Gap-junction proteins and communication in human epidermis

Salomon, Denis; Masgrau, E.; Vischer, S.; Saurat, Jean‐Hilaire; Chanson, Marc; Dc, Spray; Meda, Paolo

doi:10.1016/b978-0-444-89871-5.50037-7

Cited by 11 publications

(16 citation statements)

References 37 publications

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“…This pattern of gene expression is identical to that observed in normal skin. These results are in agreement with previous observations of connexin gene expression in normal rat and mouse skin [13,14,17,[23][24][25]271. However, in two recent studies, it was reported that in adult mouse skin, Cx26 transcript but not protein was expressed [16,26].…”

Section: Discussionsupporting

confidence: 95%

“…We do not understand the basis for this discrepancy, but perhaps the failure to detect Cx26 protein expression was due to masking of epitopes resulting from the fixation method used or to the differential sensitivity of the Cx26 antibodies used in these studies [26]. Also, in human skin, Cx26 was reported to be absent by two groups [25,28], but in a third report from one of these groups [29], expression was detected at low levels in the differentiated layers. Given the low expression levels initially reported by Salomon et al [25], perhaps the discrepancy is due to the dif- ferent detection sensitivities of Cx26 antibodies used in these various studies.…”

Section: Discussionmentioning

confidence: 83%

“…Also, in human skin, Cx26 was reported to be absent by two groups [25,28], but in a third report from one of these groups [29], expression was detected at low levels in the differentiated layers. Given the low expression levels initially reported by Salomon et al [25], perhaps the discrepancy is due to the dif- ferent detection sensitivities of Cx26 antibodies used in these various studies. Surprisingly, our in situ hybridization analysis showed that high levels of Cx26 expression in hyperplastic skin were associated with the accumulation of Cx26 transcripts in the cell nuclei.…”

Section: Discussionmentioning

confidence: 92%

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Perturbation in connexin 43 and connexin 26 gap-junction expression in mouse skin hyperplasia and neoplasia

et al. 1996

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To examine the possible role of gap junctions in mouse skin tumor progression, we generated a panel of mouse skin tissue samples exhibiting normal, hyperplastic, or neoplastic changes and characterized the expression of the gap-junction genes connexin 43 (Cx43) and connexin 26 (Cx26) by in situ hybridization and immunohistochemical analyses. In normal skin, these two gap junction genes were differentially expressed; Cx43 was found predominantly in the less differentiated lower spinous layers, whereas Cx26 was found in terminally differentiating upper spinous and granular layers. In hyperplastic epidermis exhibiting an expansion of the differentiated upper layer, i.e., epidermis with a thickened granular layer or in which the granular layer was replaced with keratinocytes exhibiting tricholemmal differentiation, expression of Cx43 and Cx26 remained segregated in the lower and upper spinous layers, respectively. However, in papillomas, Cx26 was localized in the lower but not upper spinous layer, an expression pattern identical to that of Cx43. In addition, the overall expression levels of both Cx43 and Cx26 appeared to be greatly elevated in the papillomas. It is interesting that such marked alteration in the pattern of Cx26 expression occurred within the context of hyperplastic changes histologically identical to those seen in the nonpapillomous hyperplasias. Interestingly, in neoplastic skin lesions containing a squamous cell carcinoma, Cx43 and Cx26 expression was extinguished. Moreover, expression of Cx43 was also significantly reduced in adjacent apparently nonneoplastic tissues. Overall, these observations show that perturbations in gap-junction gene expression are associated with skin hyperplasia and neoplasia. Such findings suggest a possible role for gap junctions in the malignant conversion of mouse epidermal cells.

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Section: Discussionsupporting

confidence: 95%

Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 92%

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Perturbation in connexin 43 and connexin 26 gap-junction expression in mouse skin hyperplasia and neoplasia

et al. 1996

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“…Human keratinocytes are connected by many gap junctions (Salomon et al 1988(Salomon et al ,1993Watt 1992;Wolff and Schreiner 1968). It is now established that these membrane domains allow direct cell-to-cell exchanges of multiple cytoplasmic constituents (Lowenstein and Rose 1992), but the role these exchanges may serve in skin remains uncertain.…”

Section: Discussionmentioning

confidence: 99%

“…Even though the role of gap junctions in keratinocyte function remains to be demonstrated, they have been proposed, by analogy to the roles contemplated in other systems (Lowenstein 1979;Lowenstein and Rose 1992), to be central to the regulation of keratinocyte growth and differentiation (Pitts and Finbow 1988;Watt 1992;Salomon et al 1993;Brissette et al 1994;Goliger and Paul 1995;Sawey et al 1996).…”

mentioning

confidence: 99%

In Vivo Modulation of Connexins 43 and 26 of Human Epidermis by Topical Retinoic Acid Treatment

Masgrau-Peya

Salomon

et al. 1997

J Histochem Cytochem.

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SUMMARY After 14 weeks of topical application of 0.1% all-trans -retinoic acid to the napes of volunteers, we observed a 2.5-fold increase in the thickness of epidermis, owing to an increase ( p Ͻ 0.001) in the number and size of keratinocytes and the induction of keratin 6. These changes in the differentiation of epidermal keratinocytes were paralleled by an increase in the amount of Cx43, a connexin that is normally expressed in human epidermis, and by the massive induction of Cx26, which is barely detectable in normal interfollicular epidermis, as judged at both the transcript (Northern blotting) and the protein level (immunolabeling). In contrast, retinoic acid treatment did not alter the morphology and connexin pattern of hair follicles or of sebaceous and sweat glands, and did not induce the expression of other connexins (C32, Cx37, Cx40) in either skin adnexae or epidermis. These observations suggest that the expression of two distinct connexins by interfollicular keratinocytes is related to selective changes in the differentiation program of epidermis that are induced by retinoic acid.

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Connexin expression in epidermal cell lines from SENCAR mouse skin tumors

et al. 1996

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Alteration of gap-junctional intercellular communication (GJIC) has long been proposed to be involved in carcinogenesis. Previously, we reported that the level of gap junctional intercellular communication in mouse skin carcinoma cell lines is significantly lower than in papilloma cell lines and normal mouse keratinocytes Klann et al., Cancer Res 49:699-705, 1989). Here, we present data on expression of the gap-junctional protein connexins (Cx) 26, Cx31.1, and Cx43 in a comprehensive panel of keratinocyte cell lines representing different stages of mouse skin carcinogenesis and the effect of different conditions of propagation on Cx phenotype. Northern and western blot analyses and immunostaining showed that all cell lines studied in vitro expressed Cx43 but most did not express Cx31.1 or Cx26. The abundance of Cx43 expression on plasma membranes correlated well with the level of GJIC. In vivo expression of Cx43 and Cx26 was strongly increased. Whereas none of tumorigenic cell lines expressed Cx26 gap junctions in culture, those growing as tumors in nude mice began to express Cx26 protein. The comparison of Cx expression on the keratinocyte membranes in three different groups of tumors (papillomas and squamous cell and spindle cell carcinomas) clearly revealed that the abundance of Cx43 and Cx26 expression directly correlated with the level of tumor differentiation. All studied tumors were Cx31.1 negative. These results suggest that both Cx expression and gap-junction permeability are gradually reduced during the tumor progression stage of mouse skin carcinogenesis.

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Gap-junction proteins and communication in human epidermis

Cited by 11 publications

References 37 publications

Perturbation in connexin 43 and connexin 26 gap-junction expression in mouse skin hyperplasia and neoplasia

Perturbation in connexin 43 and connexin 26 gap-junction expression in mouse skin hyperplasia and neoplasia

In Vivo Modulation of Connexins 43 and 26 of Human Epidermis by Topical Retinoic Acid Treatment

Connexin expression in epidermal cell lines from SENCAR mouse skin tumors

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