Abstract
Sleep apnea syndrome is characterized by recurrent episodes of oxygen desaturation and reoxygenation (intermittent hypoxia [IH]), and it is a known risk factor for hypertension. The upregulation of the renin-angiotensin system has been reported in IH, and the correlation between renin and CD38 has been noted. We exposed human HEK293 and mouse As4.1 renal cells to experimental IH or normoxia for 24 h and then measured the mRNA levels using a real-time reverse transcription polymerase chain reaction. The mRNA levels of Renin (Ren) and Cd38 were significantly increased by IH, indicating that they could be involved in the CD38-cyclic ADP-ribose signaling pathway. We next investigated the promotor activities of both genes, which were not increased by IH. Yet, a target mRNA search of the microRNA (miRNA) revealed both mRNAs to have a potential target sequence for miR-203. The miR-203 level of the IH-treated cells was significantly decreased when compared with the normoxia-treated cells. The IH-induced upregulation of the genes was abolished by the introduction of the miR-203 mimic, but not the miR-203 mimic NC negative control. These results indicate that IH stress downregulates the miR-203 in renin-producing cells, thereby resulting in increased mRNA levels of Ren and Cd38, which leads to hypertension.
Highlights
Sleep apnea syndrome (SAS) is a highly prevalent sleep disorder characterized by the repetitive partial or complete collapse of the pharynx during sleep
There are a number of possible reasons why the miR-203 level was decreased by IH, including (i) the fact that the mRNA levels of some enzymes involved in miRNA biosynthesis/degradation are influenced by IH and (ii) the fact that the level of miR-203 is decreased by IH, either via decreased biosynthesis or enhanced degradation
SAS patients and their organs, tissues, and cells are exposed to IH but not to sustained hypoxia
Summary
Sleep apnea syndrome (SAS) is a highly prevalent sleep disorder characterized by the repetitive partial or complete collapse of the pharynx during sleep. The pathophysiology of hypertension in cases of SAS is complex and is dependent on various factors Among those factors, the upregulation of the renin-angiotensin system (RAS) is of critical importance. Several studies have suggested the regulation of Ren to be controlled by. In addition,ADP-ribose several studies have suggested the regulation of Ren be controlled the CD38-cyclic (cADPR)-mediated signaling pathway [5].tocADPR serves by as the CD38-cyclic. CADPR serves as a a second messenger in terms of controlling thesignaling intracellular. The present study sought to investigate the gene expression of both Ren and CD38, as as well as their regulation mechanisms in response to IH stress in Ren-producing cells.
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