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Role of microRNA-130a in the pathogeneses of obstructive sleep apnea hypopnea syndrome-associated pulmonary hypertension by targeting the GAX gene.

Abstract The purpose of this study was to elucidate the role of microRNA-130a (miR-130a) in obstructive sleep apnea hypopnea syndrome (OSAHS)-associated pulmonary hypertension (PHT) by targeting the growth arrest-specific homeobox (GAX) gene.
PMID
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Regulation of angiogenesis through a microRNA (miR-130a) that down-regulates antiangiogenic homeobox genes GAX and HOXA5.

Authors

Mayor MeshTerms
Keywords
Journal Title medicine
Publication Year Start




PMID- 28514291
OWN - NLM
STAT- MEDLINE
DA  - 20170517
DCOM- 20170613
LR  - 20170613
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Linking)
VI  - 96
IP  - 20
DP  - 2017 May
TI  - Role of microRNA-130a in the pathogeneses of obstructive sleep apnea hypopnea
      syndrome-associated pulmonary hypertension by targeting the GAX gene.
PG  - e6746
LID - 10.1097/MD.0000000000006746 [doi]
AB  - OBJECTIVE: The purpose of this study was to elucidate the role of microRNA-130a
      (miR-130a) in obstructive sleep apnea hypopnea syndrome (OSAHS)-associated
      pulmonary hypertension (PHT) by targeting the growth arrest-specific homeobox
      (GAX) gene. METHODS: A total of 108 patients with OSAHS-associated PHT were
      recruited as the OSAHS-associated PHT group and 110 healthy individuals were
      randomly selected as the normal control group. Human umbilical vein endothelial
      cells (HUVECs) were selected and divided into the control, miR-130a mimic, mimic 
      negative control (NC), miR-130a inhibitor, and inhibitor-NC groups. The dual
      luciferase reporter gene assay was used to identify the relationship between
      miR-130a and the GAX gene. The quantitative real-time polymerase chain reaction
      (qRT-PCR) and Western blotting were applied for the relative expressions of
      miR-130a and the mRNA and protein expressions of GAX. Serum levels of
      endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), nitric oxide
      (NO), and super oxide dismutase (SOD) were detected. Cell apoptosis and
      angiogenic activity were analyzed by flow cytometry and cell tube formation
      assay. RESULTS: GAX was a target gene of miR-130a. Compared with the normal
      control group, the relative expression of miR-130a and the serum levels of ET-1
      and VEGF were increased, whereas the mRNA expression of GAX and the serum levels 
      of NO and SOD were decreased in the OSAHS-associated PHT group. Compared with the
      control, mimic-NC, and inhibitor-NC groups, the relative expressions of miR-130a 
      in the miR-130a mimic group were enhanced, whereas the expression of miR-130a in 
      the miR-130a inhibitor group was reduced. However, the mRNA and protein
      expressions of GAX showed an opposite trend in the miR-130a mimic and miR-130a
      inhibitor groups. In comparison to the control, mimic-NC, and inhibitor-NC
      groups, the miR-130a mimic group had an increase of ET-1 and VEGF expressions,
      whereas the expressions of NO and SOD were reduced. However, the miR-130a
      inhibitor group exhibited an opposite trend. The apoptosis rate and tube
      formation number in the miR-130a mimic group were obviously increased, whereas
      the miR-130a inhibitor group showed an obvious decrease. CONCLUSION: These data
      provided strong evidence that miR-130a may be involved in the progression of
      OSAHS-associated PHT by down-regulating GAX gene.
FAU - An, Zhe
AU  - An Z
AD  - aDepartment of Cardiology, China-Japan Union Hospital of Jilin University
      bDepartment of Breast Surgery, The Second Hospital of Jilin University
      cDepartment of Molecular Biology, College of Basic Medical Sciences, Jilin
      University dDepartment of Respiratory Medicine, the Second Hospital of Jilin
      University eDepartment of Ophthalmology, The Second Hospital of Jilin University,
      Changchun, Jilin, P.R. China.
FAU - Wang, Dan
AU  - Wang D
FAU - Yang, Guang
AU  - Yang G
FAU - Zhang, Wen-Qi
AU  - Zhang WQ
FAU - Ren, Jin
AU  - Ren J
FAU - Fu, Jin-Ling
AU  - Fu JL
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Biomarkers)
RN  - 0 (Endothelin-1)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (MEOX2 protein, human)
RN  - 0 (MIRN130 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Messenger)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - AIM
SB  - IM
MH  - Apoptosis/physiology
MH  - Biomarkers/metabolism
MH  - Cells, Cultured
MH  - Down-Regulation
MH  - Endothelin-1/blood
MH  - Female
MH  - Homeodomain Proteins/*metabolism
MH  - Human Umbilical Vein Endothelial Cells/metabolism
MH  - Humans
MH  - Hypertension, Pulmonary/*complications/*metabolism
MH  - Male
MH  - MicroRNAs/antagonists & inhibitors/genetics/*metabolism
MH  - Middle Aged
MH  - Nitric Oxide/blood
MH  - RNA, Messenger
MH  - Random Allocation
MH  - Sleep Apnea, Obstructive/*complications/*metabolism
MH  - Superoxide Dismutase/blood
MH  - Transfection
MH  - Vascular Endothelial Growth Factor A/blood
PMC - PMC5440128
EDAT- 2017/05/18 06:00
MHDA- 2017/06/14 06:00
CRDT- 2017/05/18 06:00
AID - 10.1097/MD.0000000000006746 [doi]
AID - 00005792-201705190-00008 [pii]
PST - ppublish
SO  - Medicine (Baltimore). 2017 May;96(20):e6746. doi: 10.1097/MD.0000000000006746.

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