Delayed Wound Healing in Keratin 6a Knockout Mice

Wojcik, Sonja M.; Bundman, Donnie S.; Roop, Dennis R.

doi:10.1128/mcb.20.14.5248-5255.2000

Cited by 143 publications

(124 citation statements)

References 45 publications

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“…The expression of the migrationassociated keratin K6 increases during wound healing in adult skin and is required for normal re-epithelialization (Wong and Coulombe, 2003;Wojcik et al, 2000). Activated GR can inhibit the expression of specific keratins through several mechanisms involving transcriptional and non-transcriptional events (Radoja et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid receptor antagonizes EGFR function to regulate eyelid development

Sanchís

Bayo²,

Sevilla³

et al. 2010

Int. J. Dev. Biol.

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The glucocorticoid receptor (GR) plays a crucial role in epidermal morphogenesis during embryonic development, as demonstrated by analyzing genetically modified mouse models of GR gain-and loss-of-function. Eyelid formation constitutes a useful model to study epithelial development, as it requires coordinated regulation of keratinocyte proliferation, apoptosis and migration. We have analyzed this biological process in GR -/-embryos during ontogeny. Our data demonstrate that GR deficiency results in delayed and impaired eyelid closure, as illustrated by increased keratinocyte proliferation and apoptosis along with impaired differentiation in GR -/-eyelid epithelial cells. These defects are due, at least in part, to the lack of antagonism between GR and epidermal growth factor receptor (EGFR) signaling, causing sustained activation of the MAPK/AP-1 pathway and the upregulation of keratin K6 at embryonic stage E18.5. Additionally, we demonstrate that GR regulates epithelial cell migration in vitro by interfering with EGFR-mediated signaling. Overall, GR/EGFR antagonism appears as a major mechanism regulating ocular epithelial development.

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Section: Discussionmentioning

confidence: 99%

Glucocorticoid receptor antagonizes EGFR function to regulate eyelid development

Sanchís

Bayo²,

Sevilla³

et al. 2010

Int. J. Dev. Biol.

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“…In higher vertebrates, skin wound healing has been well studied and described specific expression of Keratins (Coulombe, 2003;Pechter et al, 2012). Epidermal cells in wound healing express Keratin 6, 16, and 17 (Ishida-Yamamoto et al, 1998;Patel et al, 2006;Wojcik et al, 2000). However, in amphibians, such keratin gene expression patterns have not been described.…”

Section: Introductionmentioning

confidence: 99%

Spatiotemporal regulation of keratin 5 and 17 in the axolotl limb

Moriyasu

Makanae

Satoh

2012

Developmental Dynamics

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Background: Amphibians have greater regeneration capability than higher vertebrates. They can regenerate their limbs after an amputation. As a limb is regenerated, a regeneration-specific epithelium called the apical epithelial cap (AEC) is induced. The AEC is an essential structure for limb regeneration. Despite the importance of the AEC, molecular marker genes have not been well studied at the molecular level. Results: In the present study, keratin5 (KRT5) and KRT17 were investigated in an axolotl-regenerating limb. KRT5 and KRT17 were expressed in a regenerating limb but down-regulated in a differentiating limb. KRT5 showed characteristic regulation in a regenerating blastema. KRT5 was suppressed in the basal layer of the AEC. This KRT5 suppression was correlated to the blastema differentiation and nerve presence. Simple skin wounding could also upregulate both KRT5 and KRT17 gene expression. But these genes were suppressed within a shorter time than in limb regeneration. Conclusions: The KRT5 and KRT17 gene profile can be a useful marker gene to investigate AEC in limb regeneration. Developmental Dynamics 241:1616-1624,

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“…Increased expression of genes involved in epidermal development was surprising because all skin was removed from the joint tissue before collection, and expression was low in joint tissue collected from uninfected C57BL/6 mice. The increased expression of genes involved in wound repair, such as Krt-2a, and cell-cell interactions, such as Ly6d and Dsp, could be suggestive of a response to disseminating bacteria (35,36).…”

Section: A Novel Group Of Genes Is Selectively Increased In Infected mentioning

confidence: 99%

Gene Expression Profiling Reveals Unique Pathways Associated with Differential Severity of Lyme Arthritis

Crandall¹,

Dunn

Ma³

et al. 2006

The Journal of Immunology

132

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The murine model of Lyme disease provides a unique opportunity to study the localized host response to similar stimulus, Borrelia burgdorferi, in the joints of mice destined to develop severe arthritis (C3H) or mild disease (C57BL/6). Pathways associated with the response to infection and the development of Lyme arthritis were identified by global gene expression patterns using oligonucleotide microarrays. A robust induction of IFN-responsive genes was observed in severely arthritic C3H mice at 1 wk of infection, which was absent from mildly arthritic C57BL/6 mice. In contrast, infected C57BL/6 mice displayed a novel expression profile characterized by genes involved in epidermal differentiation and wound repair, which were decreased in the joints of C3H mice. These expression patterns were associated with disease state rather than inherent differences between C3H and C57BL/6 mice, because C57BL/6-IL-10−/− mice infected with B. burgdorferi develop more severe arthritis than C57BL/6 mice and displayed an early gene expression profile similar to C3H mice. Gene expression profiles at 2 and 4 wk postinfection revealed a common response of all strains that was likely to be important for the host defense to B. burgdorferi and mediated by NF-κB-dependent signaling. The gene expression profiles identified in this study add to the current understanding of the host response to B. burgdorferi and identify two novel pathways that may be involved in regulating the severity of Lyme arthritis.

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Delayed Wound Healing in Keratin 6a Knockout Mice

Cited by 143 publications

References 45 publications

Glucocorticoid receptor antagonizes EGFR function to regulate eyelid development

Glucocorticoid receptor antagonizes EGFR function to regulate eyelid development

Spatiotemporal regulation of keratin 5 and 17 in the axolotl limb

Gene Expression Profiling Reveals Unique Pathways Associated with Differential Severity of Lyme Arthritis

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