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瘦素通过下调 Sirt5 增加 β-连环蛋白丙二酰化修饰来减弱 BMP9 的成骨诱导潜能。

Leptin attenuates the osteogenic induction potential of BMP9 by increasing β-catenin malonylation modification via Sirt5 down-regulation.

机构信息

Department of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, People's Republic of China.

Key Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, People's Republic of China.

出版信息

Aging (Albany NY). 2024 May 3;16(9):7870-7888. doi: 10.18632/aging.205790.

DOI:10.18632/aging.205790
PMID:38709288
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11131982/
Abstract

BMP9 has demonstrated significant osteogenic potential. In this study, we investigated the effect of Leptin on BMP9-induced osteogenic differentiation. Firstly, we found Leptin was decreased during BMP9-induced osteogenic differentiation and serum Leptin concentrations were increased in the ovariectomized (OVX) rats. Both and , exogenous expression of Leptin inhibited the process of osteogenic differentiation, whereas silencing Leptin enhanced. Exogenous Leptin could increase the malonylation of β-catenin. However, BMP9 could increase the level of Sirt5 and subsequently decrease the malonylation of β-catenin; the BMP9-induced osteogenic differentiation was inhibited by silencing Sirt5. These data suggested that Leptin can inhibit the BMP9-induced osteogenic differentiation, which may be mediated through reducing the activity of Wnt/β-catenin signalling via down-regulating Sirt5 to increase the malonylation level of β-catenin partly.

摘要

BMP9 具有显著的成骨潜能。在这项研究中，我们研究了瘦素对 BMP9 诱导的成骨分化的影响。首先，我们发现瘦素在 BMP9 诱导的成骨分化过程中减少，去卵巢（OVX）大鼠的血清瘦素浓度增加。无论是过表达还是敲低瘦素，都抑制了成骨分化过程，而敲低瘦素则增强了成骨分化过程。外源性瘦素可以增加β-连环蛋白的丙二酰化。然而，BMP9 可以增加 Sirt5 的水平，从而降低β-连环蛋白的丙二酰化；沉默 Sirt5 可以抑制 BMP9 诱导的成骨分化。这些数据表明，瘦素可以抑制 BMP9 诱导的成骨分化，这可能是通过下调 Sirt5 来降低 Wnt/β-连环蛋白信号通路的活性，部分增加β-连环蛋白的丙二酰化水平来介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/d835b4dfb7c8/aging-16-205790-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/c343539dc677/aging-16-205790-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/0d1decd50f40/aging-16-205790-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/89f307eaedc6/aging-16-205790-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/f12b4774ba1d/aging-16-205790-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/4ee1c9261b46/aging-16-205790-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/14e8a51e48af/aging-16-205790-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/e1d37709a9d8/aging-16-205790-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/99ac37abba31/aging-16-205790-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/d835b4dfb7c8/aging-16-205790-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/c343539dc677/aging-16-205790-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/0d1decd50f40/aging-16-205790-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/89f307eaedc6/aging-16-205790-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/f12b4774ba1d/aging-16-205790-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/4ee1c9261b46/aging-16-205790-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/14e8a51e48af/aging-16-205790-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/e1d37709a9d8/aging-16-205790-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/99ac37abba31/aging-16-205790-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c25c/11131982/d835b4dfb7c8/aging-16-205790-g009.jpg

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