Protein Tyrosine Phosphatase, Receptor Type B (PTPRB) Inhibits Brown Adipocyte Differentiation through Regulation of VEGFR2 Phosphorylation

• Published in: Journal of microbiology and biotechnology Vol. 29; no. 4; pp. 645 - 650
• Main Authors: Kim, Ji Soo, Kim, Won Kon, Oh, Kyoung-Jin, Lee, Eun-Woo, Han, Baek Soo, Lee, Sang Chul, Bae, Kwang-Hee
• Format: Journal Article
• Language: English
• Published: Korea (South) 한국미생물·생명공학회 28.04.2019
• Subjects: Adipocytes, Brown - drug effects; Adipogenesis - physiology; Cell Differentiation - drug effects; Cell Line; Diabetes Mellitus, Type 2; Gene Expression Regulation; Humans; NADH Dehydrogenase; Obesity; Phosphorylation; Receptor-Like Protein Tyrosine Phosphatases, Class 3 - antagonists & inhibitors; Receptor-Like Protein Tyrosine Phosphatases, Class 3 - genetics; Tyrosine - metabolism; Uncoupling Protein 1 - metabolism; Vascular Endothelial Growth Factor Receptor-2 - metabolism; 생물학; Brown adipogenesis; VEGFR2; PTPRB; obesity
• ISSN: 1017-7825; 1738-8872; 1738-8872
• DOI: 10.4014/jmb.1810.10033

Brown adipocytes have an important role in the regulation of energy balance through uncoupling protein-1 (UCP-1)-mediated nonshivering thermogenesis. Although brown adipocytes have been highlighted as a new therapeutic target for the treatment of metabolic diseases, such as obesity and type II diabetes in adult humans, the molecular mechanism underlying brown adipogenesis is not fully understood. We recently found that protein tyrosine phosphatase receptor type B (PTPRB) expression dramatically decreased during brown adipogenic differentiation. In this study, we investigated the functional roles of PTPRB and its regulatory mechanism during brown adipocyte differentiation. Ectopic expression of PTPRB led to a reduced brown adipocyte differentiation by suppressing the tyrosine phosphorylation of VEGFR2, whereas a catalytic inactive PTPRB mutant showed no effects on differentiation and phosphorylation. Consistently, the expression of brown adipocyte-related genes, such as UCP-1, PGC-1α, PRDM16, PPAR-γ, and CIDEA, were significantly inhibited by PTPRB overexpression. Overall, these results suggest that PTPRB functions as a negative regulator of brown adipocyte differentiation through its phosphatase activity-dependent mechanism and may be used as a target protein for the regulation of obesity and type II diabetes.