Mammalian STE20-like kinase 2, not kinase 1, mediates photoreceptor cell death during retinal detachment View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-05-29

AUTHORS

H Matsumoto, Y Murakami, K Kataoka, H Lin, K M Connor, J W Miller, D Zhou, J Avruch, D G Vavvas

ABSTRACT

Photoreceptor cell death is the definitive cause of vision loss in retinal detachment (RD). Mammalian STE20-like kinase (MST) is a master regulator of both cell death and proliferation and a critical factor in development and tumorigenesis. However, to date the role of MST in neurodegeneration has not been fully explored. Utilizing MST1−/− and MST2−/− mice we identified MST2, but not MST1, as a regulator of photoreceptor cell death in a mouse model of RD. MST2−/− mice demonstrated significantly decreased photoreceptor cell death and outer nuclear layer (ONL) thinning after RD. Additionally, caspase-3 activation was attenuated in MST2−/− mice compared to control mice after RD. The transcription of p53 upregulated modulator of apoptosis (PUMA) and Fas was also reduced in MST2−/− mice post-RD. Retinas of MST2−/− mice displayed suppressed nuclear relocalization of phosphorylated YAP after RD. Consistent with the reduction of photoreceptor cell death, MST2−/− mice showed decreased levels of proinflammatory cytokines such as monocyte chemoattractant protein 1 and interleukin 6 as well as attenuated inflammatory CD11b cell infiltration during the early phase of RD. These results identify MST2, not MST1, as a critical regulator of caspase-mediated photoreceptor cell death in the detached retina and indicate its potential as a future neuroprotection target. More... »

PAGES

e1269-e1269

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cddis.2014.218

DOI

http://dx.doi.org/10.1038/cddis.2014.218

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1048047684

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24874741


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