PMID- 34092750
OWN - NLM
STAT- MEDLINE
DCOM- 20211122
LR  - 20231103
IS  - 1881-7122 (Electronic)
IS  - 1341-1357 (Print)
IS  - 0007-5124 (Linking)
VI  - 70
IP  - 4
DP  - 2021 Nov 10
TI  - Overexpression of miR-224-5p alleviates allergic rhinitis in mice via the 
      TLR4/MyD88/NF-kappaB pathway.
PG  - 440-449
LID - 10.1538/expanim.20-0195 [doi]
AB  - Inflammatory allergic reaction is the main cause of allergic rhinitis (AR). 
      Previous studies indicated that miR-224-5p was downregulated in the nasal mucosa 
      of patients with AR, while the function of miR-224-5p in AR remains unclear. To 
      explore this issue, AR mouse model was established using ovalbumin (OVA). For 
      treatment group, lentivirus (LV)-miR-224-5p or its control was intranasally 
      administrated to AR mice. miR-224-5p expression was detected by reverse 
      transcription-quantitative PCR, followed by assessing the immunoglobulin E (IgE) 
      level. Pathological alterations in nasal mucosa were detected using 
      Hematoxylin-Eosin staining and Sirius red staining, followed by assessing the 
      levels of inflammatory cells and factors. The NLRP3 inflammasome and 
      TLR4/MyD88/NF-kappaB pathway were measured by Western blot, and then the relationship 
      between miR-224-5p and toll-like receptor 4 (TLR4) was verified. The results 
      showed that miR-224-5p was significantly decreased in nasal mucosa of AR mice. AR 
      mice exhibited increased sneezing and nasal rubbing events, IgE level in serum, 
      and pathological alterations in nasal mucosa, while overexpression of miR-224-5p 
      markedly attenuated these changes. The levels of inflammatory cells in nasal 
      lavage fluid and pro-inflammatory factors in serum and nasal mucosa were 
      significantly increased in AR mice, which were reduced by miR-224-5p 
      overexpression. Of note, LV-miR-224-5p treatment remarkably suppressed the 
      activations of NLRP3 inflammasome and the TLR4/MyD88/NF-kappaB pathway in AR mice. 
      Furthermore, miR-224-5p could bind to 3'-untranslated region (3'-UTR) of TLR4 and 
      negatively regulate TLR4 level. Overall, we conclude that miR-224-5p may relieve 
      AR by negatively regulating TLR4/MyD88/NF-kappaB pathway, indicating that miR-224-5p 
      may be a promising target for AR treatment.
FAU - Wu, Jianhua
AU  - Wu J
AD  - Department of Otolaryngology Head and Neck Surgery, Binzhou People's Hospital, 
      No. 515, Huanghe 7th Road, Bincheng District, Binzhou, 256610, Shandong, China.
FAU - Wu, Lizhen
AU  - Wu L
AD  - Department of Otolaryngology, Beijing Shijingshan Hospital, No. 24, Shijingshan 
      Road, Beijing, 100043, China.
FAU - Zhang, Li
AU  - Zhang L
AD  - Department of Otolaryngology Head and Neck Surgery, Binzhou People's Hospital, 
      No. 515, Huanghe 7th Road, Bincheng District, Binzhou, 256610, Shandong, China.
FAU - Xu, Huanhuan
AU  - Xu H
AD  - Department of Otolaryngology Head and Neck Surgery, Binzhou People's Hospital, 
      No. 515, Huanghe 7th Road, Bincheng District, Binzhou, 256610, Shandong, China.
FAU - Wang, Min
AU  - Wang M
AD  - Department of Otolaryngology Head and Neck Surgery, Binzhou People's Hospital, 
      No. 515, Huanghe 7th Road, Bincheng District, Binzhou, 256610, Shandong, China.
FAU - Wang, Lin
AU  - Wang L
AD  - Department of Otolaryngology Head and Neck Surgery, Binzhou People's Hospital, 
      No. 515, Huanghe 7th Road, Bincheng District, Binzhou, 256610, Shandong, China.
FAU - Chen, Jie
AU  - Chen J
AD  - Department of Otolaryngology Head and Neck Surgery, Binzhou People's Hospital, 
      No. 515, Huanghe 7th Road, Bincheng District, Binzhou, 256610, Shandong, China.
FAU - Sun, Kaiyue
AU  - Sun K
AD  - Shandong Institute of Otolaryngology, Shandong Provincial ENT Hospital Affiliated 
      to Shandong University, No. 4 Duanxing West Road, Jinan, 250022, Shandong, China.
LA  - eng
PT  - Journal Article
DEP - 20210607
PL  - Japan
TA  - Exp Anim
JT  - Experimental animals
JID - 9604830
RN  - 0 (MIRN224 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (NF-kappa B)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 4)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - *Gene Expression Regulation
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - MicroRNAs/*genetics/metabolism
MH  - Myeloid Differentiation Factor 88/genetics/metabolism
MH  - NF-kappa B/genetics/metabolism
MH  - Rhinitis, Allergic/*genetics
MH  - *Signal Transduction
MH  - Toll-Like Receptor 4/genetics/metabolism
PMC - PMC8614013
OTO - NOTNLM
OT  - TLR4/MyD88/NF-kappaB pathway
OT  - allergic rhinitis
OT  - inflammatory response
OT  - miR-224-5p
COIS- The authors declare that there is no conflict of interests.
EDAT- 2021/06/08 06:00
MHDA- 2021/11/23 06:00
PMCR- 2021/01/01
CRDT- 2021/06/07 05:39
PHST- 2021/06/08 06:00 [pubmed]
PHST- 2021/11/23 06:00 [medline]
PHST- 2021/06/07 05:39 [entrez]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 20-0195 [pii]
AID - 10.1538/expanim.20-0195 [doi]
PST - ppublish
SO  - Exp Anim. 2021 Nov 10;70(4):440-449. doi: 10.1538/expanim.20-0195. Epub 2021 Jun 
      7.