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Masahide Kokado, Yuka Okada, Kazushi Ishikawa, Hiromitsu Shimada, Sakuhei Fujiwara, Masayasu Miyajima, Shizuya Saika; Knockdown Of Epiplakin In Sv40-immortalized Cultured Human Corneal Epithelial Cells Acceletrates Cell Migration Independently On P38 And C-jun N-terminal Kinase. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3573.
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© ARVO (1962-2015); The Authors (2016-present)
To examine the effect of Short-interfering RNA (siRNA)-Knockdown of epiplakin in SV40-immortalized cultured human corneal epithelial cells (HCECs) on cell migration and migration-related signaling cascades. Epiplakin is a novel component of the desmosome. We previously reported that the loss of epiplakin facilitates healing of a defect in corneal epithelium in mice (ARVO 2009).
Epiplakin siRNA transfection was performed to knockdown epiplakin in HCECs. Scratch-wound assay was employed to determine effects of epiplakin knockdown on HCEC migration. The level of transforming growth fcator β1 (TGFβ1)-dependent activation of p38 and c-Jun N-terminak kinase (JNK) and protein expression of keratin 6 were also examined in epiplakin-deficient HCECs.
siRNA transfection successfully knckdowned epiplakin protein expression in cultured HCECs. Epiplakin deficinecy accelerated migration of HCECs and also suppressed (1) After epiplakin siRNA transfection suppressed epiplakin protein expression. epiplakin knockdown by siRNA was accelerated the migration of HCEC and suppressed TGFb1 activation of p38 and JNK signals. Expression of keratin 6 was unaffected by epiplakin knockdown.
Epiplakin knockdown accelerates the migration of HCECs, but, on the other hand, suppresses TGFb1-dependent activation of cell migration-related signaling cascades, i. e., p38 and JNK. Migration-related keratin, i. e., keratin 6, expression was unaltered.
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