PMID- 30942443
OWN - NLM
STAT- MEDLINE
DCOM- 20190726
LR  - 20210816
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 19
IP  - 5
DP  - 2019 May
TI  - Comparative analysis of gene expression profiles in children with type 1 diabetes 
      mellitus.
PG  - 3989-4000
LID - 10.3892/mmr.2019.10099 [doi]
AB  - Type 1 diabetes (T1D) is an autoimmune disease that is typically diagnosed in 
      children. The aim of the present study was to identify potential genes involved 
      in the pathogenesis of childhood T1D. Two datasets of mRNA expression in children 
      with T1D were obtained from the Gene Expression Omnibus (GEO). Differentially 
      expressed genes (DEGs) in children with T1D were identified. Functional analysis 
      was performed and a protein‑protein interaction (PPI) network was constructed, as 
      was a transcription factor (TF)‑target network. The expression of selected DEGs 
      was further assessed using reverse transcription‑quantitative polymerase chain 
      reaction (RT‑qPCR) analysis. Electronic validation and diagnostic value analysis 
      of the identified DEGs [cytokine inducible SH2 containing protein (CISH), 
      SR‑related CTD associated factor 11 (SCAF11), estrogen receptor 1 (ESR1), Rho 
      GTPase activating protein 25 (ARHGAP25), major histocompatibility complex, class 
      II, DR beta4 (HLA‑DRB4) and interleukin 23 subunit alpha (IL23A)] was performed in the 
      GEO dataset. Compared with the normal control group, a total of 1,467 DEGs with 
      P<0.05 were identified in children with T1D. CISH and SCAF11 were determined to 
      be the most up‑ and downregulated genes, respectively. Heterogeneous nuclear 
      ribonucleoprotein D (HNRNPD; degree=33), protein kinase AMP‑activated catalytic 
      subunit alpha1 (PRKAA1; degree=11), integrin subunit alpha4 (ITGA4; degree=8) and ESR1 
      (degree=8) were identified in the PPI network as high‑degree genes. ARHGAP25 
      (degree=12), HNRNPD (degree=10), HLA‑DRB4 (degree=10) and IL23A (degree=9) were 
      high‑degree genes identified in the TF‑target network. RT‑qPCR revealed that the 
      expression of HNRNPD, PRKAA1, ITGA4 and transporter 2, ATP binding cassette 
      subfamily B member was consistent with the results of the integrated analysis. 
      Furthermore, the results of the electronic validation were consistent with the 
      bioinformatics analysis. SCAF11, CISH and ARHGAP25 were identified to possess 
      value as potential diagnostic markers for children with T1D. In conclusion, 
      identifying DEGs in children with T1D may contribute to our understanding of its 
      pathogenesis, and such DEGs may be used as diagnostic biomarkers for children 
      with T1D.
FAU - Qian, Liwei
AU  - Qian L
AD  - Department of Pediatrics, The Second People's Hospital of Liaocheng, Liaocheng, 
      Shandong 252000, P.R. China.
FAU - Shi, Honglei
AU  - Shi H
AD  - Department of Pediatrics, The Second People's Hospital of Liaocheng, Liaocheng, 
      Shandong 252000, P.R. China.
FAU - Ding, Meili
AU  - Ding M
AD  - Department of Pediatrics, Shandong Jining No. 1 People's Hospital, Jining, 
      Shandong 272011, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20190328
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (ESR1 protein, human)
RN  - 0 (Estrogen Receptor alpha)
RN  - 0 (SCAF11 protein, human)
RN  - 0 (Suppressor of Cytokine Signaling Proteins)
RN  - 0 (cytokine inducible SH2-containing protein)
RN  - 170974-22-8 (Serine-Arginine Splicing Factors)
MH  - Area Under Curve
MH  - Case-Control Studies
MH  - Child
MH  - Diabetes Mellitus, Type 1/*diagnosis/genetics
MH  - Estrogen Receptor alpha/genetics/metabolism
MH  - Female
MH  - Gene Regulatory Networks
MH  - Humans
MH  - Male
MH  - Protein Interaction Maps/genetics
MH  - ROC Curve
MH  - Serine-Arginine Splicing Factors/genetics/metabolism
MH  - Suppressor of Cytokine Signaling Proteins/genetics/metabolism
MH  - *Transcriptome
PMC - PMC6472094
EDAT- 2019/04/04 06:00
MHDA- 2019/07/28 06:00
PMCR- 2019/03/28
CRDT- 2019/04/04 06:00
PHST- 2017/12/20 00:00 [received]
PHST- 2018/06/22 00:00 [accepted]
PHST- 2019/04/04 06:00 [pubmed]
PHST- 2019/07/28 06:00 [medline]
PHST- 2019/04/04 06:00 [entrez]
PHST- 2019/03/28 00:00 [pmc-release]
AID - mmr-19-05-3989 [pii]
AID - 10.3892/mmr.2019.10099 [doi]
PST - ppublish
SO  - Mol Med Rep. 2019 May;19(5):3989-4000. doi: 10.3892/mmr.2019.10099. Epub 2019 Mar 
      28.