May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Immunohistochemical Observation of Diacylglycerol Kinase(DGK) in Normal and the Early Stage of Diabetic Rat
Author Affiliations & Notes
  • S. Sato
    Ophthalmology, Yamagata University, Yamagata, Japan
  • Y. Katagiri
    Anatomy & Cell Biology, Yamagata University, Yamagata, Japan
  • K. Goto
    Anatomy & Cell Biology, Yamagata University, Yamagata, Japan
  • M. Igarashi
    Laboratory Medicine, Yamagata University, Yamagata, Japan
  • H. Yamashita
    Laboratory Medicine, Yamagata University, Yamagata, Japan
  • Footnotes
    Commercial Relationships  S. Sato, None; Y. Katagiri, None; K. Goto, None; M. Igarashi, None; H. Yamashita, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 3073. doi:
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      S. Sato, Y. Katagiri, K. Goto, M. Igarashi, H. Yamashita; Immunohistochemical Observation of Diacylglycerol Kinase(DGK) in Normal and the Early Stage of Diabetic Rat . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3073.

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

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Abstract

Abstract: : Purpose: Diacylglycerol (DG) activates protein kinase C (PKC) which is involved in the signal transduction from various growth factors. Diacylglycerol kinase (DGK) phosphorylates DG to degrade into phosphatidic acid (PA), so is one of the key enzymes in the intracytoplasmic signal transduction by regulating DG level and inositol-phospholipid turnover. At present 6 isozymes of DGK (α,ß,γ,ι,ζ,ε) have been cloned in rat. Recent studies have identified that the activation of PKC and increased DG levels initiated by hyperglycemia are associated with various vascular pathological states in retina, including early stage pathophysiology of diabetic retinopathy (DMR). We observed the protein expression patterns of DGKα, PKCßIIand cytokines which are related with DMR in both normal and early stage of diabetic rat. Methods:Retina in Streptozotocin induced rats (STZ) and Spontaneously Diabetic Torii (SDT) rats (supplied by the courtesy of Torii Pharmaceutical Co., Ltd., Tokyo, Japan) were observed. SD rats were used as normal control. The expression at the protein level of DGKα and PKCßII in retina was observed immunohistochemically. We also observed the expression of cytokines (VEGF, IL-6, angiotensin II and TGFß1& 2, PEDF). Results:The expression increase of the examined cytokines was detected in the retina of the early stage of diabetes. DGKα was detected mainly in the inner plexiform layer (IPL) and the outer plexiform layer (OPL) of the normal rat retina. We could not detect the changes of DGKα localization in either STZ or SDT rat retina in comparison with the normal control. PKCßII was detected in the IPL, the OPL and the photoreceptor inner segments (IS) of the normal retina, and did not change in the early stage of diabetes. Conclusions:The localization changes of DGKα and PKCßII was not detected in early stage of diabetes by immunohistochemical methods. It is possible that DGKα and PKCßII play certain roles in the primary and baseline sites in early stage of DMR.

Keywords: diabetic retinopathy • immunohistochemistry • pathology: experimental 
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