
Periodontitis aggravates kidney injury by upregulating STAT1 expression in a mouse model of hypertension
Author(s) -
Yang Qin,
Ding Handong,
Wei Wei,
Liu Jie,
Wang Jiajia,
Ren Jie,
Chan Weicheng,
Wang Min,
Hao Liang,
Li Jinle,
Yue Yuan
Publication year - 2021
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.13081
Subject(s) - porphyromonas gingivalis , periodontitis , medicine , fibrosis , downregulation and upregulation , kidney , kidney disease , stat1 , inflammation , acute kidney injury , knockout mouse , immunology , receptor , biology , gene , biochemistry
Periodontitis is an autoimmune disease of periodontal tissues initiated by plaque. It is known that there is a close connection between periodontitis and CKD with hypertension, but the underlying mechanisms are unknown. STAT1 has been reported to play a regulatory role in hypertension and chronic kidney disease (CKD). Here, we investigated whether STAT1 regulates periodontitis‐mediated aggravation of kidney injury with accompanying hypertension. A hypertensive renal injury mouse model was established with Nos3 knockout mice, and a periodontitis model was established by implantation with the oral bacteria Porphyromonas gingivalis . The mice were intraperitoneally injected with a STAT1 inhibitor. Periodontitis aggravated kidney injury in hypertensive mice, and upregulation of STAT1 was observed when both periodontitis and hypertension were present; furthermore, STAT1 inhibitor moderated this effect. Moreover, we observed that periodontitis promoted the upregulation of inflammatory and fibrosis gene expression in the kidneys of hypertensive mice. In addition, STAT1 inhibition decreased the expression of pro‐inflammatory and pro‐fibrotic cytokines in the kidney lesion area. Periodontitis augmented the expression of inflammatory and fibrosis genes by upregulating the expression of STAT1, thereby aggravating kidney injury in the hypertensive mouse model.