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首页> 外文期刊>European review for medical and pharmacological sciences. >Effect of miR-202-5p-mediated ATG7 on autophagy and apoptosis of degenerative nucleus pulposus cells
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Effect of miR-202-5p-mediated ATG7 on autophagy and apoptosis of degenerative nucleus pulposus cells

机译:miR-202-5P介导的ATG7对退化核脉搏细胞自噬和凋亡的影响

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OBJECTIVE: This study aimed to research the effect of miR-202-5p-mediated ATG7 on autophagy and apoptosis of degenerative nucleus pulposus cells. PATIENTS AND METHODS: The intervertebral disc nucleus pulposus (NP) tissue of patients with intervertebral disc degenerative disease and normal intervertebral disc nucleus pulposus (NP) tissue of patients with spinal fractures was collected as the research object. Normal NP cells and degenerative NP cells were isolated. Low expression of miR-202-5p and overexpression of ATG7 were carried out in degenerative NP cells. The expression of miR-202-5p and ATG7 mRNA was detected by RT-PCR. The expression of ATG7, LC3-II, Bax, and Bcl-2 proteins was detected by Western blot. The autophagy of cells was detected by MDC staining. The apoptosis of NP cells was detected by flow cytometry. The targeting relationship between miR-202-5p and ATG7 was detected by Dual-Luciferase reporter. RESULTS: In the degenerative NP tissues, miR-202-5p was highly expressed and ATG7 was low expressed. The inhibition of miR-202-5p expression can effectively promote autophagy of NP cells, increase the expression of ATG7 and LC3-II, inhibit the apoptosis of NP cells, inhibit the expression of pro-apoptotic proteins Bax, and promote the expression of pro-apoptotic proteins Bcl-2 proteins. The upregulation of ATG7 expression in degenerative NP cells alone had the same effect as the downregulation of miR-202-5p. The assay of the Dual-Luciferase reporter confirmed the targeting relationship between miR-202-5p and ATG7. CONCLUSIONS: MiR-202-5p can affect the autophagy and apoptosis of degenerative nucleus pulposus cells through targeted adjustment of ATG7, which may be a new therapeutic target for intervertebral disc degenerative diseases.
机译:目的:本研究旨在研究MIR-202-5P介导的ATG7对退行性核牙髓细胞自噬和凋亡的影响。患者和方法:收集脊髓骨折患者患者椎间盘退行性疾病和正常椎间盘核髓组织(NP)组织作为研究对象。分离正常的NP细胞和退行性NP细胞。 MiR-202-5P的低表达和ATG7的过表达在退化的NP细胞中进行。通过RT-PCR检测miR-202-5P和ATG7 mRNA的表达。通过Western印迹检测ATG7,LC3-II,Bax和Bcl-2蛋白的表达。通过MDC染色检测细胞的自噬。通过流式细胞术检测NP细胞的凋亡。用双荧光素酶报告机检测miR-202-5p和ATG7之间的靶向关系。结果:在退化的NP组织中,高表达miR-202-5P,表达了催化剂。 miR-202-5P表达的抑制可以有效地促进NP细胞的自噬,增加ATG7和LC3-II的表达,抑制NP细胞的凋亡,抑制促凋亡蛋白培养的表达,促进Pro的表达-apoptotic蛋白Bcl-2蛋白。单独的退化NP细胞中ATG7表达的上调具有与miR-202-5p的下调相同的效果。双荧光素酶报告者的测定证实了MIR-202-5P和ATG7之间的靶向关系。结论:MiR-202-5P通过ATG7的靶向调节,可以影响退化核骨髓细胞的自噬和凋亡,这可能是椎间盘退行性疾病的新治疗靶标。

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