PMID- 35212609
OWN - NLM
STAT- MEDLINE
DCOM- 20220405
LR  - 20221207
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 3
DP  - 2022 Mar
TI  - Long non-coding RNA HIF1A-AS2 modulates the proliferation, migration, and 
      phenotypic switch of aortic smooth muscle cells in aortic dissection via sponging 
      microRNA-33b.
PG  - 6383-6395
LID - 10.1080/21655979.2022.2041868 [doi]
AB  - Aortic dissection (AD), also known as aortic dissecting aneurysm, is one of the 
      most common and dangerous cardiovascular diseases with high morbidity and 
      mortality. This study was aimed to investigate the functional role of long 
      non-coding RNA Hypoxia-inducible factor 1 alpha-antisense RNA 2 (lncRNA 
      HIF1A-AS2) in AD. An in vitro model of AD was established by platelet-derived 
      growth factor-BB (PDGF-BB)-mediated human aortic Smooth Muscle Cells (SMCs). 
      HIF1A-AS2 expression in human AD tissues was determined by quantitative real-time 
      PCR (qRT-PCR) and fluorescence in situ hybridization (FISH) assays, followed by 
      investigation of biological roles of HIF1A-AS2 in AD development by Cell Counting 
      Kit-8 (CCK-8), immunofluorescence, and transwell assays. Additionally, the 
      correlation between HIF1A-AS2, miR-33b, and high mobility group AT-hook2 (HMGA2) 
      were identified by RNA immunoprecipitation (RIP), RNA pull-down and luciferase 
      reporter assays. Results showed that HIF1A-AS2 was obviously increased, while the 
      contractile-phenotype markers of vascular SMCs were significantly decreased in 
      human AD tissues, when compared to normal tissues. Inhibition of HIF1A-AS2 
      attenuated SMCs proliferation and migration, whereas enhanced the phenotypic 
      switch under the stimulation of PDGF-BB. Results from RIP, RNA pull-down and 
      luciferase reporter assays demonstrated that miR-33b directly bound with 
      HIF1A-AS2, and HIF1A-AS2 silencing suppressed the expression of HMGA2, which was 
      induced by miR-33b inhibitor. In conclusion, knockdown of HIF1A-AS2 suppressed 
      the proliferation and migration, while promoted the phenotypic switching of SMCs 
      through miR-33b/HMGA2 axis, which laid a theoretical foundation for understanding 
      the development of AD and shed light on a potential target for AD treatment.
FAU - Zhang, Kai
AU  - Zhang K
AD  - Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, China.
AD  - Department of Cardiac ICU, Tianjin Chest HospitalTianjin, China , Tianjin China.
FAU - Qi, Yujuan
AU  - Qi Y
AD  - Department of Cardiac ICU, Tianjin Chest Hospital, Tianjin, China.
FAU - Wang, Meng
AU  - Wang M
AD  - Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, China.
FAU - Chen, Qingliang
AU  - Chen Q
AUID- ORCID: 0000-0001-7917-7957
AD  - Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, China.
AD  - Department of Cardiac ICU, Tianjin Chest HospitalTianjin, China , Tianjin China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (HIF1A-AS1 long non-coding RNA, human)
RN  - 0 (MIRN33b microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
SB  - IM
MH  - *Aortic Dissection/genetics/metabolism/pathology
MH  - Aorta/*cytology
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Cells, Cultured
MH  - Humans
MH  - MicroRNAs/genetics
MH  - Myocytes, Smooth Muscle/*cytology
MH  - Phenotype
MH  - RNA, Long Noncoding/*genetics
PMC - PMC8974049
OTO - NOTNLM
OT  - Aortic dissection
OT  - HIF1A-AS2
OT  - SMCs
OT  - migration
OT  - phenotypic switching
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/02/26 06:00
MHDA- 2022/04/06 06:00
PMCR- 2022/02/25
CRDT- 2022/02/25 12:15
PHST- 2022/02/25 12:15 [entrez]
PHST- 2022/02/26 06:00 [pubmed]
PHST- 2022/04/06 06:00 [medline]
PHST- 2022/02/25 00:00 [pmc-release]
AID - 2041868 [pii]
AID - 10.1080/21655979.2022.2041868 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Mar;13(3):6383-6395. doi: 10.1080/21655979.2022.2041868.