M
Michael T. Matthes
Researcher at University of California, San Francisco
Publications - 56
Citations - 6828
Michael T. Matthes is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Retinal degeneration & Retinal. The author has an hindex of 32, co-authored 56 publications receiving 6475 citations. Previous affiliations of Michael T. Matthes include Stanford University.
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Journal ArticleDOI
Mutation of the receptor tyrosine kinase gene Mertk in the retinal dystrophic RCS rat
Patricia M. D’Cruz,Douglas Yasumura,Jessica Weir,Michael T. Matthes,Hadi Abderrahim,Matthew M. LaVail,Douglas Vollrath +6 more
TL;DR: The results provide genetic evidence for an essential role of a receptor tyrosine kinase in a specialized form of phagocytosis and suggest a molecular model for ingestion of outer segments by RPE cells.
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Photoreceptor degeneration in inherited retinal dystrophy delayed by basic fibroblast growth factor
TL;DR: It is reported that subretinal injection of bFGF results in extensive rescue of photoreceptors in RCS rats for at least two months after the injection, and that intravitreal injection of the factor results in even more widespread rescue, across almost the entire retina.
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Multiple growth factors, cytokines, and neurotrophins rescue photoreceptors from the damaging effects of constant light.
Matthew M. LaVail,Kazuhiko Unoki,Douglas Yasumura,Michael T. Matthes,George D. Yancopoulos,Roy H. Steinberg +5 more
TL;DR: It is reported here that photoreceptors can be significantly protected from the damaging effects of light by intravitreal injection of eight different growth factors, cytokines, and neurotrophins that typically act through several distinct receptor families.
Journal Article
Protection of mouse photoreceptors by survival factors in retinal degenerations.
Matthew M. LaVail,Douglas Yasumura,Michael T. Matthes,Cathy Lau-Villacorta,Kazuhiko Unoki,Ching-Hwa Sung,Roy H. Steinberg +6 more
TL;DR: The slowing of degeneration in the rd/rd and Q344ter mutant mice demonstrated that intraocularly injected survival factors can protect photoreceptors from degenerating in animal models with the same or similar genetic defects as those in human inherited retinal degenerations.
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Basic fibroblast growth factor and local injury protect photoreceptors from light damage in the rat.
TL;DR: The findings indicate that the photoreceptor rescue activity of bFGF is not restricted to inherited retinal dystrophy in the rat, and that light damage is an excellent model for studying the cellular site(s), kinetics, and molecular mechanisms of both the normal function ofbFGF and its survival- promoting activity.