Human Epidermal Keratinocytes Are a Source of Tenascin-C during Wound Healing

Latijnhouwers, Mieke; Bergers, Mieke; Ponec, Maria; Dijkman, H.B.P.M.; Andriessen, M.P.M.; Schalkwijk, Joost

doi:10.1111/1523-1747.ep12292170

Cited by 53 publications

(51 citation statements)

References 65 publications

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“…This is supported by the observation that keratinocytes are capable of tenascin synthesis. [38][39][40] It can, therefore, be speculated that the data presented here are in accordance with the hypothesis that keratinocytes are involved in the aetiopathologesis of vitiligo.…”

Section: Discussionsupporting

confidence: 90%

Tenascin is overexpressed in vitiligo lesional skin and inhibits melanocyte adhesion

Poole

Wijngaard

Westerhof³

et al. 1997

British Journal of Dermatology

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SummaryThe aetiology of vitiligo remains obscure. In this study, the role of integrins in the observed inability of melanocytes to repopulate lesional skin was investigated. Antibodies directed to a 2 , a 3 , a 5 , a v , a 6 , b 1 and b 3 integrin subunits were used. Immunohistology revealed no marked differences in the overall levels of expression of integrins between control, non-lesional, perilesional or lesional skin. Moreover, no differences were noted in the level of expression of integrins or the adhesive capacity between cultured control cells derived from three separate donors and vitiligo-derived melanocytes from two donors. Rather, it was clearly observed that towards the lesion, vitiligo skin contains increasing amounts of tenascin in the basal membrane and papillary dermis in five patients employing T2H5 antihuman tenascin antibody. The anti-adhesive effect observed in vitro for this extracellular matrix molecule using normal melanocytes may contribute to loss of pigment cells in vitiligo or to ineffective repopulation of the lesions.In vitiligo, melanocytes are gradually lost in depigmenting lesions of the skin. 1 It has been suggested that defective adhesion is involved in loss of melanocytes in this pigmentary disorder. 2 Moreover, the persistence of depigmented lesions is suggestive of defective melanocyte migration which may be reversed by photochemotherapy, 2 and therefore baseline expression of adhesion molecules may differ in vitiligo as compared with control skin. Melanocyte adhesion, spreading and migration is mediated by integrins. 3 Employing antibodies to integrin subunits, the specific integrins involved in each process have been identified in vitro. 3,4 Importantly, all integrins thus far identified on melanocytes can also be found on neighbouring keratinocytes. Although immunohistology has been employed to identify integrins expressed on melanocytes in situ per se, 3 this may not be the method of choice to determine differences in the level of expression by melanocytes. Even by double immunostaining procedures, it is difficult to distinguish between integrin expression by melanocytes vs. neighbouring keratinocytes. Therefore, in vitro cultures derived from control as well as from vitiligo non-lesional skin were employed to investigate further potential differences in adhesive behaviour in vitiligo and control skin. In addition, the use of cultured cells provides the opportunity to perform functional adhesion assays. In this respect it is of great interest to note that cultured melanocytes from nonlesional vitiligo skin appear to retain disease-related characteristics. It has been demonstrated that vitiligo melanocytes have altered growth characteristics under limiting conditions. 5 Moreover, upon electron microscopic observation, dilated rough endoplasmic reticulum (RER) is apparent in diseased cells from human and mouse vitiligo subjects. 6,7 Therefore, the use of cultured cells to investigate differences in adhesive characteristics is justified.The level of expression of relevant i...

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Section: Discussionsupporting

confidence: 90%

Tenascin is overexpressed in vitiligo lesional skin and inhibits melanocyte adhesion

Poole

Wijngaard

Westerhof³

et al. 1997

British Journal of Dermatology

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“…Thus, signals were found in clustered epithelial cells at the migrating front and in the flattened cells of the epithelial sheets recovering the ulcerated surfaces, resulting in increased TN-C deposition most prominently under the sheets. A recent ISH study of skin wound healing demonstrated similar results in that TN-C mRNA was detected in the basal cells of sheets of migrating keratinocytes 2-4 days after wounding and in basally located keratinocytes of the neoepidermis after 7 days (Latijnhouwers et al 1997). It is well known that TN-C inhibits cell attachment to substrates, possibly by binding with fibronectin (Chiquet- Ehrismann et al 1988) but also due to intrinsic counteradhesive properties (Lightner and Erickson 1990;Prieto et al 1992).…”

Section: Discussionmentioning

confidence: 65%

“…In normal adult tissues, the expression is very restricted, but TN-C is re-expressed under various pathological conditions including malignancy development (Chiquet-Ehrismann et al 1986;Anbazhagan et al 1990;Hanamura et al 1997;Yoshida et al 1997), inflammation (Assad et al 1993;Tiitta et al 1994), fibrosis (Yamada et al 1992;Kaarteenaho-Wiik et al 1996), and wound healing (Mackie et al 1988;Murakami et al 1989;Latijnhouwers et al 1997). In such pathological states, as well as in embryogenesis, proliferation and migration of cells occur, followed by tissue remodeling.…”

Section: Introductionmentioning

confidence: 99%

“…Epithelial expression of TN-C has also been demonstrated in bronchi (Koch et al 1991) and mammary buds ) during embryogenesis. Keratinocytes also express TN-C mRNA in the early phase of wound healing (Latijnhouwers et al 1997). However, the functions and cellular targets of the TN-C secreted into the extracellular matrix by epithelial cells are not yet clear.…”

Section: Introductionmentioning

confidence: 99%

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Expression of tenascin-C and the integrin α9 subunit in regeneration of rat nasal mucosa after chemical injury: involvement in migration and proliferation of epithelial cells

Yoshimura

Majima

Sakakura

et al. 1999

Histochemistry and Cell Biology

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Nasal mucosa covered by pseudostratified ciliated epithelia can be injured by microbial infection and physical and chemical agents. To elucidate mechanisms of regeneration, erosion of rat nasal mucosa was produced by intranasal instillation of trichloroacetic acid, and tissue specimens were then sequentially obtained after 1-14 days. Since tenascin-C (TN-C) and its receptor, alpha 9 beta 1 integrin, are assumed to play important roles in regeneration of stratified squamous epithelia, their expression was evaluated by immunohistochemistry and in situ hybridization. Three to five days after the injury, TN-C mRNA was found in epithelial cells of migrating fronts and in epithelial sheets recovering ulcerated surfaces between the fronts and normal regions. TN-C deposition was increased under such sheets. Enhanced alpha 9 staining was also evident in the involved epithelium. 5-Bromo-2'-deoxyuridine incorporation assays revealed significant increase in proliferating cells in cell sheets over TN-C deposits at 3-7 days. Therefore, we conclude that regenerating epithelial cells produce and secrete TN-C, associated with an increase in alpha 9 expression, and that interactions between these molecules could regulate migration and proliferation of the epithelial cells in an autocrine manner.

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“…A recent ISH study on skin wound healing demonstrated TN-C mRNA in basal cells of the sheets of migrating keratinocytes 2-4 days after wounding, and in basally located keratinocytes of the neo-epidermis after 7 days [13]. It is considered that TN-C may facilitate keratinocyte migration by weakening the adhesion to fibronectin and other extracellular matrix proteins, allowing subsequent closing of the wound.…”

Section: Discussionmentioning

confidence: 99%

Involvement of tenascin-C in proliferation and migration of laryngeal carcinoma cells

Yoshida¹,

Yoshimura

H³

et al. 1999

Virchows Archiv

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Tenascin-C (TN-C) is an extracellular matrix glycoprotein upregulated in various pathological processes. In this study, we investigated its distribution in dysplasia and carcinoma of the human larynx using immunohistochemistry and in situ hybridization (ISH) techniques. In all cancer tissues, TN-C immunostaining was markedly increased in the stroma, especially around the cancer cell nests. In addition, cytoplasmic staining of cancer cells was also observed in 62.5% of the invasive cases, the cells being distributed in the periphery of the nests adjacent to the stroma. TN-C mRNA signals in cancer cells were detected in all six cases examined by ISH. Furthermore, in vitro evaluation of the roles of TN-C demonstrated an increase in the proliferating cell fraction in a dose-dependent manner. In a wound closure assay, the addition of TN-C promoted migration. We conclude that TN-C secreted by cancer cells may be involved in their proliferation and migration in an autocrine fashion.

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Human Epidermal Keratinocytes Are a Source of Tenascin-C during Wound Healing

Cited by 53 publications

References 65 publications

Tenascin is overexpressed in vitiligo lesional skin and inhibits melanocyte adhesion

Tenascin is overexpressed in vitiligo lesional skin and inhibits melanocyte adhesion

Expression of tenascin-C and the integrin α9 subunit in regeneration of rat nasal mucosa after chemical injury: involvement in migration and proliferation of epithelial cells

Involvement of tenascin-C in proliferation and migration of laryngeal carcinoma cells

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