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Cell-cycle regulatory proteins in human wound healing

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Cell-cycle regulatory proteins in human wound healing. / Bartkova, Jirina; Grøn, Birgitte; Dabelsteen, Erik; Bartek, Jiri.

I: Archives of Oral Biology, Bind 48, Nr. 2, 02.2003, s. 125-32.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Bartkova, J, Grøn, B, Dabelsteen, E & Bartek, J 2003, 'Cell-cycle regulatory proteins in human wound healing', Archives of Oral Biology, bind 48, nr. 2, s. 125-32.

APA

Bartkova, J., Grøn, B., Dabelsteen, E., & Bartek, J. (2003). Cell-cycle regulatory proteins in human wound healing. Archives of Oral Biology, 48(2), 125-32.

Vancouver

Bartkova J, Grøn B, Dabelsteen E, Bartek J. Cell-cycle regulatory proteins in human wound healing. Archives of Oral Biology. 2003 feb;48(2):125-32.

Author

Bartkova, Jirina ; Grøn, Birgitte ; Dabelsteen, Erik ; Bartek, Jiri. / Cell-cycle regulatory proteins in human wound healing. I: Archives of Oral Biology. 2003 ; Bind 48, Nr. 2. s. 125-32.

Bibtex

@article{5975689c8e534582bfc98a03a0a8a250,
title = "Cell-cycle regulatory proteins in human wound healing",
abstract = "Proper healing of mucosal wounds requires careful orchestration of epithelial cell migration and proliferation. To elucidate the molecular basis of the lack of cellular proliferation in the migrating 'epithelial tongue' during the re-epithelialization of oral mucosal wounds, the expression of cell-cycle regulators critical for G(1)-phase progression and S-phase entry was here analysed immunohistochemically. Compared to normal human mucosa, epithelia migrating to cover 2- or 3-day-old wounds made either in vivo or in an organotypic cell culture all showed loss of the proliferation marker Ki67 and cyclins D(1) and A, and reduced expression of cyclins D(3) and E, the cyclin D-dependent kinase 4 (CDK4), the MCM7 component of DNA replication origin complexes and the retinoblastoma protein pRb. Among the CDK inhibitors (CKIs), p16ink4a and p21Cip1 were moderately increased and decreased, respectively, whereas the abundance of most of the CKIs, including p27Kip1, p57Kip2, p15ink4b and p18ink4c, was relatively maintained in the migrating epithelial tongue. These data indicate that downmodulation of several G(1)/S-phase cyclins and a relative excess of CKIs may cooperate to ensure the quiescent state of migrating keratinocytes during wound healing.",
keywords = "Adult, Cell Cycle Proteins, Cell Movement, Cyclins, Epithelial Cells, G1 Phase, Humans, Mouth Mucosa, S Phase, Wound Healing",
author = "Jirina Bartkova and Birgitte Gr{\o}n and Erik Dabelsteen and Jiri Bartek",
year = "2003",
month = feb,
language = "English",
volume = "48",
pages = "125--32",
journal = "Archives of Oral Biology",
issn = "0003-9969",
publisher = "Pergamon Press",
number = "2",

}

RIS

TY - JOUR

T1 - Cell-cycle regulatory proteins in human wound healing

AU - Bartkova, Jirina

AU - Grøn, Birgitte

AU - Dabelsteen, Erik

AU - Bartek, Jiri

PY - 2003/2

Y1 - 2003/2

N2 - Proper healing of mucosal wounds requires careful orchestration of epithelial cell migration and proliferation. To elucidate the molecular basis of the lack of cellular proliferation in the migrating 'epithelial tongue' during the re-epithelialization of oral mucosal wounds, the expression of cell-cycle regulators critical for G(1)-phase progression and S-phase entry was here analysed immunohistochemically. Compared to normal human mucosa, epithelia migrating to cover 2- or 3-day-old wounds made either in vivo or in an organotypic cell culture all showed loss of the proliferation marker Ki67 and cyclins D(1) and A, and reduced expression of cyclins D(3) and E, the cyclin D-dependent kinase 4 (CDK4), the MCM7 component of DNA replication origin complexes and the retinoblastoma protein pRb. Among the CDK inhibitors (CKIs), p16ink4a and p21Cip1 were moderately increased and decreased, respectively, whereas the abundance of most of the CKIs, including p27Kip1, p57Kip2, p15ink4b and p18ink4c, was relatively maintained in the migrating epithelial tongue. These data indicate that downmodulation of several G(1)/S-phase cyclins and a relative excess of CKIs may cooperate to ensure the quiescent state of migrating keratinocytes during wound healing.

AB - Proper healing of mucosal wounds requires careful orchestration of epithelial cell migration and proliferation. To elucidate the molecular basis of the lack of cellular proliferation in the migrating 'epithelial tongue' during the re-epithelialization of oral mucosal wounds, the expression of cell-cycle regulators critical for G(1)-phase progression and S-phase entry was here analysed immunohistochemically. Compared to normal human mucosa, epithelia migrating to cover 2- or 3-day-old wounds made either in vivo or in an organotypic cell culture all showed loss of the proliferation marker Ki67 and cyclins D(1) and A, and reduced expression of cyclins D(3) and E, the cyclin D-dependent kinase 4 (CDK4), the MCM7 component of DNA replication origin complexes and the retinoblastoma protein pRb. Among the CDK inhibitors (CKIs), p16ink4a and p21Cip1 were moderately increased and decreased, respectively, whereas the abundance of most of the CKIs, including p27Kip1, p57Kip2, p15ink4b and p18ink4c, was relatively maintained in the migrating epithelial tongue. These data indicate that downmodulation of several G(1)/S-phase cyclins and a relative excess of CKIs may cooperate to ensure the quiescent state of migrating keratinocytes during wound healing.

KW - Adult

KW - Cell Cycle Proteins

KW - Cell Movement

KW - Cyclins

KW - Epithelial Cells

KW - G1 Phase

KW - Humans

KW - Mouth Mucosa

KW - S Phase

KW - Wound Healing

M3 - Journal article

C2 - 12642231

VL - 48

SP - 125

EP - 132

JO - Archives of Oral Biology

JF - Archives of Oral Biology

SN - 0003-9969

IS - 2

ER -

ID: 119593379