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微小RNA-206通过抑制血管内皮生长因子/磷脂酰肌醇-3激酶/蛋白激酶B信号通路诱导股骨头缺氧性坏死。

Microrna-206 induces hypoxic necrosis of femoral head by inhibiting VEGF/PI3K/AKT signaling pathway.

作者信息

Wu Xingjing, Tao Zhoushan, Cheng Wenjing

机构信息

Department of Orthopedics, Yijishan Hospital, Wannan Medical College, Wuhu, Anhui, China.

出版信息

Front Genet. 2023 Feb 22;14:1118831. doi: 10.3389/fgene.2023.1118831. eCollection 2023.

DOI:10.3389/fgene.2023.1118831
PMID:36911416
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9992790/
Abstract

The most common form of non-traumatic necrosis of the femoral head is anoxic necrosis of the femoral head, which is a metabolic disease, mainly involving young and middle-aged people. Apoptosis and its related signal regulation pathway play an important role in the occurrence and development of hypoxic necrosis of the femoral head. In order to investigate the possible pathological manifestations of miR-206 and VEGF/PI3K/AKT signal pathway genes and their interactions in hypoxic necrosis of the femoral head, this paper intended to systematically study the expression and regulation mechanism of miR-206 and VEGF/PI3K/AKT signal pathway genes. The interaction between miR-206 and VEGF/PI3K/AKT signaling pathway and its regulation on apoptosis, differentiation and proliferation of human osteoblast cell line hFOB1.19 (SV40 transfer of human osteoblasts) were studied by double luciferase reporter gene analysis, overexpression and inhibition of miR-206, and gene silencing of VEGF/PI3K/AKT signaling pathway. After 24 h and 48 h of intervention with MicroRNA 206 on osteoblasts, it was found that the fluorescence intensity of caspase-3 was higher than that of 0 h group ( < 0.05). This paper has provided an important research basis for the research of femoral head necrosis and the development of new diagnosis and therapeutic drugs for this kind of disease. It also has provided a reference for the further promotion of the chemotherapy drug delivery system.

摘要

股骨头非创伤性坏死最常见的形式是股骨头缺血性坏死，这是一种代谢性疾病，主要累及中青年。细胞凋亡及其相关信号调节通路在股骨头缺血性坏死的发生发展中起重要作用。为了探讨miR-206与VEGF/PI3K/AKT信号通路基因在股骨头缺血性坏死中的可能病理表现及其相互作用，本文旨在系统研究miR-206与VEGF/PI3K/AKT信号通路基因的表达及调控机制。通过双荧光素酶报告基因分析、miR-206的过表达和抑制以及VEGF/PI3K/AKT信号通路的基因沉默，研究了miR-206与VEGF/PI3K/AKT信号通路之间的相互作用及其对人成骨细胞系hFOB1.19（人成骨细胞的SV40转染）凋亡、分化和增殖的调控。用MicroRNA 206干预成骨细胞24小时和48小时后，发现caspase-3的荧光强度高于0小时组（<0.05）。本文为股骨头坏死研究及此类疾病新诊断和治疗药物的开发提供了重要的研究依据。也为进一步推进化疗药物递送系统提供了参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/3ab7a930fdcd/fgene-14-1118831-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/77f42456075a/fgene-14-1118831-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/db723ee57825/fgene-14-1118831-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/ea987825dc47/fgene-14-1118831-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/3ab7a930fdcd/fgene-14-1118831-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/545094177c6a/fgene-14-1118831-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/e0ea9acf272d/fgene-14-1118831-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/bf9b3d4aab6f/fgene-14-1118831-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/b9875fa8c9d1/fgene-14-1118831-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/77f42456075a/fgene-14-1118831-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/db723ee57825/fgene-14-1118831-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/ea987825dc47/fgene-14-1118831-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9235/9992790/3ab7a930fdcd/fgene-14-1118831-g010.jpg

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