PMID- 33557054
OWN - NLM
STAT- MEDLINE
DCOM- 20210420
LR  - 20210420
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 22
IP  - 4
DP  - 2021 Feb 4
TI  - Ubiquitous Overexpression of Chromatin Remodeling Factor SRG3 Exacerbates Atopic 
      Dermatitis in NC/Nga Mice by Enhancing Th2 Immune Responses.
LID - 10.3390/ijms22041553 [doi]
LID - 1553
AB  - The SWItch (SWI)3-related gene (SRG3) product, a SWI/Sucrose Non-Fermenting (SNF) 
      chromatin remodeling subunit, plays a critical role in regulating immune 
      responses. We have previously shown that ubiquitous SRG3 overexpression 
      attenuates the progression of Th1/Th17-mediated experimental autoimmune 
      encephalomyelitis. However, it is unclear whether SRG3 overexpression can affect 
      the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD), a 
      Th2-type immune disorder. Thus, to elucidate the effects of SRG3 overexpression 
      in AD development, we bred NC/Nga (NC) mice with transgenic mice where SRG3 
      expression is driven by the beta-actin promoter (SRG3(beta-actin) mice). We found that 
      SRG3(beta-actin) NC mice exhibit increased AD development (e.g., a higher clinical 
      score, immunoglobulin E (IgE) hyperproduction, and an increased number of 
      infiltrated mast cells and basophils in skin lesions) compared with wild-type NC 
      mice. Moreover, the severity of AD pathogenesis in SRG3(beta-actin) NC mice 
      correlated with expansion of interleukin 4 (IL4)-producing basophils and mast 
      cells, and M2 macrophages. Furthermore, this accelerated AD development is 
      strongly associated with Treg cell suppression. Collectively, our results have 
      identified that modulation of SRG3 function can be applied as one of the options 
      to control AD pathogenesis.
FAU - Lee, Sung Won
AU  - Lee SW
AUID- ORCID: 0000-0001-8059-5961
AD  - Department of Integrative Bioscience and Biotechnology, Institute of Anticancer 
      Medicine Development, Sejong University, Seoul 05006, Korea.
FAU - Park, Hyun Jung
AU  - Park HJ
AUID- ORCID: 0000-0002-8547-156X
AD  - Department of Integrative Bioscience and Biotechnology, Institute of Anticancer 
      Medicine Development, Sejong University, Seoul 05006, Korea.
FAU - Jeon, Jungmin
AU  - Jeon J
AUID- ORCID: 0000-0003-4507-660X
AD  - Department of Integrative Bioscience and Biotechnology, Institute of Anticancer 
      Medicine Development, Sejong University, Seoul 05006, Korea.
FAU - Park, Yun Hoo
AU  - Park YH
AUID- ORCID: 0000-0001-6944-8311
AD  - Department of Integrative Bioscience and Biotechnology, Institute of Anticancer 
      Medicine Development, Sejong University, Seoul 05006, Korea.
FAU - Kim, Tae-Cheol
AU  - Kim TC
AUID- ORCID: 0000-0002-9215-188X
AD  - Department of Integrative Bioscience and Biotechnology, Institute of Anticancer 
      Medicine Development, Sejong University, Seoul 05006, Korea.
FAU - Jeon, Sung Ho
AU  - Jeon SH
AD  - Department of Life Science and Multidisciplinary Genome Institute, Hallym 
      University, Chuncheon 24252, Korea.
FAU - Seong, Rho Hyun
AU  - Seong RH
AD  - School of Biological Sciences, Institute of Molecular Biology and Genetics, Seoul 
      National University, Seoul 08826, Korea.
FAU - Van Kaer, Luc
AU  - Van Kaer L
AUID- ORCID: 0000-0001-5275-2309
AD  - Department of Pathology, Microbiology and Immunology, Vanderbilt University 
      School of Medicine, Nashville, TN 37232, USA.
FAU - Hong, Seokmann
AU  - Hong S
AUID- ORCID: 0000-0002-4606-9789
AD  - Department of Integrative Bioscience and Biotechnology, Institute of Anticancer 
      Medicine Development, Sejong University, Seoul 05006, Korea.
LA  - eng
GR  - NRF-2018R1D1A1B07049495/National Research Foundation of Korea/
GR  - NRF-2016R1D1A1A09919293/National Research Foundation of Korea/
GR  - NRF-2019R1A2C1009926/National Research Foundation of Korea/
PT  - Journal Article
DEP - 20210204
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Actins)
RN  - 0 (Smarcc1 protein, mouse)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Actins/metabolism
MH  - Animals
MH  - Biopsy
MH  - *Chromatin Assembly and Disassembly
MH  - Dendritic Cells/immunology/metabolism
MH  - Dermatitis, Atopic/diagnosis/*etiology/metabolism
MH  - Disease Models, Animal
MH  - Disease Susceptibility
MH  - *Gene Expression
MH  - Immunity, Cellular
MH  - Macrophages/immunology/metabolism
MH  - Mice
MH  - Mice, Transgenic
MH  - Severity of Illness Index
MH  - Th2 Cells/*immunology/*metabolism
MH  - Transcription Factors/*genetics
PMC - PMC7913833
OTO - NOTNLM
OT  - NC/Nga
OT  - SWI3-related gene (SRG3)
OT  - Th2 cells
OT  - Treg cells
OT  - WT
OT  - atopic dermatitis
COIS- The authors declare no conflict of interest.
EDAT- 2021/02/10 06:00
MHDA- 2021/04/21 06:00
PMCR- 2021/02/04
CRDT- 2021/02/09 01:02
PHST- 2021/01/07 00:00 [received]
PHST- 2021/01/30 00:00 [revised]
PHST- 2021/02/01 00:00 [accepted]
PHST- 2021/02/09 01:02 [entrez]
PHST- 2021/02/10 06:00 [pubmed]
PHST- 2021/04/21 06:00 [medline]
PHST- 2021/02/04 00:00 [pmc-release]
AID - ijms22041553 [pii]
AID - ijms-22-01553 [pii]
AID - 10.3390/ijms22041553 [doi]
PST - epublish
SO  - Int J Mol Sci. 2021 Feb 4;22(4):1553. doi: 10.3390/ijms22041553.