Role of protein kinase Cδ in dopaminergic neurotoxic events

Eun Joo Shin, Young Gwang Hwang, Naveen Sharma, Hai Quyen Tran, Duy Khanh Dang, Choon Gon Jang, Ji Hoon Jeong, Seung Yeol Nah, Toshitaka Nabeshima, Hyoung Chun Kim

Research output: Contribution to journalReview articlepeer-review

7 Citations (Scopus)

Abstract

The pro-apoptotic role of Protein kinase Cδ (PKCδ), a member of the novel PKC subfamily, has been well-documented in various pathological conditions. In the central nervous system, the possible role of PKCδ has been studied, mainly in the condition of dopaminergic loss. It has been suggested that the phosphorylation of PKCδ at tyrosine 311 residue (Tyr311) by redox-sensitive Src family kinases (SFKs) is critical for the caspase-3-mediated proteolytic cleavage, which produces the constitutively active cleaved form of PKCδ. Mitochondrial translocation of cleaved PKCδ has been suggested to facilitate mitochondria-derived apoptosis and oxidative burdens. Moreover, it has been suggested that PKCδ contribute to neuroinflammation through the transformation of microglia into the pro-inflammatory M1 phenotype and the assembly of membrane NADPH oxidase in dopaminergic impairments. Interestingly, mitochondrial respiratory chain inhibitors or neuroinflammogens have shown to induce PKCδ activation in dopaminergic systems. Thus, PKCδ activation may be one of the pivotal causes of neuropathologic events, and could amplify these processes further in a positive feedback manner. Furthermore, PKCδ may play an intermediary role in connecting each neuropathologic event. This review affords insight into the role of PKCδ in various dopaminergic neurotoxic models, which could provide a potential target for mitigating dopaminergic neurotoxicity.

Original languageEnglish
Pages (from-to)254-261
Number of pages8
JournalFood and Chemical Toxicology
Volume121
DOIs
Publication statusPublished - 01-11-2018

All Science Journal Classification (ASJC) codes

  • Food Science
  • Toxicology

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