Long Noncoding RNA-GAS5: A Novel Regulator of Hypertension-Induced Vascular Remodeling
| Autor: | Kun Shan, Yong Ji, Biao Yan, Qin Jiang, Jia-Jian Wang, Ban Liu, Yao Jin, Mu-Di Yao, Yangyang Zhang, Yang-Ning-Zhi Wang, Xiang Li |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Vascular smooth muscle Cell 030204 cardiovascular system & hematology Biology Vascular Remodeling Transfection Sensitivity and Specificity Statistics Nonparametric Endothelial activation 03 medical and health sciences Random Allocation 0302 clinical medicine Internal medicine Rats Inbred SHR Internal Medicine medicine Animals Humans RNA Small Nucleolar Cells Cultured beta Catenin Cell Proliferation Regulation of gene expression Gene knockdown Endothelial Cells Rats Endothelial stem cell Disease Models Animal 030104 developmental biology Endocrinology medicine.anatomical_structure Gene Expression Regulation Hypertension cardiovascular system Cancer research RNA Long Noncoding GAS5 Signal transduction Signal Transduction |
| Zdroj: | Hypertension (Dallas, Tex. : 1979). 68(3) |
| ISSN: | 1524-4563 |
| Popis: | Vascular remodeling is an important pathological feature of hypertension, leading to increased vascular resistance and reduced compliance. Endothelial cell (EC) and vascular smooth muscle cell (VSMC) dysfunction is involved in vascular remodeling. Long noncoding RNAs are potential regulators of EC and VSMC function. Herein, we determined whether long noncoding RNA–growth arrest–specific 5 (GAS5) is involved in hypertension-related vascular remodeling. We revealed that GAS5 knockdown aggravated hypertension-induced microvascular dysfunction as shown by increased retinal neovascularization and capillary leakage. GAS5 regulated the remodeling of arteries, including caudal arteries, carotid arteries, renal arteries, and thoracic arteries. GAS5 was mainly expressed in ECs and VSMCs, and its expression was significantly downregulated in hypertension. GAS5 knockdown affected endothelial activation, endothelial proliferation, VSMC phenotypic conversion, and EC-VSMC communication in vivo and in vitro. Mechanistically, GAS5 regulated EC and VSMC function through β-catenin signaling. This study identified GAS5 as a critical regulator in hypertension and demonstrated the potential of gene therapy and drug development for treating hypertension. |
| Databáze: | OpenAIRE |
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