PMID- 31832126
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220411
IS  - 2040-6223 (Print)
IS  - 2040-6231 (Electronic)
IS  - 2040-6223 (Linking)
VI  - 10
DP  - 2019
TI  - CircHECTD1 mediates pulmonary fibroblast activation via HECTD1.
PG  - 2040622319891558
LID - 10.1177/2040622319891558 [doi]
LID - 2040622319891558
AB  - BACKGROUND: Circular RNA (circRNA), a new class of noncoding RNA, has been shown 
      to be important in silicosis due to its unique role as a transcription regulator 
      or as a sponge of small RNA regulators. Here, the mechanisms underlying 
      circHECTD1/HECTD1 in fibroblast activation and subsequent fibrosis induced by 
      SiO(2) were investigated. METHODS: Primary human pulmonary fibroblasts (HPF-a) 
      were utilized, combined with quantitative real-time PCR (qRT-PCR) and 
      fluorescence in situ hybridization (FISH) assays. LC3B-LV-RFP lentivirus was used 
      to evaluate the role of autophagy. The CRISPR/Cas9 system was applied to 
      specifically knock down HECTD1, combined with MTT, BrdU, and migration assays, to 
      explore the functional changes induced by SiO(2). RESULTS: After exposure to 
      SiO(2), the circHECTD1 level was decreased, which was associated with an increase 
      in HECTD1 in HPF-a cells. SiO(2)-induced autophagy was reversed by either 
      circHECTD1 overexpression or HECTD1 knockdown in HPF-a cells, with restored 
      SiO(2)-induced fibroblast activation, proliferation, and migration via downstream 
      autophagy. The lungs of mice exposed to SiO(2) confirmed the upregulation of 
      HECTD1 in pulmonary fibroblasts. CONCLUSIONS: Our data suggested a link between 
      circHECTD1/HECTD1 and fibroblast activation with subsequent fibrosis induced by 
      SiO(2), providing novel insight into the potential of circHECTD1/HECTD1 to be a 
      therapeutic target for silicosis.
CI  - (c) The Author(s), 2019.
FAU - Chu, Han
AU  - Chu H
AD  - Department of Physiology, School of Medicine, Southeast University, Nanjing, 
      Jiangsu, China.
FAU - Wang, Wei
AU  - Wang W
AD  - Department of Respiratory Medicine, Nanjing Chest Hospital, Nanjing, Jiangsu, 
      China.
FAU - Luo, Wei
AU  - Luo W
AD  - Department of Physiology, School of Medicine, Southeast University, Nanjing, 
      Jiangsu, China.
FAU - Zhang, Wei
AU  - Zhang W
AD  - Department of Physiology, School of Medicine, Southeast University, Nanjing, 
      Jiangsu, China.
FAU - Cheng, Yusi
AU  - Cheng Y
AD  - Department of Physiology, School of Medicine, Southeast University, Nanjing, 
      Jiangsu, China.
FAU - Huang, Jie
AU  - Huang J
AD  - Department of Physiology, School of Medicine, Southeast University, Nanjing, 
      Jiangsu, China.
FAU - Wang, Jing
AU  - Wang J
AD  - Department of Physiology, School of Medicine, Southeast University, Nanjing, 
      Jiangsu, China.
FAU - Dai, Xiaoniu
AU  - Dai X
AD  - Department of Physiology, School of Medicine, Southeast University, Nanjing, 
      Jiangsu, China.
FAU - Fang, Shencun
AU  - Fang S
AD  - Department of Respiratory Medicine, Nanjing Chest Hospital, Nanjing, Jiangsu, 
      China.
FAU - Chao, Jie
AU  - Chao J
AUID- ORCID: 0000-0002-7800-3557
AD  - Department of Physiology, School of Medicine, Southeast University, 87 
      Dingjiaqiao Road, Nanjing, Jiangsu, 210009, China.
LA  - eng
PT  - Journal Article
DEP - 20191127
PL  - United States
TA  - Ther Adv Chronic Dis
JT  - Therapeutic advances in chronic disease
JID - 101532140
PMC - PMC6887829
OTO - NOTNLM
OT  - HECTD1
OT  - activation
OT  - circRNA
OT  - migration
OT  - proliferation
OT  - silicosis
COIS- Conflict of interest statement: The author(s) declared no potential conflicts of 
      interest with respect to the research, authorship, and/or publication of this 
      article.
EDAT- 2019/12/14 06:00
MHDA- 2019/12/14 06:01
PMCR- 2019/11/27
CRDT- 2019/12/14 06:00
PHST- 2019/07/13 00:00 [received]
PHST- 2019/11/04 00:00 [accepted]
PHST- 2019/12/14 06:00 [entrez]
PHST- 2019/12/14 06:00 [pubmed]
PHST- 2019/12/14 06:01 [medline]
PHST- 2019/11/27 00:00 [pmc-release]
AID - 10.1177_2040622319891558 [pii]
AID - 10.1177/2040622319891558 [doi]
PST - epublish
SO  - Ther Adv Chronic Dis. 2019 Nov 27;10:2040622319891558. doi: 
      10.1177/2040622319891558. eCollection 2019.