NEDD4 对大鼠骨间充质干细胞成骨潜能的影响与 PI3K/Akt 通路有关。

IF 2.2 3区生物学 Q4 CELL BIOLOGY Differentiation Pub Date : 2025-01-01 DOI:10.1016/j.diff.2024.100830

Bo Li , Shuang Zhang , Xiaoxian Yun , Chengyi Liu , Rui Xiao , Mingjie Lu , Xiaomei Xu , Fuwei Lin

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引用次数: 0

摘要

神经前体细胞表达发育下调4 （NEDD4）是一种E3泛素连接酶，与颅面发育有关。新出现的证据表明NEDD4可能下调Akt信号，Akt信号是参与细胞分化的PI3K/Akt通路的关键元件。本研究旨在探讨NEDD4在骨间充质干细胞（BMSCs）分化中的作用及其与PI3K/Akt通路的相互作用。从SD大鼠分离骨髓间充质干细胞，NEDD4表达在成骨分化过程中增加。在诱导过程中，用siRNA沉默NEDD4可提高碱性磷酸酶（ALP）、骨钙素（OCN）、Akt和mTORC1的表达，而随后用LY294002（一种广谱PI3K抑制剂）治疗可降低Akt、mTORC1、ALP和OCN的水平。这些发现表明NEDD4可能通过抑制成骨过程中PI3K/Akt通路抑制BMSCs分化。

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NEDD4's effect on osteoblastogenesis potential of bone mesenchymal stem cells in rats concerned with PI3K/Akt pathway

Neural precursor cell expressed developmentally down-regulated 4 (NEDD4) is an E3 ubiquitin ligase implicated in craniofacial development. Emerging evidence suggests that NEDD4 may down-regulates Akt signaling, a key element of the PI3K/Akt pathway involved in cell differentiation. This study aimed to investigate NEDD4's role in bone mesenchymal stem cells (BMSCs) differentiation and its interaction with the PI3K/Akt pathway.

BMSCs were isolated from SD rats, and NEDD4 expression increased during osteogenic differentiation. Silencing NEDD4 with siRNA elevated alkaline phosphatase (ALP), osteocalcin (OCN), Akt, and mTORC1 expression during induction, while subsequent treatment with LY294002 (a broad spectrum PI3K inhibitor) reduced Akt, mTORC1, ALP, and OCN levels.

These findings suggest that NEDD4 may inhibit BMSCs differentiation by suppressing the PI3K/Akt pathway during osteogenesis.

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来源期刊

Differentiation 生物-发育生物学

CiteScore

4.10

自引率

3.40%

发文量

审稿时长

51 days

期刊介绍： Differentiation is a multidisciplinary journal dealing with topics relating to cell differentiation, development, cellular structure and function, and cancer. Differentiation of eukaryotes at the molecular level and the use of transgenic and targeted mutagenesis approaches to problems of differentiation are of particular interest to the journal. The journal will publish full-length articles containing original work in any of these areas. We will also publish reviews and commentaries on topics of current interest. The principal subject areas the journal covers are: • embryonic patterning and organogenesis • human development and congenital malformation • mechanisms of cell lineage commitment • tissue homeostasis and oncogenic transformation • establishment of cellular polarity • stem cell differentiation • cell reprogramming mechanisms • stability of the differentiated state • cell and tissue interactions in vivo and in vitro • signal transduction pathways in development and differentiation • carcinogenesis and cancer • mechanisms involved in cell growth and division especially relating to cancer • differentiation in regeneration and ageing • therapeutic applications of differentiation processes.