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Kazuhiko Yoshida

Researcher at Hokkaido University

Publications -  13
Citations -  1241

Kazuhiko Yoshida is an academic researcher from Hokkaido University. The author has contributed to research in topics: Cornea & Neurotrophic factors. The author has an hindex of 12, co-authored 13 publications receiving 1196 citations. Previous affiliations of Kazuhiko Yoshida include University of California, San Diego.

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Microglia–Müller Glia Cell Interactions Control Neurotrophic Factor Production during Light-Induced Retinal Degeneration

TL;DR: It is demonstrated the possibility that functional glia–glia interactions constitute the key mechanism by which microglia-derived NGF, brain-derived neurotrophic factor (BDNF), and CNTF indirectly influence photoreceptor survival, although the receptors for these neurotrophic factors are absent from photoreceptors.
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IKKα controls formation of the epidermis independently of NF-κB

TL;DR: It is shown that the unique function of IKKα in control of keratinocyte differentiation is not exerted through its IκB kinase activity or through NF-κB, but instead, IKK α controls production of a soluble factor that induces keratinocytes differentiation.
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Somatic gene transfer of nerve growth factor promotes the survival of axotomized septal neurons and the regeneration of their axons in adult rats.

TL;DR: The data reveal that NGF-producing grafts sustain a significantly higher proportion of NGF receptor-immunoreactive septal neurons following axotomy and promote axon regeneration and cholinergic reinnervation of dentate granular neurons by these lesioned neurons.
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Potential role of glial cell line-derived neurotrophic factor receptors in Müller glial cells during light-induced retinal degeneration

TL;DR: Observations suggest that GDNF, NTN and their receptors are involved in the regulation of trophic factor production in retinal glial cells, and that functional glia-neuron network may utilize GDNF family for the protection of neural cells during retinal degeneration.
Journal Article

Amino-terminal phosphorylation of c-Jun regulates apoptosis in the retinal ganglion cells by optic nerve transection.

TL;DR: There is a partial but significant contribution of JNP to the induction of apoptosis in RGCs by ON transection, and Retrograde labeling showed that the number of the R GCs in the retinas on the injured side of the c-Jun(AA) mice was significantly higher than in wild-type mice 14 days after the lesion.