Gene · 2025
TESC activates the C-SRC/IGF1Rβ/PI3K/AKT/VEGFA signaling pathway to promote myocardial angiogenesis in cardiac hypertrophy induced by an 8-week swimming exercise program.
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Ma Zhichao, Ding Mingchao, Hu Yarui, Mou Caiying, Xun Weiwei, Cen Yanling, Sun Jun, Bi Rui, Qui Yanli, Huo Keke, Liu Zizhang, Wang Xudong, Yu Xuedong, Jin Li
Аннотация
BACKGROUND: This study investigates the role of Tescalcin (TESC) in promoting myocardial angiogenesis during adaptive cardiac hypertrophy induced by swimming exercise.
METHODS: Female rats were divided into a control group (CN, n = 8) and an exercise training group (ET, n = 10). RNA sequencing was conducted to identify key genes involved in exercise-induced vascular remodeling. Cardiac function was evaluated by echocardiography, while myocardial hypertrophy and capillary density were assessed through histological analysis and CD31 immunostaining. Gene and protein expression levels were measured using quantitative PCR and Western blotting, respectively.
RESULTS: In the ET group, swimming exercise significantly increased the heart weight-to-body weight ratio and cardiomyocyte diameter, without upregulating markers of pathological hypertrophy. Capillary density and the expression of angiogenesis-related proteins (PI3K, p-AKT, VEGFA, and VEGFR2) were significantly elevated. RNA-seq analysis identified TESC as the most upregulated gene, a finding that was further validated by qPCR and Western blotting. To elucidate the underlying mechanisms, rat coronary microvascular endothelial cells (RCMECs) were assigned to six groups: control (Con), TESC overexpression (Ad-TESC), overexpression control (Ad-GFP), TESC knockdown (sh-TESC), knockdown control (sh-GFP), and TESC knockdown with IGF1 supplementation (sh-TESC+IGF). In the Ad-TESC group, endothelial cell proliferation and tube formation were enhanced via activation of the C-SRC/IGF1Rβ and PI3K/AKT/VEGFA pathways. Conversely, in the sh-TESC group, angiogenesis was suppressed, accompanied by reduced phosphorylation of C-SRC and IGF1Rβ, along with inhibition of downstream signaling. IGF1 treatment partially rescued the angiogenic activity.
CONCLUSION: swimming exercise promotes myocardial angiogenesis during adaptive cardiac remodeling by activating the TESC-mediated C-SRC/IGF1Rβ/ PI3K/AKT/VEGFA signaling pathway.
METHODS: Female rats were divided into a control group (CN, n = 8) and an exercise training group (ET, n = 10). RNA sequencing was conducted to identify key genes involved in exercise-induced vascular remodeling. Cardiac function was evaluated by echocardiography, while myocardial hypertrophy and capillary density were assessed through histological analysis and CD31 immunostaining. Gene and protein expression levels were measured using quantitative PCR and Western blotting, respectively.
RESULTS: In the ET group, swimming exercise significantly increased the heart weight-to-body weight ratio and cardiomyocyte diameter, without upregulating markers of pathological hypertrophy. Capillary density and the expression of angiogenesis-related proteins (PI3K, p-AKT, VEGFA, and VEGFR2) were significantly elevated. RNA-seq analysis identified TESC as the most upregulated gene, a finding that was further validated by qPCR and Western blotting. To elucidate the underlying mechanisms, rat coronary microvascular endothelial cells (RCMECs) were assigned to six groups: control (Con), TESC overexpression (Ad-TESC), overexpression control (Ad-GFP), TESC knockdown (sh-TESC), knockdown control (sh-GFP), and TESC knockdown with IGF1 supplementation (sh-TESC+IGF). In the Ad-TESC group, endothelial cell proliferation and tube formation were enhanced via activation of the C-SRC/IGF1Rβ and PI3K/AKT/VEGFA pathways. Conversely, in the sh-TESC group, angiogenesis was suppressed, accompanied by reduced phosphorylation of C-SRC and IGF1Rβ, along with inhibition of downstream signaling. IGF1 treatment partially rescued the angiogenic activity.
CONCLUSION: swimming exercise promotes myocardial angiogenesis during adaptive cardiac remodeling by activating the TESC-mediated C-SRC/IGF1Rβ/ PI3K/AKT/VEGFA signaling pathway.