TY - JOUR
T1 - Altered expression of matrix remodelling associated 7 (MXRA7) in psoriatic epidermis
T2 - Evidence for a protective role in the psoriasis imiquimod mouse model
AU - Ning, Jinling
AU - Shen, Ying
AU - Wang, Ting
AU - Wang, Mengru
AU - Liu, Wei
AU - Sun, Yonghu
AU - Zhang, Furen
AU - Chen, Lingling
AU - Wang, Yiqiang
N1 - Publisher Copyright:
© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2018/9
Y1 - 2018/9
N2 - Preliminary data mining performed with Gene Expression Omnibus data sets implied that psoriasis may involve the matrix remodelling associated 7 (MXRA7), a gene with little function information yet. To test that hypothesis, studies were performed in human samples and murine models. Immunohistochemistry in normal human skin showed that MXRA7 proteins were present across the full epidermal layer, with highest expression level detected in the basal layer. In psoriatic samples, MXRA7 proteins were absent in the basal stem cells layer, while suprabasal keratinocytes were stained at a higher level than in normal tissues. In an imiquimod-induced psoriasis-like disease model in mice, diseased skins manifested similar MXRA7 expression pattern and change as in human samples, and MXRA7-deficient mice developed severer psoriasis-like diseases than wild-type mice did. While levels of propsoriatic genes (eg IL17, IL22, IL23) in imiquimod-stimulated MXRA7-deficient mice were higher than in wild-type mice, keratinocytes isolated from MXRA7-deficient mice showed increased proliferation upon differentiation induction in culture. These data demonstrated that MXRA7 gene might function as a negative modulator in psoriasis development when propsoriatic factors attack, presumably via expression alteration or redistribution of MXRA7 proteins in keratinocytes.
AB - Preliminary data mining performed with Gene Expression Omnibus data sets implied that psoriasis may involve the matrix remodelling associated 7 (MXRA7), a gene with little function information yet. To test that hypothesis, studies were performed in human samples and murine models. Immunohistochemistry in normal human skin showed that MXRA7 proteins were present across the full epidermal layer, with highest expression level detected in the basal layer. In psoriatic samples, MXRA7 proteins were absent in the basal stem cells layer, while suprabasal keratinocytes were stained at a higher level than in normal tissues. In an imiquimod-induced psoriasis-like disease model in mice, diseased skins manifested similar MXRA7 expression pattern and change as in human samples, and MXRA7-deficient mice developed severer psoriasis-like diseases than wild-type mice did. While levels of propsoriatic genes (eg IL17, IL22, IL23) in imiquimod-stimulated MXRA7-deficient mice were higher than in wild-type mice, keratinocytes isolated from MXRA7-deficient mice showed increased proliferation upon differentiation induction in culture. These data demonstrated that MXRA7 gene might function as a negative modulator in psoriasis development when propsoriatic factors attack, presumably via expression alteration or redistribution of MXRA7 proteins in keratinocytes.
KW - Imiquimod
KW - keratinocytes
KW - matrix remodelling associated 7
KW - psoriasis
UR - http://www.scopus.com/inward/record.url?scp=85052523895&partnerID=8YFLogxK
U2 - 10.1111/exd.13687
DO - 10.1111/exd.13687
M3 - Article
C2 - 29781547
AN - SCOPUS:85052523895
SN - 0906-6705
VL - 27
SP - 1038
EP - 1042
JO - Experimental Dermatology
JF - Experimental Dermatology
IS - 9
ER -