PMID- 36254059
OWN - NLM
STAT- MEDLINE
DCOM- 20221019
LR  - 20221115
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 101
IP  - 41
DP  - 2022 Oct 14
TI  - Bioinformatics analysis identified immune infiltration, risk and drug prediction 
      models of copper-induced death genes involved in salivary glands damage of 
      primary Sjogren's syndrome.
PG  - e31050
LID - 10.1097/MD.0000000000031050 [doi]
LID - e31050
AB  - This study aimed to identify copper-induced death genes in primary Sjogren's 
      syndrome (pSS) and explore immune infiltration, risk and drug prediction models 
      for salivary glands (SGs) damage. The 3 datasets, including GSE40611, GSE23117, 
      and GSE7451 from the Gene Expression Omnibus database were downloaded. The 
      datasets were processed using the affy in R (version 4.0.3). In immune cells, 
      copper-induced death genes were strongly expressed in "activated" dendritic cells 
      (aDCs), macrophages and regulatory T cells (Treg). In immune functions, 
      copper-induced death genes were strongly expressed in major histocompatibility 
      complex (MHC) class I, human leukocyte antigen (HLA) and type I interferon (IFN) 
      response. Correlation analysis showed that 5 genes including SLC31A1, PDHA1, DLD, 
      ATP7B, and ATP7A were significantly correlated with immune infiltration. The 
      nomogram suggested that the low expression of PDHA1 was significant for 
      predicting the risk of pSS and the area under curve was 0.678. Drug model 
      suggested that "Bathocuproine disulfonate CTD 00001350," "Vitinoin CTD 00007069," 
      and "Resveratrol CTD 00002483" were the drugs most strongly associated with 
      copper-induced death genes. In summary, copper-induced death genes are associated 
      with SGs injury in pSS, which is worthy of clinicians' attention.
CI  - Copyright (c) 2022 the Author(s). Published by Wolters Kluwer Health, Inc.
FAU - Zhang, Naidan
AU  - Zhang N
AD  - Department of Clinical Laboratory, Peoples Hospital of Deyang City, Deyang, 
      China.
FAU - Ji, Chaixia
AU  - Ji C
AD  - Department of Clinical Laboratory, Peoples Hospital of Deyang City, Deyang, 
      China.
FAU - Peng, Xinyin
AU  - Peng X
AD  - Chengdu University of Chinese Medicine, Chengdu, China.
FAU - Tang, Maoju
AU  - Tang M
AD  - North Sichuan Medical College, Nanchong, China.
FAU - Bao, Xiao
AU  - Bao X
AD  - Department of Rheumatology, Peoples Hospital of Deyang City, Deyang, China.
FAU - Yuan, Chengliang
AU  - Yuan C
AUID- ORCID: 0000-0002-2187-3498
AD  - Department of Clinical Laboratory, Peoples Hospital of Deyang City, Deyang, 
      China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Interferon Type I)
RN  - 789U1901C5 (Copper)
RN  - Q369O8926L (Resveratrol)
SB  - IM
MH  - Computational Biology
MH  - Copper
MH  - Humans
MH  - *Interferon Type I
MH  - Resveratrol
MH  - Salivary Glands/metabolism
MH  - *Sjogren's Syndrome
PMC - PMC9575826
COIS- The authors have no conflicts of interest to disclose.
EDAT- 2022/10/19 06:00
MHDA- 2022/10/20 06:00
PMCR- 2022/10/14
CRDT- 2022/10/18 01:32
PHST- 2022/10/18 01:32 [entrez]
PHST- 2022/10/19 06:00 [pubmed]
PHST- 2022/10/20 06:00 [medline]
PHST- 2022/10/14 00:00 [pmc-release]
AID - 00005792-202210140-00091 [pii]
AID - 10.1097/MD.0000000000031050 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2022 Oct 14;101(41):e31050. doi: 
      10.1097/MD.0000000000031050.