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四连接蛋白通过 ERK 信号增强有丝分裂克隆扩张介导的脂肪生成功能。

Adipogenic function of tetranectin mediated by enhancing mitotic clonal expansion via ERK signaling.

机构信息

Department of Medical Biotechnology and Research Institute of Cell Culture, Yeungnam University, Gyeongsan 38541, Korea.

Department of Botany, Munshi Singh College, BR Ambedkar Bihar University, Muzaffarpur, Bihar 845401, India.

出版信息

BMB Rep. 2021 Jul;54(7):374-379. doi: 10.5483/BMBRep.2021.54.7.024.

DOI:10.5483/BMBRep.2021.54.7.024
PMID:33691910
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8328820/
Abstract

Tetranectin (TN), an adipogenic serum protein, enhances adipocyte differentiation, however, its functional mechanism has yet to be elucidated. In the present study, we investigated the adipogenic function of TN by using medium containing TN-depleted fetal bovine serum (TN-del-FBS) and recombinant mouse TN (mTN). The adipocyte differentiation of 3T3-L1 cells was significantly enhanced by mTN supplementation essentially at differentiation induction, which indicated a potential role of the protein in the early differentiation phase. The adipogenic effect of mTN was more significant with insulin in the differentiation induction cocktail, implicating their close functional relationship. mTN enhanced not only the proliferation of growing cells, but also mitotic clonal expansion (MCE) that is a prerequisite for adipocyte differentiation in the early phase. Consistently, mTN increased the phosphorylation of ERK in the early phase of adipocyte differentiation. Results of this study demonstrate that the adipogenic function of mTN is mediated by enhancing MCE via ERK signaling. [BMB Reports 2021; 54(7): 374-379].

摘要

纤连蛋白(TN)是一种成脂性血清蛋白,可增强脂肪细胞分化,但其功能机制尚不清楚。本研究通过使用 TN 耗尽胎牛血清(TN-del-FBS)和重组小鼠 TN(mTN)的培养基来研究 TN 的成脂功能。mTN 补充剂可显著增强 3T3-L1 细胞的脂肪细胞分化,主要在分化诱导期,这表明该蛋白在早期分化阶段具有潜在作用。在分化诱导混合物中添加胰岛素后,mTN 的成脂作用更为显著,表明它们具有密切的功能关系。mTN 不仅增强了生长细胞的增殖,而且还增强了有丝分裂克隆扩增(MCE),这是早期脂肪细胞分化的前提。一致地,mTN 增加了脂肪细胞分化早期 ERK 的磷酸化。本研究结果表明,mTN 的成脂功能是通过 ERK 信号增强 MCE 介导的。[BMB 报告 2021;54(7): 374-379]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/c3dd16961510/bmb-54-7-374-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/8a1598f6a521/bmb-54-7-374-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/a98bd06b0635/bmb-54-7-374-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/9dd91a355765/bmb-54-7-374-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/c3dd16961510/bmb-54-7-374-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/8a1598f6a521/bmb-54-7-374-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/a98bd06b0635/bmb-54-7-374-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/9dd91a355765/bmb-54-7-374-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a24/8328820/c3dd16961510/bmb-54-7-374-f4.jpg

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