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神经纤毛蛋白 1（NRP1）正向调控 C3H10T1/2 细胞的成脂分化。

Neuropilin 1 (NRP1) Positively Regulates Adipogenic Differentiation in C3H10T1/2 Cells.

机构信息

Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Shenyang 110002, China.

Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8525, Japan.

出版信息

Int J Mol Sci. 2023 Apr 17;24(8):7394. doi: 10.3390/ijms24087394.

DOI:10.3390/ijms24087394
PMID:37108554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10138427/
Abstract

Neuropilin 1 (NRP1), a non-tyrosine kinase receptor for several ligands, is highly expressed in many kinds of mesenchymal stem cells (MSCs), but its function is poorly understood. In this study, we explored the roles of full-length NRP1 and glycosaminoglycan (GAG)-modifiable NRP1 in adipogenesis in C3H10T1/2 cells. The expression of full-length NRP1 and GAG-modifiable NRP1 increased during adipogenic differentiation in C3H10T1/2 cells. NRP1 knockdown repressed adipogenesis while decreasing the levels of Akt and ERK1/2 phosphorylation. Moreover, the scaffold protein JIP4 was involved in adipogenesis in C3H10T1/2 cells by interacting with NRP1. Furthermore, overexpression of non-GAG-modifiable NRP1 mutant (S612A) greatly promoted adipogenic differentiation, accompanied by upregulation of the phosphorylated Akt and ERK1/2. Taken together, these results indicate that NRP1 is a key regulator that promotes adipogenesis in C3H10T1/2 cells by interacting with JIP4 and activating the Akt and ERK1/2 pathway. Non-GAG-modifiable NRP1 mutant (S612A) accelerates the process of adipogenic differentiation, suggesting that GAG glycosylation is a negative post-translational modification of NRP1 in adipogenic differentiation.

摘要

神经纤毛蛋白 1（NRP1）是一种非酪氨酸激酶受体，能够与多种配体结合，在许多间充质干细胞（MSCs）中高度表达，但它的功能尚未完全阐明。在本研究中，我们探讨了全长 NRP1 和糖胺聚糖（GAG）可修饰 NRP1 在 C3H10T1/2 细胞成脂分化中的作用。全长 NRP1 和 GAG 可修饰 NRP1 的表达在 C3H10T1/2 细胞的成脂分化过程中增加。NRP1 敲低抑制成脂分化，同时降低 Akt 和 ERK1/2 磷酸化水平。此外，支架蛋白 JIP4 通过与 NRP1 相互作用参与 C3H10T1/2 细胞的成脂分化。此外，过表达非 GAG 可修饰的 NRP1 突变体（S612A）极大地促进了成脂分化，伴随着磷酸化 Akt 和 ERK1/2 的上调。综上所述，这些结果表明，NRP1 是一种关键调节因子，通过与 JIP4 相互作用并激活 Akt 和 ERK1/2 通路，促进 C3H10T1/2 细胞的成脂分化。非 GAG 可修饰的 NRP1 突变体（S612A）加速了成脂分化的过程，表明 GAG 糖基化是 NRP1 在成脂分化中的一种负翻译后修饰。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0992/10138427/f47d35ae6393/ijms-24-07394-g006.jpg
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