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Platelet-rich plasma (PRP) is an autologous preparation used to accelerate regeneration; however, this form of therapy is not always effective. Vascular endothelial growth factor B (VEGFB), which affects vessel survival, pathological angiogenesis, and muscle development may differentiate the risk and treatment of lateral elbow tendinopathy (LET). In this study, we analyzed the influence of VEGFB gene polymorphisms on the effectiveness of LET treatment with PRP. Therapeutic effectiveness was analyzed in 107 patients (132 elbows) using patient-reported outcome measures (PROMs), specifically the visual analog scale (VAS); quick version of disabilities of the arm, shoulder, and hand score (QDASH); and patient-rated tennis elbow evaluation (PRTEE), for two years (weeks 2, 4, 8, 12, 24, 52, and 104). The polymorphisms selected for the study were rs72922019, rs12366035, rs4930152, rs594942, and rs595880, being in strong linkage disequilibrium. Patients with TT (rs72922019), TT (rs12366035), AA (rs4930152), CC (rs594942), and GG (rs595880) genotypes showed better treatment effectiveness. Statistically important differences were shown for rs72922019 VAS (week 2), QDASH (weeks 0–4), and PRTEE (week 2); rs12366035 and rs4930152 VAS (week 2), QDASH (week 2), and PRTEE (weeks 2 and 4); and rs594942 and rs595880 VAS (weeks 2 and 4), QDASH (week 2), and PRTEE (weeks 2, 52, and 104). The studied polymorphisms also showed an association with blood morphological parameters, including mean platelet volume, platelet distribution width, and eosinophil levels, as well as some comorbidities (heart failure). Genotyping due to patient selection for therapy may be considered for any of the rs72922019, rs12366035, or rs4930152 polymorphisms. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

It has been demonstrated that vascular endothelial growth factor B (VEGFB) plays a vital role in regulating vascular biological function. However, the role of VEGFB in regulating skeletal muscle cell proliferation and differentiation remains unclear. Thus, this study aimed to investigate the effects of VEGFB on C2C12 myoblast proliferation and differentiation and to explore the underlying mechanism. For proliferation, VEGFB significantly promoted the proliferation of C2C12 myoblasts with the upregulating expression of cyclin D1 and PCNA. Meanwhile, VEGFB enhanced vascular endothelial growth factor receptor 1 (VEGFR1) expression and activated the PI3K/Akt signaling pathway in a VEGFR1-dependent manner. In addition, the knockdown of VEGFR1 and inhibition of PI3K/Akt totally abolished the promotion of C2C12 proliferation induced by VEGFB, suggesting that VEGFB promoted C2C12 myoblast proliferation through the VEGFR1-PI3K/Akt signaling pathway. Regarding differentiation, VEGFB significantly stimulated the differentiation of C2C12 myoblasts via VEGFR, with elevated expressions of MyoG and MyHC. Furthermore, the knockdown of VEGFR1 rather than NRP1 eliminated the VEGFB-stimulated C2C12 differentiation. Moreover, VEGFB activated the PI3K/Akt/mTOR signaling pathway in a VEGFR1-dependent manner. However, the inhibition of PI3K/Akt/mTOR blocked the promotion of C2C12 myoblasts differentiation induced by VEGFB, indicating the involvement of the PI3K/Akt pathway. To conclude, these findings showed that VEGFB promoted C2C12 myoblast proliferation and differentiation via the VEGFR1-PI3K/Akt signaling pathway, providing new insights into the regulation of skeletal muscle development. [ABSTRACT FROM AUTHOR]