PMID- 38163156
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240103
IS  - 2405-8440 (Print)
IS  - 2405-8440 (Electronic)
IS  - 2405-8440 (Linking)
VI  - 10
IP  - 1
DP  - 2024 Jan 15
TI  - LncRNA SNHG8 upregulates MUC5B to induce idiopathic pulmonary fibrosis 
      progression by targeting miR-4701-5p.
PG  - e23233
LID - 10.1016/j.heliyon.2023.e23233 [doi]
LID - e23233
AB  - Long noncoding RNAs (lncRNAs) play a critical role in idiopathic pulmonary 
      fibrosis (IPF); however, the underlying molecular mechanisms are unclear. Our 
      study demonstrated that lncRNA small nucleolar RNA host gene 8 (SNHG8) was 
      increased in bleomycin (BLM)-induced A549 cells. LncRNA SNHG8 overexpression 
      further elevated fibrosis-related factors monocyte chemotactic protein 1 (MCP1), 
      CC motif chemokine ligand 18 (CCL18), and alpha-smooth muscle actin (alpha-SMA), as well 
      as increased collagen type I alpha-1 chain (COL1A1) and collagen type III alpha-1 
      chain (COL3A1). Meanwhile, lncRNA SNHG8 knockdown exhibited an opposite role in 
      reducing BLM-induced pulmonary fibrosis. With regard to the mechanism, SNHG8 was 
      then revealed to act as a competing endogenous RNA (ceRNA) for microRNA 
      (miR)-4701-5p in regulating Mucin 5B (MUC5B) expression. Furthermore, the 
      interactions between SNHG8 and miR-4701-5p, between miR-4701-5p and MUC5B, and 
      between SNHG8 and MUC5B on the influence of fibrosis-related indicators were 
      confirmed, respectively. In addition, SNHG8 overexpression enhanced the levels of 
      transforming growth factor (TGF)-beta1 and phosphorylation Smad2/3 (p-Smad2/3), 
      which was suppressed by SNHG8 knockdown in BLM-induced A549 cells. Moreover, 
      miR-4701-5p inhibitor-induced elevation of TGF-beta1 and p-Smad2/3 was significantly 
      suppressed by SNHG8 knockdown. In conclusion, SNHG8 knockdown attenuated 
      pulmonary fibrosis progression by regulating miR-4701-5p/MUC5B axis, which might 
      be associated with the modulation of TGF-beta1/Smad2/3 signaling. These findings 
      reveal that lncRNA SNHG8 may become a potential target for the treatment of IPF.
CI  - (c) 2023 The Authors.
FAU - Zhang, Xiaoping
AU  - Zhang X
AD  - Department of Respiratory and Critical Care Medicine, the Second Affiliated 
      Hospital of Zhengzhou University, Zhengzhou 450014, China.
FAU - Shao, Runxia
AU  - Shao R
AD  - Department of Respiratory and Critical Care Medicine, the Second Affiliated 
      Hospital of Zhengzhou University, Zhengzhou 450014, China.
LA  - eng
PT  - Journal Article
DEP - 20231203
PL  - England
TA  - Heliyon
JT  - Heliyon
JID - 101672560
PMC - PMC10756985
OTO - NOTNLM
OT  - IPF
OT  - MUC5B
OT  - TGF-beta1/Smad2/3 signaling
OT  - lncRNA SNHG8
OT  - miR-4701-5p
COIS- The authors declare that they have no known competing financial interests or 
      personal relationships that could have appeared to influence the work reported in 
      this paper.
EDAT- 2024/01/02 11:45
MHDA- 2024/01/02 11:46
PMCR- 2023/12/03
CRDT- 2024/01/01 04:36
PHST- 2023/06/28 00:00 [received]
PHST- 2023/11/28 00:00 [revised]
PHST- 2023/11/29 00:00 [accepted]
PHST- 2024/01/02 11:46 [medline]
PHST- 2024/01/02 11:45 [pubmed]
PHST- 2024/01/01 04:36 [entrez]
PHST- 2023/12/03 00:00 [pmc-release]
AID - S2405-8440(23)10441-5 [pii]
AID - e23233 [pii]
AID - 10.1016/j.heliyon.2023.e23233 [doi]
PST - epublish
SO  - Heliyon. 2023 Dec 3;10(1):e23233. doi: 10.1016/j.heliyon.2023.e23233. eCollection 
      2024 Jan 15.