Midkine expression in transient retinal ischemia in the rat
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Updated: Oct 30, 2026
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
M Miyashiro1, K Kadomatsu, N Ogata
1Department of Ophthalmology, Kansai Medical University, Osaka, Japan.
Purpose:
Midkine (MK), a 13-kDa heparin-binding growth factor, is known to exert neurotrophic activities on various nerve cells including retinal cells. To initiate studies toward determining the physiological role of endogenous MK, we investigated the spatial and temporal expression profile of MK before and after intraocular pressure-induced retinal ischemia.
Methods:
Retinal ischemia was induced in Wistar strain rats by increasing the intraocular pressure to 110 mm Hg for 45 min via cannulation into the anterior chamber. The localization and abundance of the MK protein and mRNA were determined by the use of immunohistochemistry and in situ hybridization in the normal retina, as well as the retina after reperfusion. The protein expression profile was confirmed by Western blot analysis.
Results:
Immunohistochemical analysis showed that MK protein was expressed in the ganglion cell layer, the inner portion of the inner nuclear layer, and in the retinal pigment epithelium of the normal rat. MK expression transiently decreased 3 h to 2 days after reperfusion, and then dramatically increased to a level higher than normal after 7 to 28 days. The temporal expression profile of the MK protein was confirmed by Western blot analysis. In situ hybridization analysis gave results comparable to those obtained with immunohistochemistry.
Conclusions:
MK was expressed in the neural cells of the retina in the normal state, but became more abundant after pressure-induced retinal ischemia. Thus, endogenous MK responds to ischemic treatment by an initial decrease in expression and then a period of expression above basal levels.
Insights
Midkine (MK) protein is present in normal rat retinas. Following induced retinal ischemia, MK expression initially drops then significantly increases, suggesting a role in retinal response to injury.
Area of Science:
- Ophthalmology
- Neuroscience
- Molecular Biology
Background:
- Midkine (MK) is a heparin-binding growth factor with known neurotrophic effects on retinal cells.
- Understanding the role of endogenous MK in retinal physiology is crucial.
Purpose of the Study:
- To investigate the spatial and temporal expression of Midkine (MK) in the retina.
- To determine MK expression patterns before and after induced retinal ischemia.
Main Methods:
- Retinal ischemia was induced in Wistar rats by elevating intraocular pressure.
- MK protein and mRNA localization and abundance were assessed using immunohistochemistry and in situ hybridization.
- Western blot analysis confirmed protein expression levels.
Main Results:
- In normal rat retinas, MK protein was detected in the ganglion cell layer, inner nuclear layer, and retinal pigment epithelium.
- Following ischemia, MK expression transiently decreased within 3 hours to 2 days.
- MK levels dramatically increased above baseline between 7 and 28 days post-reperfusion.
Conclusions:
- Endogenous Midkine (MK) is expressed in neural retinal cells under normal conditions.
- MK expression is altered in response to pressure-induced retinal ischemia, with an initial decrease followed by a significant increase.
- These findings highlight MK's dynamic role in the retina's response to ischemic injury.
