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抑制lncRNA-MALAT1活性通过调节mTOR信号通路改善股骨头坏死。

Suppression of lncRNA-MALAT1 activity ameliorates femoral head necrosis by modulating mTOR signaling.

作者信息

Ma Luyao, Gao Jian

机构信息

Department of Orthopaedics, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.

Second Clinical Medical College, Shanxi Medical University, Taiyuan, Shanxi, China.

出版信息

Arch Med Sci. 2020 Feb 2;20(2):612-617. doi: 10.5114/aoms.2020.92829. eCollection 2024.

DOI:10.5114/aoms.2020.92829
PMID:38757012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11094837/
Abstract

INTRODUCTION

Avascular necrosis of the femoral head (ANFH) is one of the most complicated bone disorders; management remains challenging. We evaluated the effect of lncRNA-MALAT1 suppression on ANFH rats.

MATERIAL AND METHODS

Dexamethasone was injected intravenously at 0.5 mg/kg daily for 30 days to induce ANFH; an lncRNA-MALAT1 inhibitor group received the inhibitor for the entire 30 days. LncRNA-MALAT1 suppression was evaluated by measuring blood hexosamine and hydroxyproline levels, and that of circulating endothelial progenitor cells (EPCs). Changes in femoral head bone ultrastructure were assessed via transmission electron microscopy and magnetic resonance imaging (MRI). We used reverse transcription polymerase chain reaction (RT-PCR) and Western blotting to measure gene and protein expression levels in femoral head tissue.

RESULTS

The blood hexosamine level rose and that of hydroxyproline fell in the LncRNA-MALAT1 inhibitor group compared to the ANFH group. LncRNA-MALAT1 suppression increased the level of circulating EPCs. Ultrastructural changes in the femoral bone head were alleviated by the lncRNA-MALAT1 inhibitor. LncRNA-MALAT1 suppression lowered the levels of AMPK, mTOR, and Beclin-1 in rat tissue homogenates.

CONCLUSIONS

LncRNA-MALAT1 suppression attenuated dexamethasone-induced femoral head necrosis by regulating AMPK/mTOR/Beclin-1 signaling.

摘要

引言

股骨头缺血性坏死（ANFH）是最复杂的骨疾病之一；其治疗仍然具有挑战性。我们评估了lncRNA-MALAT1抑制对ANFH大鼠的影响。

材料与方法

每天静脉注射地塞米松0.5mg/kg，持续30天以诱导ANFH；lncRNA-MALAT1抑制剂组在整个30天内接受抑制剂。通过测量血液中的己糖胺和羟脯氨酸水平以及循环内皮祖细胞（EPC）的水平来评估lncRNA-MALAT1的抑制情况。通过透射电子显微镜和磁共振成像（MRI）评估股骨头骨超微结构的变化。我们使用逆转录聚合酶链反应（RT-PCR）和蛋白质印迹法来测量股骨头组织中的基因和蛋白质表达水平。

结果

与ANFH组相比，lncRNA-MALAT1抑制剂组血液中的己糖胺水平升高，羟脯氨酸水平降低。lncRNA-MALAT1的抑制增加了循环EPC的水平。lncRNA-MALAT1抑制剂减轻了股骨头的超微结构变化。lncRNA-MALAT1的抑制降低了大鼠组织匀浆中AMPK、mTOR和Beclin-1的水平。

结论

lncRNA-MALAT1的抑制通过调节AMPK/mTOR/Beclin-1信号通路减轻了地塞米松诱导的股骨头坏死。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/4c31010f9d3f/AMS-20-2-115495-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/d9139872500b/AMS-20-2-115495-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/cb5aafe02bdf/AMS-20-2-115495-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/df73b0a7e201/AMS-20-2-115495-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/4c31010f9d3f/AMS-20-2-115495-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/d9139872500b/AMS-20-2-115495-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/112ecec1b296/AMS-20-2-115495-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/cb5aafe02bdf/AMS-20-2-115495-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/3eea9eb46594/AMS-20-2-115495-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/df73b0a7e201/AMS-20-2-115495-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d920/11094837/4c31010f9d3f/AMS-20-2-115495-g006.jpg

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