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ColXV 加剧脂肪细胞凋亡,促进小鼠细胞外基质异常重塑。

ColXV Aggravates Adipocyte Apoptosis by Facilitating Abnormal Extracellular Matrix Remodeling in Mice.

机构信息

College of Animal Science and Technology, Northwest A&F University, Yangling 712100, China.

出版信息

Int J Mol Sci. 2020 Jan 31;21(3):959. doi: 10.3390/ijms21030959.

Abstract

The extracellular matrix (ECM) is a highly dynamic structural network and plays an essential role in cell behavior and regulation during metabolic homeostasis and obesity progression. Abnormal ECM remodeling impairs adipocyte plasticity required for diverse cellular functions. Collagen XV (ColXV) is a proteoglycan localized to the outermost layer of basement membranes (BMs) and forms a bridge between the BMs and the fibrillar collagen matrix. Nevertheless, how ColXV affects ECM composition and the reason for subsequent adipocyte apoptosis is still unclear. This report found, through RNA-seq data, that ColXV is linked to cell growth and ECM remodeling. Findings show that, in response to excessive expression of extracellular ColXV, the AMPK/mTORC1 pathway is strongly activated and triggers a cascade of mitochondrial apoptosis. This is the first study to make use of ECM three-dimensional reconstruction, based on decellularization in the adipose tissues and the study reveals that ColXV is an activation factor that alters ECM remodeling in adipose tissues. It was also demonstrated that the fibroblast growth factor 2 (FGF2)/fibroblast growth factor receptor 1 (FGFR1) axis involved in ECM remodeling is suppressed by ColXV due to reduction of FGF2 translocation to FGFR1. Furthermore, ColXV induced remodeling of ECM preceding apoptosis and continued to induce apoptosis in adipocytes. Collectively, our findings establish ColXV as a basement membrane collagen with homology to ColXVIII, indicating that it is one of the positive regulators for inducing ECM remodeling and further promoting adipocyte apoptosis.

摘要

细胞外基质(ECM)是一个高度动态的结构网络,在代谢稳态和肥胖进展过程中对细胞行为和调节起着至关重要的作用。异常的 ECM 重塑会损害脂肪细胞的多样性细胞功能所必需的可塑性。XV 型胶原(ColXV)是一种定位于基底膜(BM)最外层的蛋白聚糖,在 BM 和纤维状胶原基质之间形成桥梁。然而,ColXV 如何影响 ECM 组成以及随后脂肪细胞凋亡的原因尚不清楚。本报告通过 RNA-seq 数据发现,ColXV 与细胞生长和 ECM 重塑有关。研究结果表明,在细胞外 ColXV 过度表达的情况下,AMPK/mTORC1 通路被强烈激活,并引发一连串的线粒体凋亡。这是第一项利用 ECM 三维重建的研究,该研究基于脂肪组织的脱细胞化,并揭示了 ColXV 是一种改变脂肪组织 ECM 重塑的激活因子。此外,由于 FGF2 向 FGFR1 的易位减少,ColXV 还抑制了涉及 ECM 重塑的成纤维细胞生长因子 2(FGF2)/成纤维细胞生长因子受体 1(FGFR1)轴。此外,ColXV 诱导 ECM 重塑先于细胞凋亡,并继续诱导脂肪细胞凋亡。总之,我们的研究结果确立了 ColXV 作为与 ColXVIII 同源的基底膜胶原,表明它是诱导 ECM 重塑并进一步促进脂肪细胞凋亡的正向调节因子之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9588/7037489/8238ec29104f/ijms-21-00959-g001.jpg

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