PMID- 34539308
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210921
IS  - 1617-9625 (Electronic)
IS  - 2070-7266 (Print)
IS  - 1617-9625 (Linking)
VI  - 19
DP  - 2021
TI  - The inhibitor miR-21 regulates macrophage polarization in an experimental model 
      of chronic obstructive pulmonary disease.
PG  - 69
LID - 10.18332/tid/140095 [doi]
LID - 69
AB  - INTRODUCTION: In chronic obstructive pulmonary disease (COPD), macrophages play 
      an indispensable role. In the lung tissues of COPD patients and smokers, 
      macrophages can be observed to polarize towards M2 phenotype. The molecular 
      mechanism of this process is unclear, and it has not been fully elucidated in 
      COPD. METHODS: We bought laboratory animals [C57BL/6 and miR-21(-/-) C57BL/6(F1)] 
      from the Jackson Laboratory. The model of COPD mice was established by cigarette 
      smoke (CS) exposure combined with intraperitoneal injection of cigarette smoke 
      extract (CSE). RT-PCR detected the expression levels of inflammatory factors and 
      markers associated with M1 and M2 macrophages. The ratio of M2 macrophages to M1 
      macrophages was detected by immunohistochemical staining. RESULTS: The level of 
      miR-21 was increased in RAW264.7 cells intervened by CSE and in lung tissue and 
      bone marrow-derived macrophages (BMDMs) from COPD mice. CSE can gradually over 
      time increase the level of miR-21. The proportion of M2 macrophages to M1 
      macrophages had a positive correlation with miR-21. Knockdowning miR-21 can 
      reduce lung tissue damage. CSE also increased the levels of related inflammatory 
      factors and markers associated with M2 macrophages, and an miR-21 inhibitor can 
      reverse this conversion. CONCLUSIONS: We confirmed that CSE can lead to 
      macrophage transformation to the M2 phenotype and an increase in the expression 
      level of miR-21. Knockdown of the miR-21 gene could inhibit the transformation of 
      macrophages to the M2 phenotype in COPD.
CI  - (c) 2021 Lu J.J. et al.
FAU - Lu, JunJuan
AU  - Lu J
AD  - Department of Respiratory Medicine, The Third XiangYa Hospital of Central South 
      University, Changsha, People's Republic of China.
FAU - Xie, LiHua
AU  - Xie L
AD  - Department of Respiratory Medicine, The Third XiangYa Hospital of Central South 
      University, Changsha, People's Republic of China.
FAU - Sun, ShengHua
AU  - Sun S
AD  - Department of Respiratory Medicine, The Third XiangYa Hospital of Central South 
      University, Changsha, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20210902
PL  - Greece
TA  - Tob Induc Dis
JT  - Tobacco induced diseases
JID - 101201591
PMC - PMC8409097
OTO - NOTNLM
OT  - chronic obstructive pulmonary disease
OT  - cigarette smoke extract
OT  - macrophage polarization
OT  - miR-21
COIS- The authors have completed and submitted the ICMJE Form for Disclosure of 
      Potential Conflicts of Interest and none was reported.
EDAT- 2021/09/21 06:00
MHDA- 2021/09/21 06:01
PMCR- 2021/09/02
CRDT- 2021/09/20 06:00
PHST- 2021/02/08 00:00 [received]
PHST- 2021/06/21 00:00 [revised]
PHST- 2021/07/08 00:00 [accepted]
PHST- 2021/09/20 06:00 [entrez]
PHST- 2021/09/21 06:00 [pubmed]
PHST- 2021/09/21 06:01 [medline]
PHST- 2021/09/02 00:00 [pmc-release]
AID - 69 [pii]
AID - 10.18332/tid/140095 [doi]
PST - epublish
SO  - Tob Induc Dis. 2021 Sep 2;19:69. doi: 10.18332/tid/140095. eCollection 2021.