Regulation of Renin Expression by Β1-Integrin in As4.1 Juxtaglomerular Line Cells.
Biomedicines
; 11(2)2023 Feb 09.
Article
em En
| MEDLINE
| ID: mdl-36831037
ABSTRACT
(1) Background:
Renal dysfunction and hypertension are mutually aggravating factors; however, the details of their interaction remain unclear. In a study using renal tissue from diabetic rats, we found that ß1-integrin, a cell-substrate adhesion molecule, is specifically phosphorylated in juxtaglomerular cells that secrete renin, a blood pressure regulator. (2)Methods:
A mouse juxtaglomerular cell line (As4.1 cells) was used for the following experiments drug-induced promotion of ß1-integrin phosphorylation/dephosphorylation; knockdown of ß1-integrin and the cell adhesion molecule connexin-40 (a candidate for the main body of baroreceptor); and pressurization to atmospheric pressure + 100 mmHg. culture in hypotonic liquid medium. The expression of renin under these conditions was measured by qRT-PCR. (3)Results:
Phosphorylation of ß1-integrin suppressed the expression of renin, while dephosphorylation conversely promoted it. ß1-integrin and connexin-40 knockdown both promoted the expression of renin. Pneumatic pressurization and hypotonic medium culture both decreased the expression of renin, which was restored by the knockdown of ß1-integrin. (4)Conclusions:
ß1-integrin plays an inhibitory role in the regulation of the expression of renin, which may be controlled by phosphorylation and dephosphorylation. It is hypothesized that ß1-integrin and other adhesion factors regulate the expression of renin by altering the sensitivity of baroreceptors on the plasma membrane.
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Base de dados:
MEDLINE
Idioma:
En
Revista:
Biomedicines
Ano de publicação:
2023
Tipo de documento:
Article
País de afiliação:
Japão