PMID- 35603523
OWN - NLM
STAT- MEDLINE
DCOM- 20220524
LR  - 20220716
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 5
DP  - 2022 May
TI  - Methyltransferase like 7B is upregulated in sepsis and modulates 
      lipopolysaccharide-induced inflammatory response and macrophage polarization.
PG  - 11753-11766
LID - 10.1080/21655979.2022.2068892 [doi]
AB  - Macrophages play a critical role in the regulation of the inflammatory responses 
      in sepsis. Methyltransferase like 7B (METTL7B) has been implicated in several 
      pathophysiological conditions. Nevertheless, the potential engagement of METTL7B 
      in sepsis remains to be elucidated. In this study, we retrieved transcriptomic 
      profile data of septic patients and healthy donors and compared the expression 
      level of METTL7B between septic patients and healthy controls. We also collected 
      septic patient samples to analyze METTL7B expression via RT-qPCR. Murine bone 
      marrow-derived macrophages (BMDMs) were isolated and treated with incremental 
      doses of LPS as an in vitro cell model. METTL7B was overexpressed or knocked down 
      in BMDMs, and lipopolysaccharide (LPS)-mediated inflammatory cytokines production 
      and macrophage polarization were evaluated. We found that METTL7B was upregulated 
      in the blood and peripheral blood mononuclear cells (PBMC) of septic patients, 
      which also showed a significant diagnostic potential for sepsis. In BMDMs, 
      METTL7B was induced in a time and dose-dependent manner by LPS. Modulating the 
      expression level of METTL7B could regulate LPS-mediated inflammatory cytokines 
      production and macrophage polarization. The functional role of METTL7B was also 
      validated in a septic mouse model. Our findings indicate that METTL7B is 
      implicated in the immunopathogenesis of sepsis through modulating 
      macrophage-mediated inflammatory responses. METTL7B may serve as a potential 
      diagnostic and therapeutic target for sepsis.
FAU - Huang, Dan
AU  - Huang D
AUID- ORCID: 0000-0002-1864-4002
AD  - Clinical Medical College of Chengdu Medical College, Chengdu, China.
AD  - Department of Critical Care Medicine, The First Affiliated Hospital of Chengdu 
      Medical College, Chengdu, China.
FAU - Yan, Hai
AU  - Yan H
AD  - Clinical Medical College of Chengdu Medical College, Chengdu, China.
AD  - Department of Gastrointestinal Surgery, The First Affiliated Hospital of Chengdu 
      Medical College, Chengdu, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Carrier Proteins)
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (METTL7B protein, human)
RN  - EC 2.1.1.- (Methyltransferases)
SB  - IM
MH  - Animals
MH  - Carrier Proteins
MH  - Case-Control Studies
MH  - Cytokines/metabolism
MH  - Humans
MH  - Leukocytes, Mononuclear/metabolism
MH  - *Lipopolysaccharides/metabolism
MH  - Macrophages/metabolism
MH  - Methyltransferases/genetics/metabolism
MH  - Mice
MH  - *Sepsis/genetics
PMC - PMC9275875
OTO - NOTNLM
OT  - METTL7B
OT  - inflammation
OT  - macrophages
OT  - polarization
OT  - sepsis
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/05/24 06:00
MHDA- 2022/05/25 06:00
PMCR- 2022/05/21
CRDT- 2022/05/23 05:24
PHST- 2022/05/23 05:24 [entrez]
PHST- 2022/05/24 06:00 [pubmed]
PHST- 2022/05/25 06:00 [medline]
PHST- 2022/05/21 00:00 [pmc-release]
AID - 2068892 [pii]
AID - 10.1080/21655979.2022.2068892 [doi]
PST - ppublish
SO  - Bioengineered. 2022 May;13(5):11753-11766. doi: 10.1080/21655979.2022.2068892.