Downregulation of Arntl mRNA Expression in Women with Hypertension: A Case-Control Study
Background: Previous studies have reported that disturbance of endogenous circadian rhythms enhances the chance of hypertension and suggested that circadian clock genes could have a crucial function in the onset of the disease. This case-control study was aimed to investigate the association of the...
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Veröffentlicht in: | Kidney & blood pressure research 2021-12, Vol.46 (6), p.741-748 |
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Sprache: | eng |
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Zusammenfassung: | Background: Previous studies have reported that disturbance of endogenous circadian rhythms enhances the chance of hypertension and suggested that circadian clock genes could have a crucial function in the onset of the disease. This case-control study was aimed to investigate the association of the mRNA expression of aryl hydrocarbon receptor nuclear translocator like (Arntl), clock circadian regulator (Clock), and period circadian regulators 1 and 2 (Per1 and Per2) with hypertension and blood pressure levels. Methods: A total of 172 subjects were recruited in this study, including 86 hypertension and 86 nonhypertension controls. The mRNA expression levels in peripheral blood mononuclear cells were determined by real-time quantitative polymerase chain reaction. The differences in Arntl, Clock, Per1, and Per2 mRNA expression were compared between the 2 groups, and the relationship between mRNA expression and cardiometabolic risk profiles was also assessed. Results: We found that the mRNA expression of Arntl was downregulated in the hypertension cases compared with controls in women (1.10 [0.66, 1.71] vs. 1.30 [0.99, 2.06], p = 0.031). There was a significant negative correlation between the Arntl mRNA expression and SBP (r = −0.301, p = 0.004) and DBP (r = −0.222, p = 0.034) in women. In men, a negative correlation between the Per1 mRNA expression and SBP (r = −0.247, p = 0.026) was found. Conclusions: The Arntl mRNA expression may play an important role in progression of hypertension in women. |
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ISSN: | 1420-4096 1423-0143 |
DOI: | 10.1159/000518669 |