• 제목/요약/키워드: Neuronal Differentiation

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해양심층수에 의한 해마신경세포 가지돌기 수의 증가 (Deep Seawater Increases Dendritic Branches of Cultured Rat Hippocampal Neurons)

  • 이현숙;남경수;손윤희;문일수
    • 생명과학회지
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    • 제18권6호
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    • pp.897-901
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    • 2008
  • 해양심층수(deep seawater, DSW)는 청정성과 무기물질의 풍부함 때문에 여러 분야에 응용하기 위하여 최근 많은 관심을 받고있다. 본 연구에서는 동해 양양 부근의 해저 1,100 m에서 취수하여 역삼투압 시스템으로 탈염과 농축을 한 심층수가 배양한 흰쥐해마신경세포의 형태적 분화에 미치는 영향을 조사하였다. 10%(v/v) fetal bovine serum이 첨가된 MEM 배지에서 키운 세포와 비교할 때 25%(v/v) DSW이 포함될 경우 배양 17시간째에는 차이가 없었다. 그러나 DIV3, 7, 14, 및 17에 관찰하면 경도 0 및 200의 DSW가 포함된 배지에서 자란 신경세포는 가지돌기의 수가 현저히 줄었다. 반면에 경도 600의 DSW에서 자란 신경세포는 그 가지돌기의 수가 대조군과 비슷하였으며, 경도 1000의 경우는 대조군에 비하여 거의 2배 증가하였다. 이 결과는 적당한 경도의 DSW는 신경세포의 성장 및 건강을 돕는 것으로 해석된다.

ECM 단백질이 IMR-32 및 SK-N-SH 세포주 신경축색생장에 미치는 영향 (Analyses of the Neurite Outgrowth and Signal Transduction in IMR-32 and SK-N-SH Cells by ECM Proteins)

  • 최윤정;김철우;허규정
    • 한국동물학회지
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    • 제38권4호
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    • pp.542-549
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    • 1995
  • Extracellular matrix(ECM) 단백질이 SK-N-SH 및 IMR-32 세포주가 신경계 세포로 분화되는 데 미치는 영향을 조사하였다. Laminin과 collagen으로 도말한 배양기에서 7일간 배양했을 때 SK-N-SH세포는 잘 발달된 신경측색생장을 보였으나 IMR-32세포는 뚜렷한 형태변화를 나타내지 않았다. 왜 IMR-32세포가 ECM 단백질에 반응을 하지 않는가를 규명하기 위하여 ECM단백질에 의한 초기 신호전달기작을 두 세포주에서 분석하였다. ECM 단백질을 도말한 배양기에 세포를 깔았을 때 한시간 만에 tyrosine 인산화된 단백질이 두 세포 모두 증가함을 볼 수 있었다. 아울러 focal adhesion kinase(FAK)의 tyrosine 인산화도 두 세포주 모두에서 증가하였다. 이러한 결과는 두 세포주가 ECM 단백질에 의한 초기 신호전달체계가 정상임을 의미한다. 신경세포 분화과정에 증가한다고 알려진 Bcl-2 및 NSE의 량을 ECM 단백질 처리후 조사하였을 때 SK-N-SH 세포주는 두 단백질이 증가 했지만 IMR-32 세포주는 변화가 없었다. 이러한 결과는 IMR-32 세포주가 ECM 단백질에 반응하지 않는 것이 ECM 단백질에 의한 신호전달체계에 문제가 있다기 보다 신경계세포로 분화되는 데 필요한 유전인자의 발현조절에 문제가 있음을 시사한다.

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Recent Progress on Skin-Derived Mesenchymal Stem Cells in Pigs

  • Kumar, B. Mohana;Patil, Rajreddy;Lee, Sung-Lim;Rho, Gyu-Jin
    • Reproductive and Developmental Biology
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    • 제36권4호
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    • pp.283-290
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    • 2012
  • Skin serves as an easily accessible source of multipotent stem cells with potential for cellular therapies. In pigs, stem cells from skin tissues of fetal and adult origins have been demonstrated as either floating spheres (cell aggregates) or adherent spindle-shaped mesenchymal stem cell (MSC)-like cells depending on culture conditions. The cells isolated from the epidermis and dermis of porcine skin showed plastic adherent growth in the presence of serum and positively expressed a range of surface and intracellular markers that are considered to be specific for MSCs. The properties of primitive stem cells have been observed with the expression of alkaline phosphatase and markers related to pluripotency. Further, studies have shown the ability of skin-derived MSCs to differentiate in vitro along mesodermal, neuronal and germ-line lineages. Moreover, preclinical studies have also been performed to assess their in vivo potential, and the findings appear to be effective in tissue regeneration at the defected site after transplantation. The present review describes the recent progress on the biological features of porcine skin-derived MSCs as adherent cells, and summarizes their potential in advancing stem cell based therapies.

MicroRNAs in Human Diseases: From Autoimmune Diseases to Skin, Psychiatric and Neurodegenerative Diseases

  • Ha, Tai-You
    • IMMUNE NETWORK
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    • 제11권5호
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    • pp.227-244
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    • 2011
  • MicroRNAs (miRNAs) are small noncoding RNA molecules that negatively regulate gene expression via degradation or translational repression of their target messenger RNAs (mRNAs). Recent studies have clearly demonstrated that miRNAs play critical roles in several biologic processes, including cell cycle, differentiation, cell development, cell growth, and apoptosis and that miRNAs are highly expressed in regulatory T (Treg) cells and a wide range of miRNAs are involved in the regulation of immunity and in the prevention of autoimmunity. It has been increasingly reported that miRNAs are associated with various human diseases like autoimmune disease, skin disease, neurological disease and psychiatric disease. Recently, the identification of miRNAs in skin has added a new dimension in the regulatory network and attracted significant interest in this novel layer of gene regulation. Although miRNA research in the field of dermatology is still relatively new, miRNAs have been the subject of much dermatological interest in skin morphogenesis and in regulating angiogenesis. In addition, miRNAs are moving rapidly center stage as key regulators of neuronal development and function in addition to important contributions to neurodegenerative disorder. Moreover, there is now compelling evidence that dysregulation of miRNA networks is implicated in the development and onset of human neruodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, Tourette's syndrome, Down syndrome, depression and schizophrenia. In this review, I briefly summarize the current studies about the roles of miRNAs in various autoimmune diseases, skin diseases, psychoneurological disorders and mental stress.

A Missense Variant (R239Q) in CCN3 Induces Aberrant Apoptosis in the Developing Mouse Brain

  • Kim, Hyunduk;Yang, Hayoung;Woo, Dong Kyun;Jang, Sung-Wuk;Shim, Sungbo
    • 대한의생명과학회지
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    • 제24권2호
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    • pp.64-75
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    • 2018
  • CCN3 (also known as NOV, Nephroblastoma overexpressed) proteins are involved in various pathologies during different developmental stages. We have previously shown that intracellular levels and normal extracellular secretion of CCN3 are important for neuronal differentiation. Furthermore, we demonstrated that a single amino acid in the CCN3 TSP-1 domain is important for extracellular secretion and that palmitoylation of CCN3 is required in this process. However, the effect of abnormal CCN3 accumulation on cells remains to be studied. Here, we found mutations in the TSP-1 domain of CCN3 that led to intracellular accumulation and abnormal aggregation of CCN3. It was observed that this mutation resulted in a phenomenon similar to neurodegeneration when overexpressed in the developing mouse cortex. This mutation also confirmed the activation of apoptotic gene expression in Neuro2a cells. In addition, we confirmed the in vivo transcriptional changes induced by this mutation using microarray analysis. We observed a significant increase in the expression of Anp32a, an apoptosis-related gene. Collectively, these results indicate that a single mutation in CCN3 can lead to abnormal cell death if it shows intracellular accumulation and abnormal aggregation.

Animal Models for Aging and Neurodegenerative Diseases: Brain Cell Apoptosis in the Dog and its Possible Mechanisms

  • Nakayama, Hiroyuki;Kajikawa, Satoru;Doi, Kunio
    • Toxicological Research
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    • 제17권
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    • pp.71-77
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    • 2001
  • The brain of the aged dog possesses senile plaques and amyloid angiopathy, which characterize Alzheimer's disease brains. We have defined the dementia condition of aged dogs and examined which mechanism(s) is responsible for the condition. A series of studies revealed that the dementia condition in aged dogs is significantly related to the number of apoptotic brain cells including both neurons and glial cells, but not to the number of senile plaques. On the other hand, 5-azacytidine (5AzC) is a cytidine analogue, and is thought to induce kinds of cell differentiation possibly through hypomethylation of genomic DNA. We have revealed neuronal apoptosis induced in 5AzC-treated fetal mice and PC12 cells. The ribosomal protein L4 (rpL4) gene is expressed prior to the apoptosis in the PC12 cell system. Therefore, the involvement of the rpL4 gene expression in age-related brain cell apoptosis in dogs may contribute to the investigation of Alzheimer's dementia.

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Reactive Oxygen Species are Involved in Y-27632-induced Neurite Outgrowth in PC12 Cells

  • Park, So Yeong;Moon, Seong Ah;An, Jeong Mi;Kim, Du sik;Seo, Jeong Taeg
    • International Journal of Oral Biology
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    • 제41권4호
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    • pp.231-236
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    • 2016
  • Inhibition of Rho-associated coiled coil-containing kinase (ROCK) has been reported to promote differentiation of neuronal cells. Here, we examined the effect of Y-27632, a ROCK inhibitor, on the outgrowth of neurites in PC12 cells. Y-27632 caused a rapid induction of neurite outgrowth in PC12 cells in a time-dependent manner. The neurite outgrowth, triggered by Y-27632, was accompanied by Rac1 activation, and was attenuated by Rac1 inhibitor NSC23766, in a concentration-dependent manner. Y-27632 also induced an increase in the production of reactive oxygen species (ROS). Pretreatment with N-acetylcysteine, an ROS scavenger, inhibited the ROS generation and neurite outgrowth in response to Y-27632. These results indicate that the activation of Rac1 and the generation of ROS contribute to the neurite outgrowth triggered by Y-27632 in PC12 cells.

Effect of Neurotrophic Factors on Neuronal Stem Cell Death

  • KimKwon, Yun-Hee
    • BMB Reports
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    • 제35권1호
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    • pp.87-93
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    • 2002
  • Neural cell survival is an essential concern in the aging brain and many diseases of the central nervous system. Neural transplantation of the stem cells are already applied to clinical trials for many degenerative neurological diseases, including Huntington's disease, Parkinson's disease, and strokes. A critical problem of the neural transplantation is how to reduce their apoptosis and improve cell survival. Neurotrophic factors generally contribute as extrinsic cues to promote cell survival of specific neurons in the developing mammalian brains, but the survival factor for neural stem cell is poorly defined. To understand the mechanism controlling stem cell death and improve cell survival of the transplanted stem cells, we investigated the effect of plausible neurotrophic factors on stem cell survival. The neural stem cell, HiB5, when treated with PDGF prior to transplantation, survived better than cells without PDGF. The resulting survival rate was two fold for four weeks and up to three fold for twelve weeks. When transplanted into dorsal hippocampus, they migrated along hippocampal alveus and integrated into pyramidal cell layers and dentate granule cell layers in an inside out sequence, which is perhaps the endogenous pathway that is similar to that in embryonic neurogenesis. Promotion of the long term-survival and differentiation of the transplanted neural precursors by PDGF may facilitate regeneration in the aging adult brain and probably in the injury sites of the brain.

Extracellular matrixes and neuroinflammation

  • Jang, Dong Gil;Sim, Hyo Jung;Song, Eun Kyung;Kwon, Taejoon;Park, Tae Joo
    • BMB Reports
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    • 제53권10호
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    • pp.491-499
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    • 2020
  • The extracellular matrix is a critical component of every human tissue. ECM not only functions as a structural component but also regulates a variety of cellular processes such as cell migration, differentiation, proliferation, and cell death. In addition, current studies suggest that ECM is critical for the pathophysiology of various human diseases. ECM is composed of diverse components including several proteins and polysaccharide chains such as chondroitin sulfate, heparan sulfate, and hyaluronic acid. Each component of ECM exerts its own functions in cellular and pathophysiological processes. One of the interesting recent findings is that ECM is involved in inflammatory responses in various human tissues. In this review, we summarized the known functions of ECM in neuroinflammation after acute injury and chronic inflammatory diseases of the central nerve systems.

Hepatoprotective effect of ultrasonicated ginseng berry extract on a rat mild bile duct ligation model

  • Nam, Yoonjin;Ko, Sung Kwon;Sohn, Uy Dong
    • Journal of Ginseng Research
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    • 제43권4호
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    • pp.606-617
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    • 2019
  • Background: The Panax ginseng berry extract (GBE) is well known to have an antidiabetic effect. The aim of this study is to evaluate and investigate the protective effect of ultrasonication-processed P. ginseng berry extract (UGBE) compared with GBE on liver fibrosis induced by mild bile duct ligation (MBDL) model in rats. After ultrasonication process, the composition ratio of ginsenoside in GBE was changed. The component ratio of ginsenosides Rh1, Rh4, Rg2, Rg3, Rk1, Rk3, and F4 in the extract was elevated. Methods: In this study, the protective effect of the newly developed UGBE was evaluated on hepatotoxicity and neuronal damage in MBDL model. Silymarin (150 mg/kg) was used for positive control. UGBE (100 mg/kg, 250 mg/kg, 500 mg/kg), GBE (250 mg/kg), and silymarin (150 mg/kg) were orally administered for 6 weeks after MBDL surgery. Results: The MBDL surgery induced severe hepatotoxicity that leads to liver inflammation in rats. Also, the serum ammonia level was increased by MBDL surgery. However, the liver dysfunction of MBDL surgery-operated rats was attenuated by UGBE treatment via myeloid differentiation factor 88-dependent Toll-like receptor 4 signaling pathways. Conclusion: UGBE has a protective effect on liver fibrosis induced by MBDL in rats through inhibition of the TLR4 signaling pathway in liver.