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- 저자 : KimPak, (검색결과 4 건)
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Park, Wook-Ha,KimPak, Young-Mi Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.10
Cholesterol $7{\alpha}$-hydroxylase (CYP7A1) regulates the balance between cholesterol supply and metabolism by catalyzing the rate-limiting step of bile acid biosynthesis. The transcriptional activity of CYP7A1 is tightly controlled by various nuclear receptors. A forkhead transcription factor O1 (FOXO1) plays a critical role in metabolism, and insulin inactivates FOXO1 through Akt-dependent phosphorylation and nuclear exclusion. We investigated the role of insulin- Akt-FOXO1 signaling pathway in CYP7A1 transcriptional regulation since we found putative insulin-response elements, FOXO1 binding sequences, in both rat and human CYP7A1 promoters. However, ectopic expression of FOXO1 increased the rat CYP7A1-, but mildly reduced human CYP7A1-promoter activities in a dose-dependent manner. Similarly to bile acids, insulin treatment increased small heterodimer partner (SHP) mRNA rapidly and transiently, leading to the suppression of CYP7A1 transcription in both human and rodents. Chromatin immunoprecipitation showed that FOXO1 directly bound to rat CYP1A1 promoter in the absence of insulin. FOXO1 binding to the rat promoter was diminished by insulin treatment as well as by expression of SHP. Our results suggest that the stimulation of insulin- signaling pathway of Akt-FOXO1 and SHP expression may regulate cholesterol/bile acid metabolisms in liver, linking carbohydrate and cholesterol metabolic pathways. A prolonged exposure of insulin in hyperinsulinemic insulin resistance or diabetic status represses CYP7A1 transcription and bile acid biosynthesis through SHP induction and FOXO1 inactivation, leading to impairment of the hepatic cholesterol/bile acid metabolisms.
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Choi, Joon-Sig,Choi, Min-Ji,Go, Gyeong-Su,Rhee, Byoung-Doo,KimPak, Young-Mi,Bang, In-Seok,Lee, Min-Hyung Korean Chemical Society 2006 Bulletin of the Korean Chemical Society Vol.27 No.9
It has been found that a number of diseases are associated with mutations in the mitochondrial DNA. Therapeutic gene delivery to mitochondria has been suggested as a clinical option for these diseases. In this study, we developed a gene carrier to mitochondria by the conjugation of mitochondrial leader peptide (LP) to polyethylenimine (PEI). Mitochondrial LP conjugated PEI (PEI-LP) was synthesized with low molecular weight PEI (2,000 Da, PEI2K). Gel retardation assay showed that PEI2K-LP formed complexes at a 1.0/1 weight ratio. In addition, PEI2K-LP protected DNA from the enzymatic degradation for at least 60 min, while naked DNA was completely degraded within 20 min. PEI2K-LP was compared with LP conjugated high molecular weight PEI (25,000 Da, PEI25K) in terms of toxicity and delivery efficiency. MTT assay showed that PEI2K-LP had much lower cytotoxicity than PEI25K-LP to 293 cells. In addition, cell-free DNA delivery assay showed that PEI2K-LP delivered more DNA to mitochondria at a 1.8/1 weight ratio than naked DNA or PEI. This result suggests that PEI2K-LP may be useful for the development of mitochondrial gene therapy system with lower cytotoxicity.
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Kim, Ji-Eun,Ji, Eun-Sang,Seo, Jin-Hee,Lee, Moon-Hyoung,Cho, Se-Hyung,KimPak, Young-Mi,Seo, Tae-Beom,Kim, Chang-Ju The Korean Society for Integrative Biology 2012 Animal cells and systems Vol.16 No.3
Depression is one of the most prevalent diseases of alcohol abuse. Brain-derived neurotrophic factor (BDNF) plays a critical role in cell survival in the hippocampus. Phosphorylation of extracellular signal-regulated kinase 1/2 (p-ERK1/2) is induced by BDNF, and it regulates cell proliferation and differentiation in the brain. We investigated the effects of alcohol intake on depression-like behavior, cell proliferation, expressions of BDNF and its downstream molecules in the hippocampus using Mongolian gerbils. The gerbils were divided into four groups: control group, 0.5 g/kg alcohol-treated group, 1 g/kg alcohol-treated group, 2 g/kg alcohol-treated group. Each dose of alcohol was orally administered for 3 weeks. The present results demonstrated that alcohol intake induced depression-like behavior. Both 5-hydroxytryptamine synthesis and its synthesizing enzyme tryptophan hydroxylase expression in the dorsal raphe and cell proliferation in the hippocampal dentate gyrus were decreased by alcohol intake. Alcohol intake suppressed BDNF expression, and resulted in the decrease of its downstream molecules, pERK1/2 and Bcl-2, in the hippocampus. We showed that alcohol intake may lead to a depressed-like state with reduced hippocampal cell proliferation through inhibition of the BDNF-ERK signaling pathway.
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Hypothermia alleviates hypoxic ischemia-induced dopamine dysfunction and memory impairment in rats
Ko, Il-Gyu,Cho, Han-Jin,Kim, Sung-Eun,Kim, Ji-Eun,Sung, Yun-Hee,Kim, Bo-Kyun,Shin, Mal-Soon,Cho, Seh-Yung,KimPak, Young-Mi,Kim, Chang-Ju The Korean Society for Integrative Biology 2011 Animal cells and systems Vol.15 No.4
Hypoxic ischemia injury is a common cause of functional brain damage, resulting from a decrease in cerebral blood flow and oxygen supply to the brain. The main problems associated with hypoxic ischemia to the brain are memory impairment and dopamine dysfunction. Hypothermia has been suggested to ameliorate the neurological impairment induced by various brain insults. In this study, we investigated the effects of hypothermia on memory function and dopamine synthesis following hypoxic ischemia to the brain in rats. For this purpose, a step-down avoidance task, a radial eight-arm maze task, and immunohistochemistry for tyrosine hydroxylase (TH) and 5-bromo-2'-deoxyuridine (BrdU) were performed. The present results indicated that the hypoxic ischemia-induced disturbance of the animal's performances and spatial working memory was associated with a decrement in TH expression in the substantia nigra and striatum, and an increase in cell proliferation in the hippocampal dentate gyrus. Hypothermia treatment improved the animals' performance and spatial working memory by suppressing the decrement in TH expression in the substantia nigra and striatum and the increase in cell proliferation in the dentate gyrus. We suggest that hypothermia can be an efficient therapeutic modality to facilitate recovery following hypoxic ischemia injury to the brain, presumably by modulating the dopaminergic cell loss.
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