title: Long noncoding RNA AK056155 involved in the development of Loeys-Dietz syndrome through AKT/PI3K signaling pathway.
abstract: Loeys-Dietz syndrome (LDS) is an autosomal dominant genetic connective tissue disorder, and most of LDS patients will develop into aortic aneurysm. Unfortunately, there is no known cure, and a high risk of death from aortic aneurysm rupture. However the detailed mechanism is still unknown. In order to explore the mechanism, we firstly used bioinformatics to predict, and then verified with biology methods. Firstly, we found that LncRNA AK056155 was differentially expressed in peripheral blood circulating endothelial cells between normal patients and LDS patients by bioinformatics. Then we further verified that AK056155 was also overexpressed in aortic aneurysm patients by RT-PCR. Moreover, we demonstrated that the expression of AK056155 can be enhanced by TGF-β1 in a concentration or time depended manner in HUVECs by RT-PCR. Furthermore, the expression of AK056155 was reduced with treatment of PI3K inhibitor (LY294002) or AKT inhibitor (GDC-0068) in combination with TGF-β1. These results indicate that AK056155 involved in the development of Loeys-Dietz syndrome through AKT/PI3K signaling pathway, it may provide a promising target gene to prevent LDS develop in to aortic aneurysm.
authors.affiliation: Department of Cardiology, China-Japan Union Hospital of Jilin University Changchun 130033, Jilin, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Yu
authors.affiliation: Department of Cardiology, China-Japan Union Hospital of Jilin University Changchun 130033, Jilin, China.
authors.forename: Long
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Cardiology, China-Japan Union Hospital of Jilin University Changchun 130033, Jilin, China.
authors.forename: Huan
authors.initials: H
authors.lastname: Sun
authors.affiliation: Department of Cardiology, China-Japan Union Hospital of Jilin University Changchun 130033, Jilin, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Chen
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017544:Aortic Aneurysm, Abdominal / Q000097:blood / Q000201:enzymology* / Q000235:genetics; D016022:Case-Control Studies; D002478:Cells, Cultured; D002867:Chromones / Q000494:pharmacology; D019295:Computational Biology; D030541:Databases, Genetic; D018450:Disease Progression; D004305:Dose-Response Relationship, Drug; D005260:Female; D020869:Gene Expression Profiling / Q000379:methods; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects / Q000201:enzymology*; D006801:Humans; D017543:Iliac Aneurysm / Q000097:blood / Q000201:enzymology* / Q000235:genetics; D055947:Loeys-Dietz Syndrome / Q000097:blood / Q000201:enzymology* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009025:Morpholines / Q000494:pharmacology; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism*; D000081082:Phosphoinositide-3 Kinase Inhibitors; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D034622:RNA Interference; D062085:RNA, Long Noncoding / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D014162:Transfection; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology; D015854:Up-Regulation
chemical_list: D002867:Chromones; D009025:Morpholines; D000081082:Phosphoinositide-3 Kinase Inhibitors; D047428:Protein Kinase Inhibitors; D062085:RNA, Long Noncoding; D053773:Transforming Growth Factor beta1; C000610977:long non-coding RNA AK056155, human; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D058539:Phosphatidylinositol 3-Kinase; D051057:Proto-Oncogene Proteins c-akt
keywords: AK056155; Loeys-Dietz syndrome (LDS); PI3K/AKT; TGF-β1; aortic aneurysm