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长链非编码 RNA MIR503HG 通过靶向 miR-191-5p/PLCδ1 轴负向调节腹主动脉瘤中的细胞凋亡、细胞外基质破坏和炎症。

lncRNA MIR503HG Targets miR-191-5p/PLCD1 Axis and Negatively Modulates Apoptosis, Extracellular Matrix Disruption, and Inflammation in Abdominal Aortic Aneurysm.

机构信息

Department of Vascular and Thyroid Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830000 Xinjiang Uygur Autonomous Region, China.

Department of Gastrointestinal Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830000 Xinjiang Uygur Autonomous Region, China.

出版信息

Mediators Inflamm. 2023 May 16;2023:4003618. doi: 10.1155/2023/4003618. eCollection 2023.

DOI:10.1155/2023/4003618
PMID:37228901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10205412/
Abstract

As the most prevalent subtype of aortic aneurysm, abdominal aortic aneurysm (AAA) features the apoptosis, extracellular matrix (ECM) disruption, and inflammation response of vascular smooth muscle cells (VSMCs). Noncoding RNAs (ncRNAs) are crucial factors in AAA progression, while the investigations have not been fully explained. miR-191-5p upregulation is found in aortic aneurysm. However, its role in AAA has not been addressed. This research purposed to excavate the possible and associated molecular axis of miR-191-5p in AAA. In our study, miR-191-5p level was detected to be high in the tissues from AAA patients in comparison with the control group. After miR-191-5p expression was enhanced, cell viability was repressed, cell apoptosis was boosted, and ECM disruption and the inflammation response were fortified. Furthermore, the relationship among MIR503HG, miR-191-5p, and phospholipase C delta 1 (PLCD1) in VSMCs was disclosed via mechanism assays. Decreased MIR503HG lacked the inhibition on miR-191-5p targeting PLCD1, resulting in downregulation of PLCD1, which facilitated the progression of AAA. Thus, targeting MIR503HG/miR-191-5p/PLCD1 pathway will provide an additional method for the cure of AAA patients.

摘要

作为最常见的主动脉瘤亚型,腹主动脉瘤(AAA)的特征在于血管平滑肌细胞(VSMCs)的凋亡、细胞外基质(ECM)破坏和炎症反应。非编码 RNA(ncRNA)是 AAA 进展的关键因素,但研究尚未得到充分解释。miR-191-5p 在主动脉瘤中上调。然而,其在 AAA 中的作用尚未得到解决。本研究旨在挖掘 miR-191-5p 在 AAA 中可能的相关分子轴。在我们的研究中,与对照组相比,AAA 患者组织中的 miR-191-5p 水平较高。增强 miR-191-5p 的表达后,细胞活力受到抑制,细胞凋亡增加,ECM 破坏和炎症反应增强。此外,通过机制研究揭示了 VSMCs 中 MIR503HG、miR-191-5p 和磷脂酶 C 三角洲 1(PLCD1)之间的关系。减少的 MIR503HG 缺乏对 miR-191-5p 靶向 PLCD1 的抑制作用,导致 PLCD1 下调,从而促进 AAA 的进展。因此,靶向 MIR503HG/miR-191-5p/PLCD1 途径将为 AAA 患者的治疗提供一种额外的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/e98bdb92394d/MI2023-4003618.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/4b4f8822e3e7/MI2023-4003618.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/13d5af37c6b0/MI2023-4003618.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/9807e4a75747/MI2023-4003618.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/f8c266a3a465/MI2023-4003618.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/e98bdb92394d/MI2023-4003618.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/4b4f8822e3e7/MI2023-4003618.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/13d5af37c6b0/MI2023-4003618.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/9807e4a75747/MI2023-4003618.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/f8c266a3a465/MI2023-4003618.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741d/10205412/e98bdb92394d/MI2023-4003618.005.jpg

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