LncRNA FTX Regulates Angiogenesis Through miR-342-3p/SPI1 Axis in Stroke

Abstract

Background Long non-coding RNAs (lnc-RNAs) and microRNAs (miRNAs) play key roles in the development of stroke. However, the role of lncRNA FTX in stroke is limited known. Methods Real-time polymerase chain reaction (real-time PCR) assays were used to measure the expression of lncRNA FTX, miR-342-3p and SPI1. Western blot assays were employed to examine SPI1 protein expression. The cell viability was measured by CCk8 assay. Cell migration was detected by wound healing assays and transwell assays. Angiogenesis was evaluated by matrigel tube formation assays. The interaction between lncRNA FTX, miR-342-3p and SPI1 was confirmed by site-directed mutagenesis and luciferase assays. Results The expression of lncRNA FTX was down-regulated in blood sample from stroke patients, MAO mice tissues and OGD/R treated BMECs. Overexpression of lncRNA FTX could increase the cell viability, migration and angiogenesis in OGD/R treated BMECs. LncRNA FTX could act as a ceRNA for miR-342-3p. Furthermore, miR-342-3p inhibition increased migration and angiogenesis in OGD/R-induced BMECs. Dual-luciferase reporter assay verified that SPI1 was a target of miR-342-3p. Conclusion In summary, lncRNA FTX enhanced the angiogenesis in stroke by acting as a sponge of miR-342-3p to regulate the expression of SPI1 level.

Flow-Responsive Noncoding RNAs in the Vascular System: Basic Mechanisms for the Clinician

“…Most studies on miR-92a have focused on its role in ECs function. Inhibition of miR-92a significantly enhances endothelial recovery in carotid arteries after balloon injury or arterial stenting [62]. In line with those findings, it has been shown that inhibition of miR-92a in ECs increases endothelial recovery and thus prevents neointimal formation following wire-induced injury in mice [110].…”

“…LncRNA are able to exert an array of biological func tions, including: (1) regulation of DNA transcription by acting with a transcription facto (2) epigenetic silencing and repressing the histone modification via chromatin interaction (3) mRNA translation (4) post-translational regulation through miRNA sponges o circRNA, (5) scaffold of protein complex, (6) shorter ncRNAs (siRNA) generation (Figur 1B). Noncoding RNAs are largely involved in cardiovascular physiology, atherosclerosi [35], and multiple cardiovascular diseases [36], as chronic and acute coronary syndrome [6,[37][38][39][40][41], vascular remodeling [29,42], valvular heart disease [43][44][45][46][47], generation and pro gression of ectopic calcifications in the cardiovascular system [48][49][50][51][52][53][54], platelet functio [55][56][57][58][59], heart failure and stroke [60][61][62][63][64][65][66][67][68][69][70]. Evidence of the impact of flow conditions on cir culating ncRNA derives both from observations on pathological changes, such as cardia valve disease, vascular stenoses or aneurysm, but also from physiological conditions, suc as exercise [68].…”

“…This review focuses on regulatory noncoding RNAs that are directly or indirectl responsive to flow and their involvement with cardiovascular effects of altered bloo flow, with a focus on the potential clinical relevance and the underlying molecular mech anisms and their possible use as clinical biomarkers [71]. As relevant evidence is no equally available for all ncRNAs sub-categories, some specific ncRNAs, including siR NAs, snoRNA or piRNA are not mentioned in this review due to lack of evidence in rela Noncoding RNAs are largely involved in cardiovascular physiology, atherosclerosis [35], and multiple cardiovascular diseases [36], as chronic and acute coronary syndromes [6,[37][38][39][40][41], vascular remodeling [29,42], valvular heart disease [43][44][45][46][47], generation and progression of ectopic calcifications in the cardiovascular system [48][49][50][51][52][53][54], platelet function [55][56][57][58][59], heart failure and stroke [60][61][62][63][64][65][66][67][68][69][70]. Evidence of the impact of flow conditions on circulating ncRNA derives both from observations on pathological changes, such as cardiac valve disease, vascular stenoses or aneurysm, but also from physiological conditions, such as exercise…”

Molecular subtype identification of cerebral ischemic stroke based on ferroptosis-related genes

“…In IS, miR-1224 contributes to dysfunction of natural killer cell by targeting Sp1 signaling 66 . In stroke, FTX transcript, XIST regulator (FTX) can regulate angiogenesis through miR-342-3p/SPI1 axis 67 . It is indicated that MAPK3 and WAS may be involved in the process of CIS under the regulation of TFs of TWIST1, ETS1, MYB, SP1, and SPI1.…”