TMIGD1 Inhibited Abdominal Adhesion Formation by Alleviating Oxidative Stress in the Mitochondria of Peritoneal Mesothelial Cells.
TMIGD1 Inhibited Abdominal Adhesion Formation by Alleviating Oxidative Stress in the Mitochondria of Peritoneal Mesothelial Cells.
复制标题
TMIGD1 通过减轻腹膜间皮细胞线粒体的氧化应激抑制腹部粘连形成
DOI：
10.1155/2021/9993704
复制
发表时间：
2021
影响因子：
--
通讯作者：
Wei G
中科院分区：
文献类型：
--
作者：
Wu Y;Li E;Wang Z;Shen T;Shen C;Liu D;Gao Q;Li X;Wei G
背景术后腹腔粘连是腹部手术后常见的并发症之一，缺乏有效的干预措施。腹膜间皮细胞损伤和愈合在粘连形成过程中起着至关重要的作用，确定这种机制可能为这种疾病的可能新的治疗策略提供新的见解。跨膜免疫球蛋白结构域1（Transmembrane and immunoglobulin domain-containing 1，TMIGD 1）是一种新型的粘附分子，具有保护肾上皮细胞免受氧化应激损伤的作用。在这里，我们研究了TMIGD 1的作用及其在粘附形成中的可能机制。材料与方法采用免疫组化、qPCR和免疫荧光法检测TMIGD 1的表达。采用粘连分级和粘连强度评分评价粘连形成情况。建立了TMIGD 1过表达的HMrSV 5细胞系。采用MTT法、Western印迹法、Annexin V细胞凋亡分析和CK 19染色来测量间皮细胞的活力、细胞凋亡和完整性。ROS和MDA检测用于测量间皮细胞氧化应激水平。JC-1染色，IHF和透射电子显微镜进行评估线粒体功能。采用创伤实验和粘附实验评价间皮细胞的粘附能力。结果首先，我们发现TMIGD 1在小鼠腹腔粘连组织和腹膜间皮细胞中表达减少。其次，TMIGD 1过表达抑制粘连形成。第三，TMIGD 1过表达保护间皮细胞免受过氧化氢（H2 O2-）诱导的氧化应激损伤。第四，TMIGD 1过表达通过保护间皮细胞的线粒体功能减轻氧化应激。此外，TMIGD 1过表达增强间皮细胞粘附。结论TMIGD 1可能通过保护正常腹腔粘连组织中线粒体功能而保护间皮细胞免受氧化应激损伤。此外，TMIGD 1增强腹膜间皮细胞粘附以促进愈合。
Background Postoperative abdominal adhesion remains one of the frequent complications after abdominal surgery and lacks effective intervention. Peritoneal mesothelial cell injury and healing play crucial roles in the process of adhesion formation, and identifying this mechanism might provide new insight into possible new therapeutic strategies for this disease. Transmembrane and immunoglobulin domain-containing 1 (TMIGD1) has been proven to protect renal epithelial cells from injury induced by oxidative stress and has also been identified as a novel adhesion molecule. Here, we investigated the role of TMIGD1 and its possible mechanism in adhesion formation. Materials and Methods Immunohistochemistry (IHC), qPCR, and immunofluorescence (IHF) were used to detect the expression of TMIGD1. The grade and tenacity score of adhesion were used to evaluate the adhesion formation conditions. A TMIGD1-overexpressing HMrSV5 cell line was established. MTT assay, Western blotting, Annexin V apoptosis analysis, and CK19 staining were used to measure mesothelial cell viability, apoptosis, and completeness. ROS and MDA detection were used to measure mesothelial cell oxidative stress levels. JC-1 staining, IHF, and transmission electron microscopy were performed to assess mitochondrial function. Scratch-wound and adhesion assays were used to evaluate the adhesion ability of mesothelial cells. Results First, we showed that TMIGD1 was decreased in mouse abdominal adhesion tissue and peritoneal mesothelial cells. Second, TMIGD1 overexpression inhibited adhesion formation. Third, TMIGD1 overexpression protected mesothelial cells from hydrogen peroxide- (H2O2-) induced oxidative stress injury. Fourth, TMIGD1 overexpression alleviated oxidative stress by protecting the mitochondrial function of mesothelial cells. In addition, TMIGD1 overexpression enhanced mesothelial cell adhesion. Conclusion Our findings suggest that TMIGD1 protects mesothelial cells from oxidative stress injury by protecting their mitochondrial function, which is decreased in regular abdominal adhesion tissue. In addition, TMIGD1 enhances peritoneal mesothelial cell adhesion to promote healing.
登录
查看更多内容
影响因子：
4.1
作者：
Kitamura, Shinji;Horimoto, Naoya;Makino, Hirofumi
通讯作者：
Makino, Hirofumi
影响因子：
7.3
作者：
Sandoval, Pilar;Jimenez-Heffernan, Jose A.;Lopez-Cabrera, Manuel
通讯作者：
Lopez-Cabrera, Manuel
影响因子：
--
作者：
Liakopoulos V;Roumeliotis S;Gorny X;Eleftheriadis T;Mertens PR
通讯作者：
Mertens PR
DOI：
10.1159/000380971
发表时间：
2015-01-01
期刊：
CHRONIC KIDNEY DISEASES - RECENT ADVANCES IN CLINICAL AND BASIC RESEARCH
影响因子：
--
作者：
Kawanishi, Kunio;Nitta, Kosaku
通讯作者：
Nitta, Kosaku
影响因子：
2.2
作者：
ten Raa, Sander;van den Tol, M. Petrousjka;Jeekel, Hans
通讯作者：
Jeekel, Hans