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Am J Physiol Cell Physiol 284: C51-C59, 2003. First published September 4, 2002; doi:10.1152/ajpcell.00205.2002
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Vol. 284, Issue 1, C51-C59, January 2003

Ultraviolet A radiation transiently disrupts gap junctional communication in human keratinocytes

Nicolas Provost1, Marielle Moreau1,3, Armelle Leturque2, and Carine Nizard1,3

1 Laboratoire de Pharmacologie Cellulaire, Ecole Pratique des Hautes Etudes-Institut National de la Santé et de la Recherche Médicale U505, Université Pierre et Marie Curie; 2 Institut National de la Santé et de la Recherche Médicale U505, Université Pierre et Marie Curie, 75006 Paris; and 3 LVMH, Research and Development Laboratory, Perfumes and Cosmetics Division, 45804 Saint Jean de Braye-Cedex, France

Ultraviolet A (UVA) (320-400 nm) radiation is known to cause cutaneous aging and skin cancer. We studied the effect of UVA (365 nm) radiation on the human epidermis by focusing on keratinocyte gap junction-mediated intercellular communication (GJIC). We observed a dose-dependent 10-fold decrease in GJIC induced by UVA in normal human keratinocytes. This decrease in GJIC was associated with time-dependent internalization of connexin43 (Cx43). UVA radiation also damaged the actin cytoskeleton, as shown by microfilament disappearance. Importantly, the decrease in GJIC was transient when keratinocytes were irradiated with 10 J/cm2 UVA, with a return to baseline values after 8 h. Concomitantly, Cx43 was relocalized and the actin cytoskeleton was restored. UVA irradiation and 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment activated protein kinase C and reduced GJIC. However, Cx43 localization and phosphorylation were differently regulated by the two treatments. This suggests that at least two different pathways may mediate the observed fall in GJIC. These findings identify keratinocyte GJIC as a new UVA target that might sensitize human skin to photoaging and cancer formation.

GJIC; connexin43; skin physiology; actin cytoskeleton; photoaging


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