CD73 alleviates podocytes injury in adriamycin-induced nephrotic syndrome.

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell Pub Date : 2024-12-01 DOI:10.1016/j.tice.2024.102647

Yanji Zhu, Guiling Xie, Fangyan Qi, ShenWei Tang, Wenlong Xun

{"title":"CD73 alleviates podocytes injury in adriamycin-induced nephrotic syndrome.","authors":"Yanji Zhu, Guiling Xie, Fangyan Qi, ShenWei Tang, Wenlong Xun","doi":"10.1016/j.tice.2024.102647","DOIUrl":null,"url":null,"abstract":"<p><p>Podocyte injury is considered one of the main causes of kidney diseases occurrence and development. We have demonstrated that Ecto-5'-Nucleotidase (CD73) upregulated during podocyte injury, yet its function in podocyte is still unclear. Mouse podocytes cell line (MPC5) were exposed to the adriamycin (ADR, 0.25 μg/ml) to establish the model of podocytes injury, as well as low expression CD73 with lentivirus transfected shRNA. CD73 expression was verified by western blot and immunofluorescence assay. Cytokines (IL-1β, IL-18), apoptosis and apoposis-related protein (Bax, Caspase-3, Desmin) levels were measured using ELISA assay, Flow cytometry and Western blot, respectively. CD73, the cytokines of IL-1β and IL-18, apoptosis rate and the expression of Bax, Caspase-3 and Desmin were significantly increased in ADR group compared with the control group. Moreover, we also successfully constructed a CD73 down-expressed podocytes cell line. However, in comparsion with the ADR group, the cytokines of IL-1β and IL-18, apoptosis rate and the expression of Bax, Caspase-3 and Desmin protein were remarkably lowered in the ADR+CD73 shRNA group. These findings demonstrate that CD73 alleviates podocyte damage by reducing the inflammation and increasing apoptosis.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102647"},"PeriodicalIF":2.7000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue & cell","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/j.tice.2024.102647","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Podocyte injury is considered one of the main causes of kidney diseases occurrence and development. We have demonstrated that Ecto-5'-Nucleotidase (CD73) upregulated during podocyte injury, yet its function in podocyte is still unclear. Mouse podocytes cell line (MPC5) were exposed to the adriamycin (ADR, 0.25 μg/ml) to establish the model of podocytes injury, as well as low expression CD73 with lentivirus transfected shRNA. CD73 expression was verified by western blot and immunofluorescence assay. Cytokines (IL-1β, IL-18), apoptosis and apoposis-related protein (Bax, Caspase-3, Desmin) levels were measured using ELISA assay, Flow cytometry and Western blot, respectively. CD73, the cytokines of IL-1β and IL-18, apoptosis rate and the expression of Bax, Caspase-3 and Desmin were significantly increased in ADR group compared with the control group. Moreover, we also successfully constructed a CD73 down-expressed podocytes cell line. However, in comparsion with the ADR group, the cytokines of IL-1β and IL-18, apoptosis rate and the expression of Bax, Caspase-3 and Desmin protein were remarkably lowered in the ADR+CD73 shRNA group. These findings demonstrate that CD73 alleviates podocyte damage by reducing the inflammation and increasing apoptosis.

查看原文本刊更多论文

求助全文

约1分钟内获得全文求助全文

来源期刊

Tissue & cell 医学-解剖学与形态学

CiteScore

3.90

自引率

0.00%

发文量

234

期刊介绍： Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.