays a pivotal role in the development of adipose tissue through PI3K/Akt pathway.