PMID- 32019674
OWN - NLM
STAT- MEDLINE
DCOM- 20201014
LR  - 20210108
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 524
IP  - 3
DP  - 2020 Apr 9
TI  - A systems biology approach for defining the potential molecular framework of 
      idiopathic hypereosinophilic syndrome with cutaneous involvement.
PG  - 567-574
LID - S0006-291X(20)30214-X [pii]
LID - 10.1016/j.bbrc.2020.01.131 [doi]
AB  - Hypereosinophilic syndrome (HES) is a rare multisystem disease that predominantly 
      includes skin with severe and persistent itching. A lack of understanding about 
      the pathological condition and mechanism of dermatosis caused by HES hinders its 
      treatment. In the present study, we applied a quantitative proteomics approach to 
      characterize the cellular responses of skin tissue to idiopathic HES (IHES) at 
      the proteome level. We identified hundreds of skin tissue proteins that were 
      differentially expressed between IHES patients and healthy individuals. IHES 
      patients display severely damaged microenvironment, including extracellular 
      matrix (ECM) organization and disassembly, immune disorders, decreased metabolic 
      capacity, and susceptibility to microbial infection. Moreover, there was abnormal 
      proliferation of basal epidermal stem cells, which was closely related to high 
      expression of the epigenetic regulator, histone deacetylase 2, providing 
      mechanistic insight into the abnormal epidermal thickening of IHES skin tissues. 
      Overall, our study provides a comprehensive framework for a system-level 
      understanding of IHES-induced dermatosis (IHESiD) tissues at the protein and cell 
      pathway levels. Our findings may facilitate a new approach to diagnosis and 
      treatment to alleviate skin clinical symptoms, monitor the activity of IHES, and 
      determine therapeutic effects.
CI  - Copyright (c) 2020 Elsevier Inc. All rights reserved.
FAU - Wang, Wenjuan
AU  - Wang W
AD  - Department of Dermatology, PLA General Hospital, Beijing, China.
FAU - Ma, Jie
AU  - Ma J
AD  - State Key Laboratory of Proteomics, Beijing Proteome Research Center, National 
      Center for Protein Sciences (Beijing), Beijing Institute of Life Omics, Beijing, 
      China.
FAU - Sun, Xuer
AU  - Sun X
AD  - Tissue Engineering Lab, Institute of Health Service and Transfusion Medicine, 
      Beijing, China.
FAU - Ba, Wei
AU  - Ba W
AD  - Department of Dermatology, PLA General Hospital, Beijing, China.
FAU - Meng, Xianfu
AU  - Meng X
AD  - Department of Dermatology, PLA General Hospital, Beijing, China.
FAU - Zhu, Yunping
AU  - Zhu Y
AD  - State Key Laboratory of Proteomics, Beijing Proteome Research Center, National 
      Center for Protein Sciences (Beijing), Beijing Institute of Life Omics, Beijing, 
      China.
FAU - Leng, Ling
AU  - Leng L
AD  - Department of Medical Science Research Center, Peking Union Medical College 
      Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, 
      Beijing, China. Electronic address: zhenlinger@126.com.
FAU - Li, Chengxin
AU  - Li C
AD  - Department of Dermatology, PLA General Hospital, Beijing, China. Electronic 
      address: chengxinderm@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200201
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - EC 3.5.1.98 (Histone Deacetylase 2)
SB  - IM
EIN - Biochem Biophys Res Commun. 2021 Feb 19;541:104. PMID: 33413980
MH  - Cell Proliferation
MH  - Down-Regulation
MH  - Epidermis/pathology
MH  - Histone Deacetylase 2/metabolism
MH  - Humans
MH  - Hypereosinophilic Syndrome/*pathology
MH  - Mass Spectrometry
MH  - Proteomics
MH  - Skin/*pathology
MH  - Stem Cells/pathology
MH  - *Systems Biology
OTO - NOTNLM
OT  - Epidermal stem cells
OT  - Idiopathic hypereosinophilic syndrome
OT  - Proteomics
COIS- Declaration of competing interests The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2020/02/06 06:00
MHDA- 2020/10/21 06:00
CRDT- 2020/02/06 06:00
PHST- 2020/01/04 00:00 [received]
PHST- 2020/01/23 00:00 [accepted]
PHST- 2020/02/06 06:00 [pubmed]
PHST- 2020/10/21 06:00 [medline]
PHST- 2020/02/06 06:00 [entrez]
AID - S0006-291X(20)30214-X [pii]
AID - 10.1016/j.bbrc.2020.01.131 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2020 Apr 9;524(3):567-574. doi: 
      10.1016/j.bbrc.2020.01.131. Epub 2020 Feb 1.