PMID- 34040396
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220423
IS  - 1178-6965 (Print)
IS  - 1178-6965 (Electronic)
IS  - 1178-6965 (Linking)
VI  - 14
DP  - 2021
TI  - MiR-21-5p in Macrophage-Derived Exosomes Targets Smad7 to Promote Epithelial 
      Mesenchymal Transition of Airway Epithelial Cells.
PG  - 513-524
LID - 10.2147/JAA.S307165 [doi]
AB  - BACKGROUND: Asthma is usually associated with airway inflammation and airway 
      remodeling. Epithelial mesenchymal transition (EMT) often occurs in airway 
      remodeling. The purpose of this study is to identify the effect of miR-21-5p and 
      Smad7 signaling pathway in macrophage-derived exosomes on EMT of airway 
      epithelial cells. METHODS: HE staining and Masson staining were used to verify 
      the successful establishment of the asthma model. The levels of epithelial cell 
      adhesion factor and stromal cell markers were detected by Western blot. The 
      levels of miR-21-5p were detected by qRT-PCR. The expression of miR-21-5p in lung 
      tissue was further verified by fluorescence in situ hybridization (FISH). Exosome 
      morphology was observed by transmission electron microscopy (TEM) and 
      nanoparticle tracking analysis (NTA). Luciferase reporter assay was applied to 
      analyze the interaction of miR-21-5p with Smad7. RESULTS: The expression of 
      miR-21-5p was upregulated in macrophages of rats in vivo with OVA-induced asthma. 
      In vitro cultured alveolar macrophages stimulated by LPS could secrete exosomes 
      with high levels of miR-21-5p. The exosome-derived miR-21-5p promotes EMT in rat 
      tracheal epithelial cells through TGFbeta1/Smad signaling pathway by downregulating 
      Smad7. This process can be blocked by miR-21-5p inhibitor. CONCLUSION: Rat 
      alveolar macrophages produced high levels of miR-21-5p-containing exosomes, which 
      transported miR-21-5p to tracheal epithelial cells, thus promoting EMT through 
      TGF-beta1/Smad signaling pathway by targeting Smad7.
CI  - (c) 2021 Li et al.
FAU - Li, Xiang
AU  - Li X
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 
      Shenyang, Liaoning, 110004, People's Republic of China.
FAU - Yang, Nan
AU  - Yang N
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 
      Shenyang, Liaoning, 110004, People's Republic of China.
FAU - Cheng, Qi
AU  - Cheng Q
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 
      Shenyang, Liaoning, 110004, People's Republic of China.
FAU - Zhang, Han
AU  - Zhang H
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 
      Shenyang, Liaoning, 110004, People's Republic of China.
FAU - Liu, Fen
AU  - Liu F
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 
      Shenyang, Liaoning, 110004, People's Republic of China.
FAU - Shang, Yunxiao
AU  - Shang Y
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 
      Shenyang, Liaoning, 110004, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20210518
PL  - New Zealand
TA  - J Asthma Allergy
JT  - Journal of asthma and allergy
JID - 101543450
PMC - PMC8140948
OTO - NOTNLM
OT  - Smad7
OT  - asthma
OT  - epithelial mesenchymal transition
OT  - exosomes
OT  - miR-21-5p
OT  - miRNA
COIS- The authors declare that they have no conflicts of interest for this work.
EDAT- 2021/05/28 06:00
MHDA- 2021/05/28 06:01
PMCR- 2021/05/18
CRDT- 2021/05/27 06:37
PHST- 2021/02/18 00:00 [received]
PHST- 2021/04/21 00:00 [accepted]
PHST- 2021/05/27 06:37 [entrez]
PHST- 2021/05/28 06:00 [pubmed]
PHST- 2021/05/28 06:01 [medline]
PHST- 2021/05/18 00:00 [pmc-release]
AID - 307165 [pii]
AID - 10.2147/JAA.S307165 [doi]
PST - epublish
SO  - J Asthma Allergy. 2021 May 18;14:513-524. doi: 10.2147/JAA.S307165. eCollection 
      2021.