PMID- 29473816
OWN - NLM
STAT- MEDLINE
DCOM- 20190311
LR  - 20190311
IS  - 1531-2267 (Electronic)
IS  - 1094-8341 (Linking)
VI  - 50
IP  - 5
DP  - 2018 May 1
TI  - DNA methylation signatures of pulmonary arterial smooth muscle cells in chronic 
      thromboembolic pulmonary hypertension.
PG  - 313-322
LID - 10.1152/physiolgenomics.00069.2017 [doi]
AB  - Chronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening 
      disease, which is often underpinned by vascular remodeling. Pulmonary arterial 
      smooth muscle cells (PASMCs) are the main participants in vascular remodeling. 
      However, their biological role in CTEPH is not entirely clear. In the present 
      study, we analyzed the whole epigenome-wide DNA methylation profile of cultured 
      PASMCs from CTEPH and control cell lines with the Illumina Human Methylation 450K 
      BeadChip. A total of 6,829 significantly differentially methylated probes (DMPs) 
      were detected between these two groups. Among these, 4,246 DMPs were 
      hypermethylated, while 2,583 DMPs were hypomethylated. The functional enrichment 
      analysis of 1,743 DMPs in the promoter regions and corresponding genes indicated 
      that DNA hypermethylation and hypomethylation might be involved in the regulation 
      of genes that have multifarious biological roles, including roles in 
      cancer-related diseases, the regulation of the actin cytoskeleton, cell adhesion, 
      and pattern specification processes. The observed methylations were categorized 
      into the most important functions, including those involved in cell 
      proliferation, immunity, and migration. We speculate that these methylations were 
      most likely involved in the possible pathophysiology of CTEPH. Gene interaction 
      analysis pertaining to signal networks confirmed that PIK3CA and PIK3R1 were 
      important mediators in these whole networks. The mRNA levels of PIK3CA, HIC1, and 
      SSH1 were verified by qPCR and corresponded with DNA methylation differences. 
      Understanding epigenetic features associated with CTEPH may provide new insights 
      into the mechanism that underlie this condition.
FAU - Wang, Ying
AU  - Wang Y
AD  - Department of Clinical Laboratory, Beijing Chao-Yang Hospital, Capital Medical 
      University , Beijing , People's Republic of China.
AD  - Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of 
      Respiratory Medicine , Beijing , People's Republic of China.
FAU - Huang, Xiaoxi
AU  - Huang X
AD  - Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of 
      Respiratory Medicine , Beijing , People's Republic of China.
AD  - Medical Research Center, Beijing Chao-Yang Hospital, Capital Medical University , 
      Beijing , People's Republic of China.
FAU - Leng, Dong
AU  - Leng D
AD  - Department of Clinical Laboratory, Beijing Chao-Yang Hospital, Capital Medical 
      University , Beijing , People's Republic of China.
AD  - Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of 
      Respiratory Medicine , Beijing , People's Republic of China.
FAU - Li, Jifeng
AU  - Li J
AD  - Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of 
      Respiratory Medicine , Beijing , People's Republic of China.
AD  - Department of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, 
      Capital Medical University , Beijing , People's Republic of China.
FAU - Wang, Lei
AU  - Wang L
AD  - Department of Pulmonary and Critical Care Medicine, Xuanwu Hospital, Capital 
      Medical University , Beijing , People's Republic of China.
FAU - Liang, Yan
AU  - Liang Y
AD  - Department of Clinical Laboratory, Beijing Chao-Yang Hospital, Capital Medical 
      University , Beijing , People's Republic of China.
AD  - Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of 
      Respiratory Medicine , Beijing , People's Republic of China.
FAU - Wang, Jun
AU  - Wang J
AD  - Department of Physiology, Capital Medical University , Beijing , People's 
      Republic of China.
FAU - Miao, Ran
AU  - Miao R
AD  - Department of Clinical Laboratory, Beijing Chao-Yang Hospital, Capital Medical 
      University , Beijing , People's Republic of China.
AD  - Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of 
      Respiratory Medicine , Beijing , People's Republic of China.
FAU - Jiang, Tao
AU  - Jiang T
AD  - Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University 
      , Beijing , People's Republic of China.
AD  - Beijing Neurosurgical Institute, Capital Medical University , Beijing , People's 
      Republic of China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180223
PL  - United States
TA  - Physiol Genomics
JT  - Physiological genomics
JID - 9815683
SB  - IM
MH  - Adult
MH  - Cell Line
MH  - Cells, Cultured
MH  - Chronic Disease
MH  - CpG Islands/genetics
MH  - *DNA Methylation
MH  - Epigenomics/*methods
MH  - Female
MH  - Humans
MH  - Hypertension, Pulmonary/etiology/*genetics/pathology
MH  - Male
MH  - Middle Aged
MH  - Muscle, Smooth, Vascular/pathology
MH  - Myocytes, Smooth Muscle/*metabolism
MH  - Promoter Regions, Genetic/genetics
MH  - Pulmonary Artery/pathology
MH  - Pulmonary Embolism/complications
OTO - NOTNLM
OT  - DNA methylation profile
OT  - chronic thromboembolic pulmonary hypertension
OT  - functional enrichment analysis
OT  - pulmonary artery smooth muscle cells
EDAT- 2018/02/24 06:00
MHDA- 2019/03/12 06:00
CRDT- 2018/02/24 06:00
PHST- 2018/02/24 06:00 [pubmed]
PHST- 2019/03/12 06:00 [medline]
PHST- 2018/02/24 06:00 [entrez]
AID - 10.1152/physiolgenomics.00069.2017 [doi]
PST - ppublish
SO  - Physiol Genomics. 2018 May 1;50(5):313-322. doi: 
      10.1152/physiolgenomics.00069.2017. Epub 2018 Feb 23.