Psoriasis Risk Genes of the Late Cornified Envelope-3 Group Are Distinctly Expressed Compared with Genes of Other LCE Groups
Deletion of the late cornified envelope (LCE) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes of LCE groups 1, 2, 3, 5, and 6 was examined in vivo and in vitro. Quantitative PCR demonstrated that moderate to high LCE expression was largel...
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Published in | The American journal of pathology Vol. 178; no. 4; pp. 1470 - 1477 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
Elsevier Inc
01.04.2011
American Society for Investigative Pathology |
Subjects | |
Online Access | Get full text |
ISSN | 0002-9440 1525-2191 1525-2191 |
DOI | 10.1016/j.ajpath.2010.12.017 |
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Abstract | Deletion of the late cornified envelope (LCE) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes of LCE groups 1, 2, 3, 5, and 6 was examined in vivo and in vitro. Quantitative PCR demonstrated that moderate to high LCE expression was largely confined to skin and a few oropharyngeal tissues. Genes of the LCE3 group demonstrated increased expression in lesional psoriatic epidermis and were induced after superficial injury of normal skin, whereas expression of members of other LCE groups was down-regulated under these conditions. Immunohistochemistry and immunoelectron microscopy demonstrated that LCE2 protein expression was restricted to the uppermost granular layer and the stratum corneum. Stimulation of in vitro reconstructed skin by several psoriasis-associated cytokines resulted in induction of LCE3 members. The data suggest that LCE proteins of groups 1, 2, 5, and 6 are involved in normal skin barrier function, whereas LCE3 genes encode proteins involved in barrier repair after injury or inflammation. These findings may provide clues to the mechanistic role of LCE3B/C deletion in psoriasis. |
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AbstractList | Deletion of the late cornified envelope (
LCE
) genes
LCE3B
and
LCE3C
has recently been identified as a risk factor for psoriasis. Expression of 16
LCE
genes of
LCE
groups 1, 2, 3, 5, and 6 was examined
in vivo
and
in vitro
. Quantitative PCR demonstrated that moderate to high
LCE
expression was largely confined to skin and a few oropharyngeal tissues. Genes of the
LCE3
group demonstrated increased expression in lesional psoriatic epidermis and were induced after superficial injury of normal skin, whereas expression of members of other
LCE
groups was down-regulated under these conditions. Immunohistochemistry and immunoelectron microscopy demonstrated that LCE2 protein expression was restricted to the uppermost granular layer and the stratum corneum. Stimulation of
in vitro
reconstructed skin by several psoriasis-associated cytokines resulted in induction of
LCE3
members. The data suggest that LCE proteins of groups 1, 2, 5, and 6 are involved in normal skin barrier function, whereas
LCE
3 genes encode proteins involved in barrier repair after injury or inflammation. These findings may provide clues to the mechanistic role of
LCE
3
B/C
deletion in psoriasis. Deletion of the late cornified envelope (LCE) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes of LCE groups 1, 2, 3, 5, and 6 was examined in vivo and in vitro. Quantitative PCR demonstrated that moderate to high LCE expression was largely confined to skin and a few oropharyngeal tissues. Genes of the LCE3 group demonstrated increased expression in lesional psoriatic epidermis and were induced after superficial injury of normal skin, whereas expression of members of other LCE groups was down-regulated under these conditions. Immunohistochemistry and immunoelectron microscopy demonstrated that LCE2 protein expression was restricted to the uppermost granular layer and the stratum corneum. Stimulation of in vitro reconstructed skin by several psoriasis-associated cytokines resulted in induction of LCE3 members. The data suggest that LCE proteins of groups 1, 2, 5, and 6 are involved in normal skin barrier function, whereas LCE3 genes encode proteins involved in barrier repair after injury or inflammation. These findings may provide clues to the mechanistic role of LCE3B/C deletion in psoriasis. Deletion of the late cornified envelope (LCE) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes of LCE groups 1, 2, 3, 5, and 6 was examined in vivo and in vitro. Quantitative PCR demonstrated that moderate to high LCE expression was largely confined to skin and a few oropharyngeal tissues. Genes of the LCE3 group demonstrated increased expression in lesional psoriatic epidermis and were induced after superficial injury of normal skin, whereas expression of members of other LCE groups was down-regulated under these conditions. Immunohistochemistry and immunoelectron microscopy demonstrated that LCE2 protein expression was restricted to the uppermost granular layer and the stratum corneum. Stimulation of in vitro reconstructed skin by several psoriasis-associated cytokines resulted in induction of LCE3 members. The data suggest that LCE proteins of groups 1, 2, 5, and 6 are involved in normal skin barrier function, whereas LCE3 genes encode proteins involved in barrier repair after injury or inflammation. These findings may provide clues to the mechanistic role of LCE3B/C deletion in psoriasis.Deletion of the late cornified envelope (LCE) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes of LCE groups 1, 2, 3, 5, and 6 was examined in vivo and in vitro. Quantitative PCR demonstrated that moderate to high LCE expression was largely confined to skin and a few oropharyngeal tissues. Genes of the LCE3 group demonstrated increased expression in lesional psoriatic epidermis and were induced after superficial injury of normal skin, whereas expression of members of other LCE groups was down-regulated under these conditions. Immunohistochemistry and immunoelectron microscopy demonstrated that LCE2 protein expression was restricted to the uppermost granular layer and the stratum corneum. Stimulation of in vitro reconstructed skin by several psoriasis-associated cytokines resulted in induction of LCE3 members. The data suggest that LCE proteins of groups 1, 2, 5, and 6 are involved in normal skin barrier function, whereas LCE3 genes encode proteins involved in barrier repair after injury or inflammation. These findings may provide clues to the mechanistic role of LCE3B/C deletion in psoriasis. Deletion of the late cornified envelope ( LCE ) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes of LCE groups 1, 2, 3, 5, and 6 was examined in vivo and in vitro . Quantitative PCR demonstrated that moderate to high LCE expression was largely confined to skin and a few oropharyngeal tissues. Genes of the LCE3 group demonstrated increased expression in lesional psoriatic epidermis and were induced after superficial injury of normal skin, whereas expression of members of other LCE groups was down-regulated under these conditions. Immunohistochemistry and immunoelectron microscopy demonstrated that LCE2 protein expression was restricted to the uppermost granular layer and the stratum corneum. Stimulation of in vitro reconstructed skin by several psoriasis-associated cytokines resulted in induction of LCE3 members. The data suggest that LCE proteins of groups 1, 2, 5, and 6 are involved in normal skin barrier function, whereas LCE 3 genes encode proteins involved in barrier repair after injury or inflammation. These findings may provide clues to the mechanistic role of LCE 3 B/C deletion in psoriasis. |
Author | Thuret, Jean-Yves Tjabringa, Geuranne S. Rodijk-Olthuis, Diana Jansen, Patrick A.M. Ishida-Yamamoto, Akemi Narita, Masashi Schalkwijk, Joost van Vlijmen-Willems, Ivonne M.J.J. Zeeuwen, Patrick L.J.M. Bergboer, Judith G.M. Kamsteeg, Marijke |
AuthorAffiliation | Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, United Kingdom Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands Department of Dermatology, Asahikawa Medical University, Asahikawa, Japan |
AuthorAffiliation_xml | – name: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands – name: Department of Dermatology, Asahikawa Medical University, Asahikawa, Japan – name: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, United Kingdom |
Author_xml | – sequence: 1 givenname: Judith G.M. surname: Bergboer fullname: Bergboer, Judith G.M. organization: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands – sequence: 2 givenname: Geuranne S. surname: Tjabringa fullname: Tjabringa, Geuranne S. organization: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands – sequence: 3 givenname: Marijke surname: Kamsteeg fullname: Kamsteeg, Marijke organization: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands – sequence: 4 givenname: Ivonne M.J.J. surname: van Vlijmen-Willems fullname: van Vlijmen-Willems, Ivonne M.J.J. organization: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands – sequence: 5 givenname: Diana surname: Rodijk-Olthuis fullname: Rodijk-Olthuis, Diana organization: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands – sequence: 6 givenname: Patrick A.M. surname: Jansen fullname: Jansen, Patrick A.M. organization: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands – sequence: 7 givenname: Jean-Yves surname: Thuret fullname: Thuret, Jean-Yves organization: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, United Kingdom – sequence: 8 givenname: Masashi surname: Narita fullname: Narita, Masashi organization: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, United Kingdom – sequence: 9 givenname: Akemi surname: Ishida-Yamamoto fullname: Ishida-Yamamoto, Akemi organization: Department of Dermatology, Asahikawa Medical University, Asahikawa, Japan – sequence: 10 givenname: Patrick L.J.M. surname: Zeeuwen fullname: Zeeuwen, Patrick L.J.M. organization: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands – sequence: 11 givenname: Joost surname: Schalkwijk fullname: Schalkwijk, Joost email: j.schalkwijk@ncmls.ru.nl organization: Department of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands |
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ContentType | Journal Article |
Copyright | 2011 American Society for Investigative Pathology American Society for Investigative Pathology 2015 INIST-CNRS Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved. 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved. 2011 American Society for Investigative Pathology |
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Keywords | Skin disease Anatomic pathology Late Gene Psoriasis Risk factor Genetics Risk Gene expression Comparative study |
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Snippet | Deletion of the late cornified envelope (LCE) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes of... Deletion of the late cornified envelope ( LCE ) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes... Deletion of the late cornified envelope ( LCE ) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes... |
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SubjectTerms | Biological and medical sciences Case-Control Studies Cornified Envelope Proline-Rich Proteins - biosynthesis Cornified Envelope Proline-Rich Proteins - metabolism Dermatology Gene Deletion Gene Expression Regulation Gene Frequency Humans Immunohistochemistry - methods Inflammation Investigative techniques, diagnostic techniques (general aspects) Medical sciences Microscopy, Fluorescence - methods Microscopy, Immunoelectron - methods Pathology Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Psoriasis - diagnosis Psoriasis - genetics Psoriasis - pathology Psoriasis. Parapsoriasis. Lichen Regular Risk Skin - metabolism |
Title | Psoriasis Risk Genes of the Late Cornified Envelope-3 Group Are Distinctly Expressed Compared with Genes of Other LCE Groups |
URI | https://www.clinicalkey.com/#!/content/1-s2.0-S0002944010002804 https://www.clinicalkey.es/playcontent/1-s2.0-S0002944010002804 https://dx.doi.org/10.1016/j.ajpath.2010.12.017 https://www.ncbi.nlm.nih.gov/pubmed/21435436 https://www.proquest.com/docview/858778782 https://pubmed.ncbi.nlm.nih.gov/PMC3078472 |
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