Oligodendrocyte Dysfunction after Induction of Experimental Anterior Optic Nerve Ischemia

Abstract

After rAION induction oligodendrocytes, as well as RGCs, undergo progressive stress, with dysfunction and apoptosis. The findings lead to a proposal that progressive retrograde oligodendrocyte stress, away from the primary lesion, is an important factor after ischemic optic neuropathy. Postinduction demyelination must be addressed for effective neuroprotection of ischemic and hypoxic white matter.

Functional rescue of experimental ischemic optic neuropathy with αB-crystallin

“…Photochemical thrombosis animal models of AION have been instrumental in elucidating the events following ON head ischemia. [5][6][7][8][9] In experimental AION, there is early glial and axonal dysfunction, with ON oligodendrocyte apoptosis occurring by day 6 and progressive nerve demyelination within 2 weeks. 5,8,9 Retinal ganglion cell (RGC) loss peaks during weeks 2 and 3.…”

“…[5][6][7][8][9] In experimental AION, there is early glial and axonal dysfunction, with ON oligodendrocyte apoptosis occurring by day 6 and progressive nerve demyelination within 2 weeks. 5,8,9 Retinal ganglion cell (RGC) loss peaks during weeks 2 and 3. 7,8,10,11 During these 3 weeks of critical period for treatment considerations, there are important signs of self repair, such as the upregulation of retinal heat shock proteins HSP 70, 84, and 86.…”

“…5,8,9 Retinal ganglion cell (RGC) loss peaks during weeks 2 and 3. 7,8,10,11 During these 3 weeks of critical period for treatment considerations, there are important signs of self repair, such as the upregulation of retinal heat shock proteins HSP 70, 84, and 86. 5,8 Heat shock proteins act as molecular chaperones and are thought to have important roles in optic neuropathies, retinal diseases, and central nervous system inflammatory and neurodegenerative diseases.…”

“…7,8,10,11 During these 3 weeks of critical period for treatment considerations, there are important signs of self repair, such as the upregulation of retinal heat shock proteins HSP 70, 84, and 86. 5,8 Heat shock proteins act as molecular chaperones and are thought to have important roles in optic neuropathies, retinal diseases, and central nervous system inflammatory and neurodegenerative diseases. [12][13][14][15][16] In this study, we used a mouse model for AION via photochemical thrombosis [5][6][7][8]10,11,17 to examine the early changes following ON head ischemia.…”

“…5,8 Heat shock proteins act as molecular chaperones and are thought to have important roles in optic neuropathies, retinal diseases, and central nervous system inflammatory and neurodegenerative diseases. [12][13][14][15][16] In this study, we used a mouse model for AION via photochemical thrombosis [5][6][7][8]10,11,17 to examine the early changes following ON head ischemia. We then assessed the effectiveness of a small heat shock protein named aB-crystallin (aBC) in the treatment of experimental AION, using functional and histological approaches.…”