PMID- 31786325
OWN - NLM
STAT- MEDLINE
DCOM- 20201005
LR  - 20201005
IS  - 1878-5875 (Electronic)
IS  - 1357-2725 (Linking)
VI  - 118
DP  - 2020 Jan
TI  - Lung myofibroblast transition and fibrosis is regulated by circ0044226.
PG  - 105660
LID - S1357-2725(19)30237-7 [pii]
LID - 10.1016/j.biocel.2019.105660 [doi]
AB  - BACKGROUND AND PURPOSE: Idiopathic pulmonary fibrosis (IPF) is a life-threatening 
      progressive disease characterized by aberrant fibroblast activation. This study 
      aims to explore the role of the circ0044226 on fibroblast-to-myofibroblast 
      transition (FMT). METHODS: Bleomycin and TGF-beta1 were respectively used to induce 
      the IPF mice model and human lung fibroblasts to myofibroblast differentiation. 
      The mRNA and protein levels were examined by qRT-PCR and western blot. 
      Localization of alpha-SMA was evaluated by immunofluorescence staining. Cell 
      viability and proliferation were evaluated by CCK8 and EDU test. Dual-luciferase 
      reporter assay was used to analyze the interaction between miR-7 and circ0044226 
      or sp1. Fluorescence in situ hybridization (FISH) assay was used for the 
      identification of sub-location of circ0044226 and miR-7 in cells. The IPF model 
      mice received intratracheal injection of AAV-sh-NC and AAV-sh- circ0044226, and 
      lung fibrosis was detected by HE staining, Masson staining and 
      immunohistochemistry assay. RESULTS: The circ0044226 was upregulated while miR-7 
      was downregulated in IPF mice model and FMT-derived myofibroblasts. miR-7 was a 
      target of circ0044226 and sp1 was a target of miR-7. circ0044226 was distributed 
      mostly in the cytoplasm and functioned as a miR-7 sponge to positively regulate 
      the expression of sp1. Intervention of circ0044226 could ameliorate FMT and 
      suppress fibroblast viability and proliferation by functioning as an endogenous 
      miR-7 sponge. CONCLUSION: Circ0044226 knockdown alleviates fibroblast 
      proliferation and FMT by functioning as a competing endogenous RNA, which may 
      represent a promising therapy for pulmonary fibrosis.
CI  - Copyright (c) 2019 Elsevier Ltd. All rights reserved.
FAU - Zhang, Lijuan
AU  - Zhang L
AD  - Department of Respiratory and Critical Care Medicine, The First Affiliated 
      Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China.
FAU - Chi, Xiaowen
AU  - Chi X
AD  - Pediatrics, The First Affiliated Hospital of Harbin Medical University, Harbin, 
      Heilongjiang, 150036, China.
FAU - Luo, Wen
AU  - Luo W
AD  - Department of Respiratory and Critical Care Medicine, The First Affiliated 
      Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China.
FAU - Yu, Shihuan
AU  - Yu S
AD  - Department of Respiratory and Critical Care Medicine, The First Affiliated 
      Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China.
FAU - Zhang, Jiawen
AU  - Zhang J
AD  - Department of Respiratory and Critical Care Medicine, The First Affiliated 
      Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China.
FAU - Guo, Yuening
AU  - Guo Y
AD  - Department of Respiratory and Critical Care Medicine, The First Affiliated 
      Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China.
FAU - Ren, Qiu
AU  - Ren Q
AD  - Department of Respiratory, Heilongjiang Province Hospital, Harbin, Heilongjiang, 
      150001, China.
FAU - Zhang, Wei
AU  - Zhang W
AD  - Department of Respiratory and Critical Care Medicine, The First Affiliated 
      Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China. 
      Electronic address: weizh52121@163.com.
LA  - eng
PT  - Journal Article
DEP - 20191128
PL  - Netherlands
TA  - Int J Biochem Cell Biol
JT  - The international journal of biochemistry & cell biology
JID - 9508482
RN  - 0 (Actins)
RN  - 0 (MIRN7 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Circular)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (Tgfb1 protein, mouse)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (alpha-smooth muscle actin, mouse)
RN  - 11056-06-7 (Bleomycin)
SB  - IM
MH  - Actins/genetics
MH  - Animals
MH  - Bleomycin/pharmacology
MH  - Cell Differentiation/drug effects
MH  - Cell Proliferation/drug effects
MH  - Fibroblasts/metabolism/pathology
MH  - Humans
MH  - Idiopathic Pulmonary Fibrosis/*genetics/pathology
MH  - In Situ Hybridization, Fluorescence
MH  - Lung/metabolism/pathology
MH  - Mice
MH  - MicroRNAs/*genetics
MH  - Myofibroblasts/metabolism
MH  - RNA, Circular/*genetics
MH  - Signal Transduction/drug effects
MH  - Sp1 Transcription Factor/*genetics
MH  - Transforming Growth Factor beta1/genetics
OTO - NOTNLM
OT  - Circ0044226
OT  - Fibroblast-to-myofibroblast transition
OT  - Pulmonary fibrosis
OT  - miR-7
EDAT- 2019/12/02 06:00
MHDA- 2020/10/06 06:00
CRDT- 2019/12/02 06:00
PHST- 2019/09/20 00:00 [received]
PHST- 2019/11/26 00:00 [revised]
PHST- 2019/11/27 00:00 [accepted]
PHST- 2019/12/02 06:00 [pubmed]
PHST- 2020/10/06 06:00 [medline]
PHST- 2019/12/02 06:00 [entrez]
AID - S1357-2725(19)30237-7 [pii]
AID - 10.1016/j.biocel.2019.105660 [doi]
PST - ppublish
SO  - Int J Biochem Cell Biol. 2020 Jan;118:105660. doi: 10.1016/j.biocel.2019.105660. 
      Epub 2019 Nov 28.