April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Investigation of protein kinase C alpha in corneal epithelial cells derived from a gelatinous drop-like corneal dystrophy patient
Author Affiliations & Notes
  • Koji Kitazawa
    Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Satoshi Kawasaki
    Kyoto Prefectural Univ of Med, Kyoto, Japan
    Ophthalmology, Osaka Univ, Osaka, Japan
  • Morio Ueno
    Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Hiroshi Tanaka
    Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Katsuhiko Shinomiya
    Kyoto Prefectural Univ of Med, Kyoto, Japan
    Ophthalmic Research Center, R&D Division, Santen Pharmaceutical Co., Ltd., Ikoma, Japan
  • Mina Nakatsukasa
    Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Shigeru Kinoshita
    Kyoto Prefectural Univ of Med, Kyoto, Japan
  • Footnotes
    Commercial Relationships Koji Kitazawa, None; Satoshi Kawasaki, None; Morio Ueno, None; Hiroshi Tanaka, None; Katsuhiko Shinomiya, None; Mina Nakatsukasa, None; Shigeru Kinoshita, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 5506. doi:https://doi.org/
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      Koji Kitazawa, Satoshi Kawasaki, Morio Ueno, Hiroshi Tanaka, Katsuhiko Shinomiya, Mina Nakatsukasa, Shigeru Kinoshita; Investigation of protein kinase C alpha in corneal epithelial cells derived from a gelatinous drop-like corneal dystrophy patient. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5506. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Gelatinous drop-like corneal dystrophy (GDLD) is a rare autosomal recessive disorder caused by biallelic loss-of-function mutations within the tumor-associated calcium signal transducer 2 (TACSTD2) gene, and is characterized by the reduction of tight junction-related proteins and a resultant loss of barrier function. Protein kinase C-alpha (PKC-alpha) is known to be involved in altering the function of tight-junctions. The purpose of this present study was to investigate the involvement of PKC-alpha in GDLD.

Methods: Immortalized corneal epithelial cells (CECs), which we previously established to have similar characteristics as in vivo GDLD CECs, were seeded on a culture well and then cultured in growth medium. After the cells had reached 100% confluence, the medium was switched to a differentiation medium and the cells were cultured for an additional 7 days. The expression levels of PKC-alpha mRNA , PKC-alpha protein, and tight junction-related proteins claudin (CLDN)-1 and CLDN7 were then examined using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis.

Results: The expression levels of CLDN1 and CLDN7 proteins in GDLD CECs was significantly lower compared to the normal CECs. The mRNA level of PKC-alpha in the GDLD cells was upregulated compared to the normal cells. In addition, the PKC-alpha protein was found to be highly expressed in the GDLD cells.

Conclusions: The findings of this study show that PKC-alpha may be involved in the tight- junction complex in GDLD.

Keywords: 480 cornea: basic science • 482 cornea: epithelium • 494 degenerations/dystrophies  
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