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Corin 在肾缺血/再灌注损伤中下调,与肾移植后延迟肾功能恢复有关。

Corin Is Downregulated in Renal Ischemia/Reperfusion Injury and Is Associated with Delayed Graft Function after Kidney Transplantation.

机构信息

Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.

Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China.

出版信息

Dis Markers. 2019 Jan 14;2019:9429323. doi: 10.1155/2019/9429323. eCollection 2019.

DOI:10.1155/2019/9429323
PMID:30766618
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6350528/
Abstract

Renal ischemia/reperfusion (IR) injury is one of the most important risk factors for the occurrence of delayed graft function (DGF) after kidney transplantation; however, its mechanism remains not fully understood. In the present study, we screened differentially expressed genes in a murine model of renal IR injury by using high-throughput assays. We identified as one of the most significantly downregulated genes among 2218 differentially expressed genes (≥2-fold, < 0.05). By using a real-time qPCR assay, we observed that the expression of renal in IR-injured mice was reduced to 11.5% of the sham-operated mice and that the protein level of renal Corin in IR-injured mice was also downregulated. Interestingly, renal IR injury in mice induced the downregulation of Corin in heart tissues, suggesting that the overall synthesis of Corin may be suppressed. We recruited 11 recipients complicated with DGF and 16 without DGF, and plasma Corin concentrations were determined by ELISA. We observed that the plasma Corin levels were indeed reduced in recipients complicated with DGF (0.98 vs. 1.95 ng/ml, < 0.05). These findings demonstrate that Corin may be a potential biomarker of DGF after kidney transplantation and may participate in the regulation of renal IR injury.

摘要

肾缺血/再灌注(IR)损伤是肾移植后发生延迟移植物功能障碍(DGF)的最重要危险因素之一;然而,其机制仍不完全清楚。在本研究中,我们通过高通量检测筛选了肾 IR 损伤小鼠模型中的差异表达基因。我们发现,在 2218 个差异表达基因(≥2 倍, < 0.05)中, 是下调最显著的基因之一。通过实时 qPCR 检测,我们观察到 IR 损伤小鼠的肾组织中 Corin 的表达降低至 sham 手术组的 11.5%,并且肾组织中 Corin 的蛋白水平也下调。有趣的是,小鼠的肾 IR 损伤诱导了心脏组织中 Corin 的下调,表明 Corin 的整体合成可能受到抑制。我们招募了 11 名伴有 DGF 的受者和 16 名无 DGF 的受者,并通过 ELISA 测定了血浆 Corin 浓度。我们观察到伴有 DGF 的受者的血浆 Corin 水平确实降低(0.98 与 1.95ng/ml, < 0.05)。这些发现表明 Corin 可能是肾移植后 DGF 的潜在生物标志物,并可能参与肾 IR 损伤的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/3d09091831ed/DM2019-9429323.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/9878ccdecf75/DM2019-9429323.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/d48b2037ed59/DM2019-9429323.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/0bb698b9ac1e/DM2019-9429323.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/3d09091831ed/DM2019-9429323.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/9878ccdecf75/DM2019-9429323.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/d48b2037ed59/DM2019-9429323.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/0bb698b9ac1e/DM2019-9429323.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca6/6350528/3d09091831ed/DM2019-9429323.004.jpg

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