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糖尿病肾病中的系膜血管生成和间质嗜酸性粒细胞浸润与CD248表达升高有关。

Mesangial angiogenesis and interstitial eosinophilic infiltration in diabetic nephropathy are associated with elevated CD248 expression.

作者信息

Li Xiangmeng, Zhang Jiao, Wang Ying, Yu Tianyu, Jiang Shimin, Gao Yan, Zhang Haisong, Li Wenge

机构信息

Department of Nephrology, China-Japan Friendship Hospital, Beijing, China.

China-Japan Friendship Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

出版信息

Ren Fail. 2025 Dec;47(1):2510552. doi: 10.1080/0886022X.2025.2510552. Epub 2025 Jun 1.

DOI:10.1080/0886022X.2025.2510552
PMID:40451785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12128132/
Abstract

OBJECTIVES

To investigate the factors associated with angiogenesis within the glomerular mesangial area and interstitial eosinophilic infiltration in diabetic nephropathy (DN).

METHODS

The NCBI database identified differentially expressed genes (DEGs) in DN patients linked to angiogenesis and inflammation. Bioinformatics analyzed these genes and mechanisms. (DN patients and db/db mice) and experiments explored glomerular mesangial angiogenesis and interstitial eosinophilic infiltration mechanisms.

RESULTS

Twenty-five independent DEGs associated with DN were identified, and CD248 was associated with vessel formation and inflammatory cells. Biological analysis suggested CD248 mainly promoted vessel formation and eosinophilic infiltration VEGFC and CCL-5, respectively. In DN patients, neovascularization with CD31-positive endothelial cells was observed in the mesangial regions, which was accompanied by increased expression of CD248 and VEGFC. Eosinophilic infiltration was observed in the renal interstitium, and the degree of eosinophilic infiltration was positively correlated with the intensity of CD248 expression. Serial section analysis revealed that areas with increased eosinophilic infiltration exhibited stronger infiltration of CD3-positive cells and elevated CCL-5 expression. Similar findings were discovered in the db/db mice, with WB results demonstrating higher expression levels of CD248, CCL-5, and VEGFC in the renal tissues of db/db mice compared with m/m mice. , CD248 expression is low in mesangial cells, but increased under high-glucose/LPS. CD248 siRNA reduced high-glucose/LPS-induced VEGFC/CCL-5.

CONCLUSION

In DN, CD248 may contribute to mesangial angiogenesis and renal interstitial eosinophilic infiltration; these pathological processes may be associated with the elevated expressions of VEGFC and CCL-5, respectively.

摘要

目的

探讨糖尿病肾病（DN）肾小球系膜区血管生成及间质嗜酸性粒细胞浸润的相关因素。

方法

NCBI数据库鉴定出与血管生成和炎症相关的DN患者差异表达基因（DEG）。生物信息学分析这些基因及其机制。（DN患者和db/db小鼠）并通过实验探究肾小球系膜血管生成和间质嗜酸性粒细胞浸润机制。

结果

鉴定出25个与DN相关的独立DEG，CD248与血管形成和炎症细胞相关。生物学分析表明，CD248主要分别通过VEGFC和CCL-5促进血管形成和嗜酸性粒细胞浸润。在DN患者中，系膜区观察到CD31阳性内皮细胞的新生血管形成，同时伴有CD248和VEGFC表达增加。在肾间质观察到嗜酸性粒细胞浸润，嗜酸性粒细胞浸润程度与CD248表达强度呈正相关。连续切片分析显示，嗜酸性粒细胞浸润增加的区域CD3阳性细胞浸润更强且CCL-5表达升高。在db/db小鼠中也发现了类似结果，WB结果显示与m/m小鼠相比，db/db小鼠肾组织中CD248、CCL-5和VEGFC表达水平更高。系膜细胞中CD248表达低，但在高糖/LPS条件下增加。CD248 siRNA降低了高糖/LPS诱导的VEGFC/CCL-5。

结论

在DN中，CD248可能促进系膜血管生成和肾间质嗜酸性粒细胞浸润；这些病理过程可能分别与VEGFC和CCL-5表达升高有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/b506fc9d1b54/IRNF_A_2510552_F0008_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/8fefeaf7c1c6/IRNF_A_2510552_UF0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/cd92405cd36a/IRNF_A_2510552_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/04071c1c8bad/IRNF_A_2510552_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/62b836fbca2a/IRNF_A_2510552_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/db9fdcc35de2/IRNF_A_2510552_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/47f72f10caa1/IRNF_A_2510552_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/bd46c0db1526/IRNF_A_2510552_F0006_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/6aa53f542205/IRNF_A_2510552_F0007_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/b506fc9d1b54/IRNF_A_2510552_F0008_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/8fefeaf7c1c6/IRNF_A_2510552_UF0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/cd92405cd36a/IRNF_A_2510552_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/04071c1c8bad/IRNF_A_2510552_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/62b836fbca2a/IRNF_A_2510552_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/db9fdcc35de2/IRNF_A_2510552_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/47f72f10caa1/IRNF_A_2510552_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/bd46c0db1526/IRNF_A_2510552_F0006_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/6aa53f542205/IRNF_A_2510552_F0007_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63f/12128132/b506fc9d1b54/IRNF_A_2510552_F0008_C.jpg

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