PMID- 38163574
OWN - NLM
STAT- MEDLINE
DCOM- 20240122
LR  - 20240202
IS  - 1089-8646 (Electronic)
IS  - 0888-7543 (Linking)
VI  - 116
IP  - 1
DP  - 2024 Jan
TI  - Identification of rat Vstm1 with conservative anti-inflammatory effect between 
      rat and human homologs.
PG  - 110774
LID - S0888-7543(23)00218-5 [pii]
LID - 10.1016/j.ygeno.2023.110774 [doi]
AB  - Human VSTM1 (also known as SIRL1) is an inhibitory immune checkpoint receptor 
      involved in leukocyte activation. Identification of the homologous genes in other 
      species, such as mice and rats, will undoubtedly contribute to functional studies 
      and clinical applications. Here, we successfully cloned the Vstm1 gene in rats, 
      as supported by high-throughput sequencing data. However, Vstm1 is degenerated to 
      a pseudogene in the mouse genome. Rat Vstm1 mRNA contains a complete open reading 
      frame (ORF) of 630 nucleotides encoding 209 amino acids. Rat Vstm1 is highly 
      expressed in bone marrow, especially in granulocytes. The expression levels of 
      Vstm1 gradually increase with the development of granulocytes in bone marrow but 
      are downregulated in response to inflammatory stimuli. Rat VSTM1 does not have an 
      immunoreceptor tyrosine-based inhibitory motif (ITIM), however, it shows a 
      conservative function of inflammatory inhibition with human VSTM1, and both are 
      anti-correlated with many inflammatory cytokines, such as IL-1alpha and TNF-alpha. In 
      bone marrow-derived macrophages (BMDMs), either rat or human VSTM1 suppressed the 
      secretion of inflammatory cytokines in response to LPS stimulation. Further 
      analysis in lung cancer microenvironment revealed that VSTM1 is mainly expressed 
      in myeloid cells, anti-correlated with inflammatory cytokines and associated with 
      tumor development and metastasis.
CI  - Copyright (c) 2024 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Hu, Yuzhe
AU  - Hu Y
AD  - Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking 
      University), School of Basic Medical Sciences, Peking University Health Science 
      Center, Beijing, China; Peking University Center for Human Disease Genomics, 
      Beijing, China.
FAU - Sun, Yingzhe
AU  - Sun Y
AD  - Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking 
      University), School of Basic Medical Sciences, Peking University Health Science 
      Center, Beijing, China; Peking University Center for Human Disease Genomics, 
      Beijing, China.
FAU - Li, Ting
AU  - Li T
AD  - Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking 
      University), School of Basic Medical Sciences, Peking University Health Science 
      Center, Beijing, China; Peking University Center for Human Disease Genomics, 
      Beijing, China.
FAU - Han, Wenling
AU  - Han W
AD  - Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking 
      University), School of Basic Medical Sciences, Peking University Health Science 
      Center, Beijing, China; Peking University Center for Human Disease Genomics, 
      Beijing, China. Electronic address: hanwl@bjmu.edu.cn.
FAU - Wang, Pingzhang
AU  - Wang P
AD  - Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking 
      University), School of Basic Medical Sciences, Peking University Health Science 
      Center, Beijing, China; Peking University Center for Human Disease Genomics, 
      Beijing, China. Electronic address: wangpzh@bjmu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20231230
PL  - United States
TA  - Genomics
JT  - Genomics
JID - 8800135
RN  - 0 (Cytokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Humans
MH  - Rats
MH  - Animals
MH  - Mice
MH  - *Cytokines
MH  - *Macrophages/metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
MH  - Anti-Inflammatory Agents/pharmacology/therapeutic use
MH  - Lipopolysaccharides
OTO - NOTNLM
OT  - Homologous gene
OT  - Immune checkpoint
OT  - Immunosuppressive
OT  - Inflammation
OT  - VSTM1
COIS- Declaration of competing interest The authors declare no competing financial 
      interests.
EDAT- 2024/01/02 11:41
MHDA- 2024/01/22 06:42
CRDT- 2024/01/01 19:14
PHST- 2023/09/15 00:00 [received]
PHST- 2023/11/17 00:00 [revised]
PHST- 2023/12/29 00:00 [accepted]
PHST- 2024/01/22 06:42 [medline]
PHST- 2024/01/02 11:41 [pubmed]
PHST- 2024/01/01 19:14 [entrez]
AID - S0888-7543(23)00218-5 [pii]
AID - 10.1016/j.ygeno.2023.110774 [doi]
PST - ppublish
SO  - Genomics. 2024 Jan;116(1):110774. doi: 10.1016/j.ygeno.2023.110774. Epub 2023 Dec 
      30.