PMID- 34709954
OWN - NLM
STAT- MEDLINE
DCOM- 20211101
LR  - 20220531
IS  - 1945-8932 (Electronic)
IS  - 1945-8932 (Linking)
VI  - 35
IP  - 6
DP  - 2021 Nov
TI  - LncRNA MIAT Promotes Allergic Inflammation and Symptoms by Targeting MiR-10b-5p 
      in Allergic Rhinitis Mice.
PG  - 781-789
LID - 10.1177/1945892421998143 [doi]
AB  - BACKGROUND: Allergic rhinitis (AR) is one of the most common noninfectious 
      respiratory diseases caused by immunoglobulin E (IgE) response. OBJECTIVE: The 
      study sought to explore the relationship between lncRNA MIAT and miR-10b-5p and 
      their interaction in the regulation of allergic phenotypes in allergic rhinitis 
      (AR) mice. METHODS: A mice model of AR was constructed using ovalbumin (OVA) 
      sensitization. AR mice were treated with miR-10b-5p agomiR and LNA mediated 
      lncRNA MIAT. The targeting relationship between MIAT and miR-10b-5p was analyzed 
      by the ENCORI website and dual-luciferase reporter assay. The numbers of rubbing 
      and sneezing of mice were counted. Hematoxylin-eosin (HE) staining visualized the 
      eosinophils infiltration in nasal mucosa tissues of mice. The percentage of Th17 
      cells was quantitated by flow cytometry analysis. ELISA was used to detect the 
      levels of serum OVA-specific IgE, the Th12 cytokine IL-4, and in fl ammatory 
      cytokines (IL-6, IL-17). RESULTS: MIAT was up-regulated in the nasal mucosa of AR 
      mice, while miR-10b-5p was down-regulated. MIAT directly suppressed miR-10b-5p 
      expression in AR mice. The numbers of rubbing and sneezing, the percentage of 
      Th17 cells, and the levels of OVA-specific IgE, IL-4, IL-6, and IL-17 in AR mice 
      were decreased by miR-10b-5p overexpression, which was reversed by MIAT 
      overexpression. The eosinophils infiltration in AR mice was inhibited by 
      miR-10b-5p overexpression, which was also reversed by MIAT overexpression. 
      CONCLUSION: The present study demonstrates that MIAT overexpression Promotes 
      allergic inflammation and symptoms by activating Th17 immune response via 
      miR-10b-5p inhibition.
FAU - Ma, Zhiqi
AU  - Ma Z
AD  - Department of Otorhinolaryngology, Affiliated Hangzhou First People's Hospital, 
      Zhejiang University School of Medicine, Hangzhou, China.
FAU - Lian, Haijuan
AU  - Lian H
AD  - Hangzhou Medical College, Binjiang District, Hangzhou, China.
FAU - Lin, Xiaoyan
AU  - Lin X
AD  - Department of Otorhinolaryngology, Affiliated Hangzhou First People's Hospital, 
      Zhejiang University School of Medicine, Hangzhou, China.
FAU - Li, Yong
AU  - Li Y
AUID- ORCID: 0000-0003-2403-7935
AD  - Department of Otorhinolaryngology, Affiliated Hangzhou First People's Hospital, 
      Zhejiang University School of Medicine, Hangzhou, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Rhinol Allergy
JT  - American journal of rhinology & allergy
JID - 101490775
RN  - 0 (Cytokines)
RN  - 0 (Miat long non-coding RNA)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Animals
MH  - Cytokines
MH  - Disease Models, Animal
MH  - Inflammation
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - *MicroRNAs/genetics
MH  - Nasal Mucosa
MH  - Ovalbumin
MH  - *RNA, Long Noncoding
MH  - *Rhinitis, Allergic
OTO - NOTNLM
OT  - LncRNA MIAT
OT  - Th17 cells
OT  - allergic rhinitis
OT  - inflammation
OT  - miR-10b-5p
EDAT- 2021/10/29 06:00
MHDA- 2021/11/03 06:00
CRDT- 2021/10/28 17:15
PHST- 2021/10/28 17:15 [entrez]
PHST- 2021/10/29 06:00 [pubmed]
PHST- 2021/11/03 06:00 [medline]
AID - 10.1177/1945892421998143 [doi]
PST - ppublish
SO  - Am J Rhinol Allergy. 2021 Nov;35(6):781-789. doi: 10.1177/1945892421998143.