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Knockdown of VEGFB/VEGFR1 Signaling Promotes White Adipose Tissue Browning and Skeletal Muscle Development
Authors:Mingfa Ling  Xumin Lai  Lulu Quan  Fan Li  Limin Lang  Yiming Fu  Shengchun Feng  Xin Yi  Canjun Zhu  Ping Gao  Xiaotong Zhu  Lina Wang  Gang Shu  Qingyan Jiang  Songbo Wang
Affiliation:1.Guangdong Provincial Key Laboratory of Animal Nutrition Control, College of Animal Science, South China Agricultural University, Guangzhou 510642, China; (M.L.); (X.L.); (L.Q.); (F.L.); (L.L.); (Y.F.); (S.F.); (X.Y.); (C.Z.); (P.G.); (X.Z.); (L.W.); (G.S.); (Q.J.);2.National Engineering Research Center for the Breeding Swine Industry, South China Agricultural University, Guangzhou 510642, China
Abstract:It has been demonstrated that vascular endothelial growth factor B (VEGFB) and vascular endothelial growth factor receptor 1 (VEGFR1) play a vital role in regulating vascular biological function. However, the role of VEGFB and VEGFR1 in regulating fat deposition and skeletal muscle growth remains unclear. Therefore, this study was conducted to investigate the effects of VEGFB and VEGFR1 on fat deposition and skeletal muscle growth in mice. Our results showed that knockdown of VEGFB decreased body weight and iWAT index, stimulated the browning of mice iWAT with increased expression of UCP1, decreased the diameters of adipocytes, and elevated energy expenditure. In contrast, knockdown of VEGFB increased gastrocnemius (GAS) muscle index with increased proliferation of GAS muscle by expression of PCNA and Cyclin D1. Meanwhile, knockdown of endothelial VEGFR1 induced the browning of iWAT with increased expression of UCP1 and decreased diameters of adipocytes. By contrast, knockdown of endothelial VEGFR1 inhibited GAS muscle differentiation with decreased expression of MyoD. In conclusion, these results suggested that the loss of VEGFB/VEGFR1 signaling is associated with enhanced browning of inguinal white adipose tissue and skeletal muscle development. These results provided new insights into the regulation of skeletal muscle growth and regeneration, as well as fat deposition, suggesting the potential application of VEGFB/VEGFR1 as an intervention for the restriction of muscle diseases and obesity and related metabolic disorders.
Keywords:VEGFB   VEGFR1   skeletal muscle   proliferation   differentiation   iWAT browning
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