Effects of SPARCL1 on the proliferation and differentiation of sheep preadipocytes.

IF 3.5 4区 生物学 Q2 ENDOCRINOLOGY & METABOLISM
Cheng Xiao, Hai Guo Jin, Li Chun Zhang, Jian Qiang Liu, Ming He, Hui Hai Ma, Yong Sheng Yu, Yang Cao
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引用次数: 7

Abstract

Important candidate genes that regulate lipid metabolism have the potential to increase the content of intramuscular fat (IMF) and improve meat quality. Secreted protein acidic and rich in cysteine like 1(SPARCL1) is a secreted glycoprotein with important physiological functions and is involved in the proliferation and differentiation of various cells. However, the role of the SPARCL1 gene in sheep preadipocytes and its regulatory mechanism is still unclear. In this study, we explored the effect of SPARCL1 on the proliferation and differentiation of sheep preadipocytes. The results showed that the expression level of the SPARCL1 gene is higher in fat tissue than in other tissues, and the gene was significantly increased on the 6th day of preadipocyte differentiation. In the preadipocyte proliferation stage, interference of SPARCL1 gene reduced cell viability and increased cell apoptosis. In preadipocyte differentiation stage, SPARCL1 overexpression significantly inhibited lipid droplets accumulation and triglyceride content by increasing Wnt10b, Fzd8, IL6, and β-catenin and inhibiting PPARγ, C/EBPα, LPL, and IGF1 genes expression, whereas SPARCL1 deficiency significantly promoted cell differentiation by inhibiting β-catenin and increasing GSK3β, PPARγ, C/EBPα, and LPL. The results of this study suggest that SPARCL1 plays a negative role during preadipocyte differentiation and may become a novel target for regulating preadipocyte differentiation and improving IMF.Abbreviations:IMF: Intramuscular fat SPARCL1: Secreted protein acidic and rich in cysteine like 1 PPARγ: Peroxisome proliferator-activated receptor γ C/EBPα: CCAAT/enhancer-binding protein-α LPL: Lipoprotein lipase IGF1: Insulin-like growth factor 1 Wnt10b: Wnt family member 10B Fzd8: Frizzled class receptor 8 IL6: Interleukin 6 β-catenin: Catenin beta interacting protein 1 GSK3β: Glycogen synthase kinase 3 beta LRP5/6: Low-density lipoprotein receptor-related protein 5/6.

Abstract Image

Abstract Image

Abstract Image

SPARCL1对绵羊前脂肪细胞增殖和分化的影响。
调节脂质代谢的重要候选基因有可能增加肌内脂肪(IMF)含量并改善肉品质。酸性且富含半胱氨酸的分泌蛋白如1(SPARCL1)是一种具有重要生理功能的分泌糖蛋白,参与多种细胞的增殖和分化。然而,SPARCL1基因在绵羊前脂肪细胞中的作用及其调控机制尚不清楚。在本研究中,我们探讨了SPARCL1对绵羊前脂肪细胞增殖和分化的影响。结果表明,SPARCL1基因在脂肪组织中的表达水平高于其他组织,且在前脂肪细胞分化第6天显著升高。在前脂肪细胞增殖阶段,干扰SPARCL1基因可降低细胞活力,增加细胞凋亡。在脂肪前细胞分化阶段,SPARCL1过表达通过增加Wnt10b、Fzd8、IL6和β-catenin,抑制PPARγ、C/EBPα、LPL和IGF1基因表达,显著抑制脂滴积累和甘油三酯含量,而SPARCL1过表达通过抑制β-catenin,增加GSK3β、PPARγ、C/EBPα和LPL,显著促进细胞分化。本研究结果提示SPARCL1在前脂肪细胞分化过程中发挥负向作用,可能成为调节前脂肪细胞分化和改善IMF的新靶点。缩写:IMF:肌内脂肪SPARCL1:分泌蛋白酸性和富含半胱氨酸样1 PPARγ:过氧化物酶体增殖物激活受体γ C/EBPα: CCAAT/增强子结合蛋白-α LPL:脂蛋白脂肪酶IGF1:胰岛素样生长因子1 Wnt10b: Wnt家族成员10B Fzd8:毛状类受体8 IL6:白细胞介素6 β-连环蛋白:连环蛋白β相互作用蛋白1 GSK3β:糖原合成酶激酶3β LRP5/6:低密度脂蛋白受体相关蛋白5/6。
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来源期刊
Adipocyte
Adipocyte Medicine-Histology
CiteScore
6.50
自引率
3.00%
发文量
46
审稿时长
32 weeks
期刊介绍: Adipocyte recognizes that the adipose tissue is the largest endocrine organ in the body, and explores the link between dysfunctional adipose tissue and the growing number of chronic diseases including diabetes, hypertension, cardiovascular disease and cancer. Historically, the primary function of the adipose tissue was limited to energy storage and thermoregulation. However, a plethora of research over the past 3 decades has recognized the dynamic role of the adipose tissue and its contribution to a variety of physiological processes including reproduction, angiogenesis, apoptosis, inflammation, blood pressure, coagulation, fibrinolysis, immunity and general metabolic homeostasis. The field of Adipose Tissue research has grown tremendously, and Adipocyte is the first international peer-reviewed journal of its kind providing a multi-disciplinary forum for research focusing exclusively on all aspects of adipose tissue physiology and pathophysiology. Adipocyte accepts high-profile submissions in basic, translational and clinical research.
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