Renal lysophospholipase A1 contributes to Enterococcus faecalis-induced hypertension by enhancing sodium reabsorption

Yuting Liu; Qing Zhu; Yufeng Tao; Yuting Zeng; Shasha Li; Liangyu Zeng; Chun Zhang; Yang Chen; Lei Wang

doi:10.1016/j.isci.2022.105403

Renal lysophospholipase A1 contributes to Enterococcus faecalis-induced hypertension by enhancing sodium reabsorption

iScience. 2022 Oct 19;25(12):105403. doi: 10.1016/j.isci.2022.105403. eCollection 2022 Dec 22.

Authors

Yuting Liu¹, Qing Zhu², Yufeng Tao¹, Yuting Zeng¹, Shasha Li³, Liangyu Zeng¹, Chun Zhang⁴, Yang Chen¹, Lei Wang¹

Affiliations

¹ School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, China.
² Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, China.
³ Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, China.
⁴ Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China.

Abstract

Our recent study has found that gut bacteria Enterococcus faecalis contributes to hypertension and upregulates lysophospholipase A1 (LYPLA1) in the renal medulla of rats. This work aimed to investigate the role of LYPLA1 in the development of E. faecalis-induced hypertension. Compared to control, E. faecalis treatment increased blood pressure (BP), serum angiotensin II, sodium reabsorption, and expression of αENaC and LYPLA1 in the renal medulla of mice, and these effects were attenuated by knockdown of LYPLA1. Moreover, the intrarenal lypla1 overexpression increased sodium reabsorption and BP. Further studies showed that LYPLA1 promoted the accumulation of renal glycerophosphocholine (GPC), which directly elevated the expression of αENaC and sodium reabsorption. In addition, enriched abundance of LYPLA1 in the renal medulla and urine was also observed in other hypertensive animals. Overall, our results demonstrate that LYPLA1 contributes to E. faecalis-induced hypertension by accumulating GPC and activating ENaC in the renal medulla.

Keywords: Biological sciences; Endocrine regulation; Endocrinology; Microbial metabolism.