December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Expression of Matrix Metalloproteinases (MMPs) and Their Natural Tissue Inhibitors (TIMPs) Following Retinal Ischemia-Reperfusion in Rats
Author Affiliations & Notes
  • N Mathalone
    Ophthalmology
    Carmel Medical Center Haifa Israel
  • MA Rahat
    Serology Laboratory
    Carmel Medical Center Haifa Israel
  • N Lahat
    Serology Laboratory
    Carmel Medical Center Haifa Israel
  • O Geyer
    Ophthalmology
    Carmel Medical Center Haifa Israel
  • Footnotes
    Commercial Relationships   N. Mathalone, None; M.A. Rahat, None; N. Lahat, None; O. Geyer, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 4093. doi:
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      N Mathalone, MA Rahat, N Lahat, O Geyer; Expression of Matrix Metalloproteinases (MMPs) and Their Natural Tissue Inhibitors (TIMPs) Following Retinal Ischemia-Reperfusion in Rats . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4093.

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

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Abstract

Abstract: : Purpose: Microvascular integrity is lost during retinal ischemia. The degradation of the basal lamina and extracellular matrix are, in part, responsible for the loss of vascular integrity. Matrix metalloproteinases (MMPs) and the natural tissue inhibitors of metalloproteinases (TIMPs) play a role in basal lamina degradation and the resulting tissue damage. Our present study evaluated the changes in the expression of MMP-2, MMP-9, TIMP-1 and TIMP-2 following retinal ischemia-reperfusion injury. Methods: Retinal ischemia was achieved by installation of sterile saline into the anterior chamber of the rat study eye at a pressure of 140 cm H2O for 90 minutes. The counter eye served as a non-ischemic control. Gelatin zymography was conducted to measure MMP-2 and MMP-9 levels in the ischemic retinal tissue, zero to 120 hours after ischemia. TIMP-1 and TIMP-2 levels were studied by means of western blot analysis following the same periods of reperfusion. Results: MMPs expression was low during ischemia and significantly increased (P<0.05) on reperfusion. Maximum levels of MMP-9 were recorded at 24 hours of reperfusion (7-fold of control), persisting at reduced levels for 5 days. Levels of MMP-2 peaked at 48 hours of reperfusion (2.6-fold of control), then decreased but remained above normal levels for 5 days. We noted no significant difference in TIMP-1 and TIMP-2 expression following ischemia-reperfusion compared to normal controls. Conclusion: Our results suggest that MMPs may play a role in retinal ischemia-reperfusion injury.

Keywords: 448 ischemia • 316 animal model • 614 vascular cells 
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