Effects of all-trans retinoic acid on orphan receptor APJ signaling in spontaneously hypertensive rats
JC Zhong, DY Huang, GF Liu, HY Jin… - Cardiovascular …, 2005 - academic.oup.com
JC Zhong, DY Huang, GF Liu, HY Jin, YM Yang, YF Li, XH Song, K Du
Cardiovascular research, 2005•academic.oup.comObjective: Studies show general agreement that all-trans retinoic acid (atRA) has been
linked to the regulation of G protein-coupled receptor (GPCRs) signaling. To further validate
effects of atRA on the cardiovascular GPCRs, the present study was designed to assess
whether atRA will modulate orphan receptor APJ, a homologue of angiotensin II type 1 (AT1)
receptor. Methods: Real-time polymerase chain reaction and Western blot methods were
performed to examine the expression of APJ and its endogenous ligand apelin in …
linked to the regulation of G protein-coupled receptor (GPCRs) signaling. To further validate
effects of atRA on the cardiovascular GPCRs, the present study was designed to assess
whether atRA will modulate orphan receptor APJ, a homologue of angiotensin II type 1 (AT1)
receptor. Methods: Real-time polymerase chain reaction and Western blot methods were
performed to examine the expression of APJ and its endogenous ligand apelin in …
Abstract
Objective: Studies show general agreement that all-trans retinoic acid (atRA) has been linked to the regulation of G protein-coupled receptor (GPCRs) signaling. To further validate effects of atRA on the cardiovascular GPCRs, the present study was designed to assess whether atRA will modulate orphan receptor APJ, a homologue of angiotensin II type 1 (AT1) receptor.
Methods: Real-time polymerase chain reaction and Western blot methods were performed to examine the expression of APJ and its endogenous ligand apelin in spontaneously hypertensive rats (SHR) and Wistar–Kyoto (WKY) rats after chronic atRA treatment.
Results: APJ and apelin expression were markedly depressed in placebo-treated SHR, compared with WKY rats (p<0.01). However, in atRA-treated SHR, a significant upregulation of APJ and apelin expression was observed in both heart and aorta (p<0.05), accompanied by a reduction of AT1 expression, an elevation of serum nitric oxide levels and a subsequent decrease of blood pressure.
Conclusions: Chronic atRA treatment activates gene and protein expression of APJ and apelin and reduces blood pressure in SHR, suggesting that atRA may regulate the balance between apelin-APJ and angiotensin II-AT1 signaling and have potential clinical value in the prevention and treatment of human hypertension.
Oxford University Press