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S100钙结合蛋白A16通过抑制SMAD家族成员4信号传导来抑制大鼠骨髓间充质干细胞的成骨分化。

S100 calcium‑binding protein A16 suppresses the osteogenic differentiation of rat bone marrow mesenchymal stem cells by inhibiting SMAD family member 4 signaling.

作者信息

Xin Jing, Wang Zhaoxu, Shen Yanju, Bai Jing, Shen Yafei

机构信息

Department of Endocrinology and Diabetes, Luohe Central Hospital, Luohe First People's Hospital, The First Affiliated Hospital of Luohe Medical College, Luohe, Henan 462000, P.R. China.

出版信息

Exp Ther Med. 2024 Apr 15;27(6):250. doi: 10.3892/etm.2024.12538. eCollection 2024 Jun.

DOI:10.3892/etm.2024.12538
PMID:38682113
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11046178/
Abstract

Osteogenesis is a complex process of bone formation regulated by various factors, yet its underlying molecular mechanisms remain incompletely understood. The present study aimed to investigate the role of S100A16, a novel member of the S100 protein family, in the osteogenic differentiation of rat bone marrow mesenchymal stem cells (BMSCs) and uncover a novel Smad4-mitogen-activated protein kinase (MAPK)/Jun N-terminal kinase (JNK) signaling axis. In the present study, the expression level of S100A16 in bone tissues and BMSCs from ovariectomized rats was evaluated and then the impact of S100A16 silencing on osteogenic differentiation was examined. Increased S100A16 expression was observed in bone tissues and BMSCs from ovariectomized rats, and S100A16 silencing promoted osteogenic differentiation. Further transcriptomic sequencing revealed that the Smad4 pathway was involved in S100A16 silencing-induced osteogenesis. The results of western blot analysis revealed that S100A16 overexpression not only downregulated Smad4 but also activated MAPK/JNK signaling, which was validated by treatment with MAPK and JNK inhibitors U0126 and SP600125. Overall, in the present study, the novel regulatory factors influencing osteogenic differentiation were elucidated and mechanistic insights that could aid in the development of targeted therapeutic strategies for patients with osteoporosis were provided.

摘要

骨生成是一个由多种因素调节的复杂骨形成过程，但其潜在的分子机制仍未完全阐明。本研究旨在探讨S100蛋白家族新成员S100A16在大鼠骨髓间充质干细胞（BMSCs）成骨分化中的作用，并揭示一条新的Smad4-丝裂原活化蛋白激酶（MAPK）/Jun氨基末端激酶（JNK）信号轴。在本研究中，评估了去卵巢大鼠骨组织和BMSCs中S100A16的表达水平，然后检测了S100A16沉默对成骨分化的影响。在去卵巢大鼠的骨组织和BMSCs中观察到S100A16表达增加，并且S100A16沉默促进了成骨分化。进一步的转录组测序显示，Smad4通路参与了S100A16沉默诱导的成骨过程。蛋白质印迹分析结果显示，S100A16过表达不仅下调Smad4，还激活MAPK/JNK信号，这通过用MAPK和JNK抑制剂U0126和SP600125处理得到验证。总体而言，本研究阐明了影响成骨分化的新调节因子，并提供了有助于为骨质疏松症患者制定靶向治疗策略的机制性见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/859c545dee5a/etm-27-06-12538-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/866eae091b72/etm-27-06-12538-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/cdd2def8c298/etm-27-06-12538-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/321ef24cc908/etm-27-06-12538-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/5b1ca0eb32f5/etm-27-06-12538-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/859c545dee5a/etm-27-06-12538-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/866eae091b72/etm-27-06-12538-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/cdd2def8c298/etm-27-06-12538-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/321ef24cc908/etm-27-06-12538-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/5b1ca0eb32f5/etm-27-06-12538-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35e/11046178/859c545dee5a/etm-27-06-12538-g04.jpg

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