Abstract
Aquaporins (AQPs)are integral membrane proteins transporting water or neutral partials in cells. AQPs have been demonstrated that facilitate epidermal cells migration and proliferation during the process of wound healing.AQPs generate wound healing via polarization and osmolarity change to regulate the distribution and remodeling of actin. This study was to observe the cell migration and adhesion regulated by AQP3 and actin, and to investigate how AQP3 conferred on the phenomenon of polarization for actin location and cell remolding in wound healing in order to establish the model of cell migration through AQP3 and actin. The result of traditional wound healing assay showed that AQP3 was inhibited by nickel chloride (NiCl2)resulting in impaired cell migration and wound healing. The polymerization of AQP3 and actin were inhibited in accompanied with no lamellipodium generation. It indicated that the polymerization of AQP3 and actin mediated lamellipodium generation to facilitate cell migration during wound healing. The immunofluorescence assay explored that AQP3 generally distributed around nuclei, and actin monomers colocalized with AQP3 distribution to polymerize radically along lamellipodium. Moreover, AQP3 deficiency interfered with polarization of AQP3, and caused the location of polymerized actin parallel and undirected. The assay of electric cell-substrate impedance sensing (ECIS) detected AQP3 mediated cell lamellipodium generation to affect cell migration and distribution resulting in impaired cell migration. Otherwise,the impedance change (± 50 ohm) was detectable in the forward and backward movement during cell migration, and the impedance was significantly decreased when AQP3 was repressed. It suggested that AQP3 mediated cell morphology for cell migration, extension and adhesion. Regarding the findings of this study, it speculated and established a model of cell migration during wound healing. In the process of cell migration for wound healing, AQP3 induced cells to form lamellipodium and attract actin monomers to the location of AQP3 distribution, and lamellipodium further extended and actin filaments were formed from actin monomers to maintain the shape of lamellipodium. The ECIS assay can detect in real time that AQP3 regulated cell migration for wound healing.