PMID- 33338031
OWN - NLM
STAT- MEDLINE
DCOM- 20210104
LR  - 20210816
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 26
DP  - 2020 Dec 18
TI  - Functional Analysis of Estrogen Receptor 1 in Diabetic Wound Healing: A Knockdown 
      Cell-Based and Bioinformatic Study.
PG  - e928788
LID - 10.12659/MSM.928788 [doi]
AB  - BACKGROUND Diabetic wound (DW) treatment is a serious challenge for clinicians, 
      and the underlying mechanisms of DWs remain elusive. We sought to identify the 
      critical genes in the development of DWs and provide potential targets for DW 
      therapies. MATERIAL AND METHODS Datasets of GSE38396 from the Gene Expression 
      Omnibus (GEO) database were reviewed. Pathway analysis was performed using the 
      Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology term analyses were 
      carried out, and Cytoscape software (Cytoscape 3.7.2) was used to construct the 
      protein interaction network. Serum samples from patients with diabetes and 
      control participants were collected, and the expression of estrogen receptor 1 
      (ESR1) was measured by quantitative reverse-transcription polymerase chain 
      reaction. In addition, the function of ESR1 in human skin fibroblasts was 
      investigated in vitro. RESULTS Eight samples were analyzed using the Morpheus 
      online tool, which identified 637 upregulated and 448 downregulated 
      differentially expressed genes. The top 5 KEGG pathways of upregulated 
      differentially expressed genes were associated with sphingolipid metabolism, 
      estrogen signaling, ECM-receptor interaction, MAPK signaling, and PI3K-Akt 
      signaling. The hub genes for DWs were JUN, ESR1, CD44, SMARCA4, MMP2, BMP4, 
      GSK3B, WDR5, PTK2, and PTGS2. JUN, MMP2, and ESR1 were the upregulated hub genes, 
      and ESR1 was found to be consistently enriched in DW patients. Inhibition of ESR1 
      had a stimulative role in human skin fibroblasts. CONCLUSIONS ESR1 was identified 
      as a crucial gene in the development of DWs, which suggests potential therapeutic 
      targets for DW healing.
FAU - Qi, Sha
AU  - Qi S
AD  - Department of Hand Surgery, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China 
      (mainland).
FAU - Han, Qiong
AU  - Han Q
AD  - Department of Hand Surgery, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China 
      (mainland).
FAU - Xing, Danmou
AU  - Xing D
AD  - Department of Hand Surgery, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China 
      (mainland).
FAU - Qian, Long
AU  - Qian L
AD  - Department of Hand Surgery, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China 
      (mainland).
FAU - Yu, Xiang
AU  - Yu X
AD  - Department of Hand Surgery, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China 
      (mainland).
FAU - Ren, Dong
AU  - Ren D
AD  - Department of Hand Surgery, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China 
      (mainland).
FAU - Wang, Huan
AU  - Wang H
AD  - Department of Hand Surgery, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China 
      (mainland).
FAU - Chen, Quan
AU  - Chen Q
AD  - Department of Hand Surgery, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China 
      (mainland).
LA  - eng
PT  - Journal Article
DEP - 20201218
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (ESR1 protein, human)
RN  - 0 (Estrogen Receptor alpha)
SB  - IM
MH  - Cells, Cultured
MH  - Databases, Genetic
MH  - Diabetes Complications/*genetics
MH  - Estrogen Receptor alpha/*genetics
MH  - Fibroblasts/*metabolism
MH  - Gene Expression Regulation
MH  - Gene Ontology
MH  - Humans
MH  - Signal Transduction
MH  - *Skin Ulcer/etiology/genetics/metabolism
MH  - Wound Healing/genetics
PMC - PMC7754692
EDAT- 2020/12/19 06:00
MHDA- 2021/01/05 06:00
PMCR- 2020/12/18
CRDT- 2020/12/18 17:11
PHST- 2020/12/18 17:11 [entrez]
PHST- 2020/12/19 06:00 [pubmed]
PHST- 2021/01/05 06:00 [medline]
PHST- 2020/12/18 00:00 [pmc-release]
AID - 928788 [pii]
AID - 10.12659/MSM.928788 [doi]
PST - epublish
SO  - Med Sci Monit. 2020 Dec 18;26:e928788. doi: 10.12659/MSM.928788.