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Naoyuki Morishige, Shizuka Murata, Haruya Azumi, Ryutaro Shin-gyou-uchi, Yukiko Morita, Kazuhiro Kimura, Koh-hei Sonoda; Coordinated Regulation of Palladin and α-Smooth Muscle Actin by Transforming Growth Factor-β in Human Corneal Fibroblast. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1937.
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To investigate the role of palladin, actin assembly-related protein, in the cornea, we examined expression of palladin in normal, diseased, or injured corneal tissue as well as in cultured corneal fibroblasts.
Expression of palladin and α-smooth muscle actin (α-SMA) in the rat cornea with an incision wound, in the human cornea (normal, bullous keratopathy, or keratoconus), and in cultured human corneal fibroblasts was examined by immunofluorescence or immunoblot analysis.
The expression of both palladin and α-SMA was detected at the lesion site during wound healing in the rat cornea. Whereas neither palladin nor α-SMA was detected in the normal human cornea or a cornea affected by bullous keratopathy, both proteins were detected in association with scarring in a keratoconic cornea. The expression of both palladin and α-SMA in cultured human corneal fibroblasts was increased by transforming growth factor-β (TGF-β) in a manner sensitive to inhibition by blockers of mitogen-activated protein kinase (MAPK) signaling. Finally, RNA interference-mediated depletion of palladin attenuated the TGF-β-induced up-regulation of α-SMA expression in human corneal fibroblasts.
Palladin was expressed in the rat and human cornea in association with scar formation. The expression of palladin in human corneal fibroblasts was increased by TGF-β in a manner dependent on MAPK signaling and was required for the TGF-β-induced up-regulation of α-SMA. Our data thus implicate palladin in scar formation in the corneal stroma and suggest that it contributes to the up-regulation of α-SMA by TGF-β in corneal fibroblasts.
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