Alterations in protein expression and membrane properties during Müller cell gliosis in a murine model of transient retinal ischemia.
Retinal Müller glial cells are involved in K+ ion homeostasis of the tissue. Inwardly rectifying K(+) (Kir) channels play a decisive role in the process of spatial K+ buffering. It has been demonstrated that Kir-mediated currents of Müller cells are downregulated in various cases of retinal neurodegeneration. However, this has not yet been verified for any murine animal model. The aim of the present study was to investigate Müller cells after transient retinal ischemia in mice. High intraocular pressure was applied for 1h; the retina was analysed 1 week later. We studied protein expression in the tissue by immunohistochemistry, and membrane currents of isolated cells by patch-clamp experiments. We found the typical indicators of reactive gliosis such as upregulation of glial fibrillary acidic protein. Moreover, the membrane capacitance of isolated Müller cells was increased and the amplitudes of Kir-mediated currents were slightly, but significantly decreased. This murine high intraocular pressure model of transient retinal ischemia is proposed as a versatile tool for further studies on Müller cell functions in retinal degeneration.
Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig, Jahnallee 59, D-04109 Leipzig, Germany.
Petra G
PG
Hirrlinger
Elke
E
Ulbricht
Ianors
I
Iandiev
Andreas
A
Reichenbach
Thomas
T
Pannicke
D000818:Animals; D051401:Aquaporin 4 / Q000096:biosynthesis; D002352:Carrier Proteins / Q000096:biosynthesis; D004195:Disease Models, Animal; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D005911:Gliosis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D005974:Glutamate-Ammonia Ligase / Q000096:biosynthesis; D007150:Immunohistochemistry; D007429:Intraocular Pressure; D007511:Ischemia / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008564:Membrane Potentials; D051379:Mice; D008810:Mice, Inbred C57BL; D009457:Neuroglia / Q000473:pathology* / Q000502:physiology*; D018408:Patch-Clamp Techniques; D024661:Potassium Channels, Inwardly Rectifying / Q000096:biosynthesis; D012160:Retina / Q000378:metabolism* / Q000473:pathology*; D012171:Retinal Vessels / Q000503:physiopathology; D014746:Vimentin / Q000096:biosynthesis; D000098854:Kcnj10 Channel
C020932:11-cis-retinal-binding protein; C496031:Aqp4 protein, mouse; D051401:Aquaporin 4; D002352:Carrier Proteins; D005904:Glial Fibrillary Acidic Protein; D000098854:Kcnj10 Channel; D024661:Potassium Channels, Inwardly Rectifying; D014746:Vimentin; D005974:Glutamate-Ammonia Ligase