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김세환,문경준,오용석,박정하,신원호,정재영,최광식,진병관,Nikolai Kholodilov,Robert E Burke,김형준,하창만,이석근,김상룡 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
We recently reported that adeno-associated virus serotype 1 (AAV1) transduction of murine nigral dopaminergic (DA) neurons with constitutively active ras homolog enriched in brain with a mutation of serine to histidine at position 16 [Rheb(S16H)] induced the production of neurotrophic factors, resulting in neuroprotective effects on the nigrostriatal DA system in animal models of Parkinson’s disease (PD). To further investigate whether AAV1-Rheb(S16H) transduction has neuroprotective potential against neurotoxic inflammation, which is known to be a potential event related to PD pathogenesis, we examined the effects of Rheb(S16H) expression in nigral DA neurons under a neurotoxic inflammatory environment induced by the endogenous microglial activator prothrombin kringle-2 (pKr-2). Our observations showed that Rheb(S16H) transduction played a role in the neuroprotection of the nigrostriatal DA system against pKr-2-induced neurotoxic inflammation, even though there were similar levels of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1-beta (IL-1β), in the AAV1- Rheb(S16H)-treated substantia nigra (SN) compared to the SN treated with pKr-2 alone; the neuroprotective effects may be mediated by the activation of neurotrophic signaling pathways following Rheb(S16H) transduction of nigral DA neurons. We conclude that AAV1-Rheb(S16H) transduction of neuronal populations to activate the production of neurotrophic factors and intracellular neurotrophic signaling pathways may offer promise for protecting adult neurons from extracellular neurotoxic inflammation.
In Vivo AAV1 Transduction With hRheb(S16H) Protects Hippocampal Neurons by BDNF Production
Jeon, Min-Tae,Nam, Jin Han,Shin, Won-Ho,Leem, Eunju,Jeong, Kyoung Hoon,Jung, Un Ju,Bae, Young-Seuk,Jin, Young-Ho,Kholodilov, Nikolai,Burke, Robert E,Lee, Seok-Geun,Jin, Byung Kwan,Kim, Sang Ryong Elsevier Science B.V., Amsterdam 2015 MOLECULAR THERAPY Vol.23 No.3