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The lncRNA MALAT1 protects the endothelium against ox‐LDL‐induced dysfunction via upregulating the expression of the miR‐22‐3p target genes CXCR2 and AKT
Author(s) -
Tang Yong,
Jin Xian,
Xiang Yin,
Chen Yu,
Shen Cheng-xing,
Zhang Ya-chen,
Li Yi-gang
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.08.046
Subject(s) - malat1 , endothelium , gene silencing , downregulation and upregulation , cancer research , competing endogenous rna , endothelial dysfunction , small interfering rna , protein kinase b , signal transduction , microbiology and biotechnology , biology , gene , rna , endocrinology , biochemistry , long non coding rna
CXCR2 plays a key role in protecting the integrity of the endothelium. Emerging evidence has demonstrated that the long ncRNAs (lncRNA) Human metastasis associated lung adenocarcinoma transcript 1 (MALAT1) participates in the regulation of the pathophysiological processes. However, whether there is crosstalk between CXCR2 and MALAT1 remains unknown. In this study, we demonstrated that MALAT1 was upregulated in patients with unstable angina. MALAT1 silencing significantly downregulated the expression of the miR‐22‐3p target gene CXCR2 via reversing the effect of the miR‐22‐3p, resulting in the aggravation of Oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial injury; this process was associated with the AKT pathway. Thus, MALAT1 protects the endothelium from ox‐LDL‐induced endothelial dysfunction partly through competing with miR‐22‐3p for endogenous RNA.