Abstract

BackgroundEssential hypertension (EH) is an inflammatory disease, and endothelial dysfunction induced by chronic inflammation is one of the pathogeneses of EH. The expression of some inflammatory mediators may be regulated by the interaction of circular RNAs (circRNAs) and microRNAs (miRNAs).MethodsAn Agilent human circRNA microarray was used to identify the expression profile of circRNAs in EH. qRT‐PCR was used to evaluate the relative expression of circRNAs in 48 pairs of human whole blood samples (sex and age ± 3 years matched) and endothelial cells. TNF‐α was applied to induce endothelial cells inflammation. CircRNA‐miRNA network was predicted by MiRanda software.ResultsThere were 287 circRNAs differentially expressed in the microarray. The top 10 up‐regulated circRNAs in the EH group were hsa_circ_0014243, hsa_circ_0133228, hsa‐circRNA14116‐3, hsa_circ_0079536, hsa‐circRNA13649‐1, hsa_circ_0117886, hsa_circ_0007075, hsa‐circRNA15285‐1, hsa‐circRNA10088‐9, and hsa‐circRNA14119‐10; the top 10 down‐regulated circRNAs were hsa_circ_0100094, hsa_circ_0127342, hsa_circ_0093773, hsa_circ_0096334, hsa_circ_0131618, hsa_circ_0063886, hsa_circ_0097804, hsa_circ_0126640, hsa‐circRNA8935‐1, and hsa_circ_0039978 (fold change in descending order). Hsa_circ_0105015 has two predicted binding sites with hsa‐miR‐637. The relative expression of hsa_circ_0105015 in EH patients was significantly higher than healthy controls (P = .002), and similar results appeared in TNF‐α‐induced endothelial cells. The area under the curve after hsa_circ_0105015 combined with hsa‐miR‐637 was 0.703, P < .001.ConclusionHyperexpression of hsa_circ_0105015 is a significant risk factor of EH and its association with EH involves inflammatory pathways. Hyperexpression of hsa_circ_0105015 combined with hypoexpression of hsa‐miR‐637 indicates vascular inflammation or endothelial dysfunction and has potential as a biomarker for early diagnosis of EH.

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