EGFR-mediated expression of aquaporin-3 is involved in human skin fibroblast migration.

@article{citeulike:1809589, abstract = {AQP3 (aquaporin-3), known as an integral membrane channel in epidermal keratinocytes, facilitates water and glycerol movement into and out of the skin. Here, we demonstrate that AQP3 is also expressed in cultured human skin fibroblasts, which under normal wound healing processes migrate from surrounding tissues to close the wound. EGF (epidermal growth factor), which induced fibroblast migration, also induced AQP3 expression in a time- and dose-dependent manner. CuSO4 and NiCl2, previously known as AQP3 water transport inhibitors, as well as two other bivalent heavy metals Mn2+ and Co2+, inhibited EGF-induced cell migration in human skin fibroblasts. AQP3 knockdown by small interfering RNA inhibited EGF-induced AQP3 expression and cell migration. Furthermore, an EGFR (EGF receptor) kinase inhibitor, PD153035, blocked EGF-induced AQP3 expression and cell migration. MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase]/ERK inhibitor U0126 and PI3K (phosphoinositide 3-kinase) inhibitor LY294002 also inhibited EGF-induced AQP3 expression and cell migration. Collectively, our findings show for the first time that AQP3 is expressed in human skin fibroblasts and that EGF induces AQP3 expression via EGFR, PI3K and ERK signal transduction pathways. We have provided evidence for a novel role of AQP3 in human skin fibroblast cell migration, which occurs during normal wound healing.}, address = {Department of Biology, Providence College, 549 River Ave., Providence, RI 02918, USA.}, author = {Cao, C. and Sun, Y. and Healey, S. and Bi, Z. and Hu, G. and Wan, S. and Kouttab, N. and Chu, W. and Wan, Y. }, citeulike-article-id = {1809589}, doi = {10.1042/BJ20060816}, issn = {1470-8728}, journal = {Biochem J}, month = {December}, number = {2}, pages = {225--234}, posted-at = {2007-10-23 09:07:43}, priority = {2}, title = {EGFR-mediated expression of aquaporin-3 is involved in human skin fibroblast migration.}, url = {http://dx.doi.org/10.1042/BJ20060816}, volume = {400}, year = {2006} }

TY - JOUR ID - citeulike:1809589 L3 - citeulike-article-id:1809589 TI - EGFR-mediated expression of aquaporin-3 is involved in human skin fibroblast migration. JF - Biochem J VL - 400 IS - 2 SP - 225 EP - 234 AD - Department of Biology, Providence College, 549 River Ave., Providence, RI 02918, USA. SN - 1470-8728 N2 - AQP3 (aquaporin-3), known as an integral membrane channel in epidermal keratinocytes, facilitates water and glycerol movement into and out of the skin. Here, we demonstrate that AQP3 is also expressed in cultured human skin fibroblasts, which under normal wound healing processes migrate from surrounding tissues to close the wound. EGF (epidermal growth factor), which induced fibroblast migration, also induced AQP3 expression in a time- and dose-dependent manner. CuSO4 and NiCl2, previously known as AQP3 water transport inhibitors, as well as two other bivalent heavy metals Mn2+ and Co2+, inhibited EGF-induced cell migration in human skin fibroblasts. AQP3 knockdown by small interfering RNA inhibited EGF-induced AQP3 expression and cell migration. Furthermore, an EGFR (EGF receptor) kinase inhibitor, PD153035, blocked EGF-induced AQP3 expression and cell migration. MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase]/ERK inhibitor U0126 and PI3K (phosphoinositide 3-kinase) inhibitor LY294002 also inhibited EGF-induced AQP3 expression and cell migration. Collectively, our findings show for the first time that AQP3 is expressed in human skin fibroblasts and that EGF induces AQP3 expression via EGFR, PI3K and ERK signal transduction pathways. We have provided evidence for a novel role of AQP3 in human skin fibroblast cell migration, which occurs during normal wound healing. AU - Cao, C AU - Sun, Y AU - Healey, S AU - Bi, Z AU - Hu, G AU - Wan, S AU - Kouttab, N AU - Chu, W AU - Wan, Y PY - 2006/12/01/ UR - http://dx.doi.org/10.1042/BJ20060816 ER -