期刊
AGING CELL
卷 21, 期 4, 页码 -出版社
WILEY
DOI: 10.1111/acel.13597
关键词
ageing; degeneration; Muller glia; proliferation; regeneration; retina; telomerase; Zebrafish
资金
- National Institutes of Health [NEI R01EY026551, R21EY031526]
- Wellcome Trust [210152/Z/18/Z, UNS35121]
- University of Sheffield
- Royal Society [UNS35121]
- Biotechnology and Biological Sciences Research Council [BB/S010386/1]
- Wellcome Trust [210152/Z/18/Z] Funding Source: Wellcome Trust
Ageing affects the regenerative capacity of Müller glia cells in the retina, but is insufficient to stimulate neurodegeneration. Müller glia cells undergo morphological aberrations and loss of vision with ageing.
Ageing is a significant risk factor for degeneration of the retina. Muller glia cells (MG) are key for neuronal regeneration, so harnessing the regenerative capacity of MG in the retina offers great promise for the treatment of age-associated blinding conditions. Yet, the impact of ageing on MG regenerative capacity is unclear. Here, we show that the zebrafish retina undergoes telomerase-independent, age-related neurodegeneration but that this is insufficient to stimulate MG proliferation and regeneration. Instead, age-related neurodegeneration is accompanied by MG morphological aberrations and loss of vision. Mechanistically, yes-associated protein (Yap), part of the Hippo signalling, has been shown to be critical for the regenerative response in the damaged retina, and we show that Yap expression levels decline with ageing. Despite this, morphologically and molecularly altered aged MG retain the capacity to regenerate neurons after acute light damage, therefore, highlighting key differences in the MG response to high-intensity acute damage versus chronic neuronal loss in the zebrafish retina.
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