• Title/Summary/Keyword: brain mitochondria

Search Result 103, Processing Time 0.032 seconds

CoMIC, the hidden dynamics of mitochondrial inner compartments

  • Cho, Bongki;Sun, Woong
    • BMB Reports
    • /
    • v.50 no.12
    • /
    • pp.597-598
    • /
    • 2017
  • Mitochondria have evolutionarily, functionally and structurally distinct outer- (OMM) and inner-membranes (IMM). Thus, mitochondrial morphology is controlled by independent but coordinated activity of fission and fusion of the OMM and IMM. Constriction and division of the OMM are mediated by endocytosis-like machineries, which include dynamin-related protein 1 with additional cytosolic vesicle scissoring machineries such as actin filament and Dynamin 2. However, structural alteration of the IMM during mitochondrial division has been poorly understood. Recently, we found that the IMM and the inner compartments undergo transient and reversible constriction prior to the OMM division, which we termed CoMIC, ${\underline{C}}onstriction$ ${\underline{o}}f$ ${\underline{M}}itochondrial$ ${\underline{I}}nner$ ${\underline{C}}ompartment$. In this short review, we further discuss the evolutionary perspective and the regulatory mechanism of CoMIC during mitochondrial division.

Effect of Pine Needle Extract (PNE) on Physiological Activity of SD Rats II. Feeding Effect of PNE on Oxygen Radicals and Their Scavenger Enztmes in Brain Membranes of SD Rats (흰쥐의 생리활성에 미치는 송엽 추출물(PNE)의 영향 II. 뇌세포막의 산소라디칼 및 제거효소의 활성에 미치는 PNE의 투여효과)

  • 최진호;김정화;김동우;김경석;이종수;백영호
    • Journal of Life Science
    • /
    • v.8 no.1
    • /
    • pp.91-96
    • /
    • 1998
  • Pine(Pinus densiflora Sieb et Zucc.) is one of rhe popular plant drugs which has been used as a medicine in Asia. To investigate the effect of pine needle extract (PNE) on oxygen radicals and their scavenger enzymes in brain membranes of Sprague- Dawley (SD), make SD rats were fed basic diets(control group), and experimental diets (PNE group) with 0.5 and 1.0% of PNE 6 weeks. Mitochondrial hydroxyl radical levels in brain of 0.5%-PNE and 1.0%-PNE groups were significantly inhibited to 30% and 25%, respectively, and microsomal hydrogen peroxide levels in brain of 0.5%-PNE and 1.0%-PNE groups were significantly inhibited to 15% compared with control group. Cytosolic superoxide rdical levels in 1.0%-PNE group were significantly inhibited to 20% compared with control group. Lipid peroxide(LPO) levels in brain mitochondria of 0.5%-PNE and 1.0%-PNE groups were significantly lower(25% and 35%) than that in control group. Mn-superoxide disumtase (SOD) activities in brain of 0.5%-PNE and 1.0%-PNE groups were significantly higher(18% and 12%) than those in control groups, but Cu,Zn-SOD activities in brain of 0.5%-PNE were significantly activated to 15% compared with control group. Glutathione peroxidase(GSHPx) activities in brain of 1.5%-PNE and 1.0% PNE groups were significantly higher(14% and 12%) than those in control group. These results suggest that more beneficial effects such as inhibition of oxygen radicals and lipid peroxide(LPO). and oncreases of scavenger enzymes in brain membranes of SD rats may be effectively modulated by administration of pine needle extract (PNE)

  • PDF

Inhibition of Proliferation and Neurogenesis of Mouse Subventricular Zone Neural Stem Cells by a Mitochondrial Inhibitor Rotenone (미토콘드리아 억제제 rotenone에 의한 쥐의 뇌실 하 영역 신경 줄기 세포의 증식과 신경 세포로의 분화 억제)

  • Park, Ki-Youb;Kim, Man Su
    • Journal of Life Science
    • /
    • v.28 no.12
    • /
    • pp.1397-1405
    • /
    • 2018
  • Mitochondria have multiple functions in cells: providing chemical energy, storing cellular $Ca^{2+}$, generating reactive oxygen species, and regulating apoptosis. Through these functions, mitochondria are also involved in the maintenance, proliferation, and differentiation of stem/progenitor cells. In the brain, the subventricular zone (SVZ) is one of the neurogenic regions that contains neural stem cells (NSCs) throughout a lifetime. However, reports on the role of mitochondria in SVZ NSCs are scarce. Here, we show that rotenone, a complex I inhibitor of mitochondria, inhibits the proliferation and differentiation of SVZ NSCs in different ways. In proliferating NSCs, rotenone decreases mitosis as measured through phosphorylated histone H3 detection; moreover, apoptosis is not induced by rotenone at 50 nM. In differentiating NSCs, rotenone blocks neurogenesis and oligodendrogenesis while glial fibrillary acidic protein-positive astrocytes are not affected. Interestingly, in this study there were more cells in the differentiating NSCs treated with rotenone for 4-6 days than in the vehicle control group which was a different effect from the reduced number of cells in the proliferating NSCs. We examined both apoptosis and mitosis and found that rotenone decreased apoptosis as detected by staining cleaved caspase-3 but did not affect mitosis. Our results suggest that functional mitochondria are necessary in both the proliferation and differentiation of SVZ NSCs. Furthermore, mitochondria might be involved in the mitosis and apoptosis that occur during those processes.

Evidence for the Drp1-dependent Mitochondrial Fission in the Axon of the Rat Cerebral Cortex Neurons (흰쥐 대뇌 피질 신경세포의 축삭에서 Drp1 의존적 미토콘드리아의 분열)

  • Cho, Bong-Ki;Lee, Seung-Bok;Sun, Woong;Kim, Young-Hwa
    • Applied Microscopy
    • /
    • v.41 no.4
    • /
    • pp.249-255
    • /
    • 2011
  • Neurons utilize a large quantity of energy for their survival and function, and thereby require active mitochondrial function. Mitochondrial morphology shows dynamic changes, depending on the cellular condition, and mitochondrial dynamics are required for neuronal development and function. In this study, we found that the length of mitochondria in the distal axon is significantly shorter than that of mitochondria in dendrites or proximal axons of cerebral cortical neurons, and the reason for this difference is the local fission within the axon. We also found that suppression of Drp1, a key regulator of mitochondrial fission, resulted in significant elongation of mitochondria in axons. Collectively, these results suggest that local mitochondrial fission within the axon contributes to region-dependent mitochondrial length differences in the axons of cortical neurons.

Effect of Pine Needle Extract (PNE) on Physilolgical Activity of SD Rats III. Feeding Effect of PNE on Fluidity and Neurotransmitter-Related Enztmes in Brain Membranes of SD Rats (흰쥐의 생리활성에 미치는 송엽(松葉) 추출물(PNE)의 영향 III. 뇌세포막의 유동성 및 신경전달관련 효소의 활성에 미치는 PNE의 투여효과)

  • Choi, Jin-Ho;Kim, Jung-Hwa;Kim, Dong-Woo;Hwang, Chan-Ho;Kim, Dae-Ik;Lee, Jong-Soo
    • Journal of Life Science
    • /
    • v.8 no.2
    • /
    • pp.167-172
    • /
    • 1998
  • To investigate the effect of pine needle extract (PNE) on membrane fluidirt and neurotransmiter-related enzymes in brain of Spragu-Dawley(SD), male SD rats were fed basic diets (control group), and experimantal diets (PNE group)with 0.5% and 0.1% fo PNE for 6 weeks. pine (pinus tabulaeformis C$_{ARR}$ is one of the popular plant drugs which has used as a medicine in Asia. Cholesterol levels in brain mitochondria of 0.5%-PNE and 0.1%-PNDE groups were significantly decreased in 15% and 25%, respectively, compared with control group, but cholesterol levels in brain microsomes of these PNE groups howed almost no change compared with control group. Lipofuscin accumulations in brain membranes of 0.5%-PNE and 0.1%-PNE groups were sgnificantly inhibited in 18% and 21%, respectively, compared with control group. Brain memberance fluidity was also activated in 50% and 100% by the administration of 0.5%-PNE and 0.1%-PNE. higher acetylcholinesterase(15% and25%) and lower monoamine oxidase B (25% and 15%0 activities were effectively modulated by the administration of 0.5%-PNE and 0.1%-PNDE. These results suggest that more beneficial effects such as inhibition of cholesterol and lipofuscin, increase of membrane fluidity, higher acetylcholinesterase and lower monoamone oxidase activities in brain membranes of SD rats may be effectively modulated by administration of pine needle extract (PNE).

  • PDF

The end effector of circadian heart rate variation: the sinoatrial node pacemaker cell

  • Yaniv, Yael;Lakatta, Edward G.
    • BMB Reports
    • /
    • v.48 no.12
    • /
    • pp.677-684
    • /
    • 2015
  • Cardiovascular function is regulated by the rhythmicity of circadian, infradian and ultradian clocks. Specific time scales of different cell types drive their functions: circadian gene regulation at hours scale, activation-inactivation cycles of ion channels at millisecond scales, the heart's beating rate at hundreds of millisecond scales, and low frequency autonomic signaling at cycles of tens of seconds. Heart rate and rhythm are modulated by a hierarchical clock system: autonomic signaling from the brain releases neurotransmitters from the vagus and sympathetic nerves to the heart's pacemaker cells and activate receptors on the cell. These receptors activating ultradian clock functions embedded within pacemaker cells include sarcoplasmic reticulum rhythmic spontaneous Ca2+ cycling, rhythmic ion channel current activation and inactivation, and rhythmic oscillatory mitochondria ATP production. Here we summarize the evidence that intrinsic pacemaker cell mechanisms are the end effector of the hierarchical brain-heart circadian clock system.

Identification of Novel Metabolic Proteins Released by Insulin Signaling of the Rat Hypothalmus Using Liquid Chromatography-Mass Spectrometry (LC-MS)

  • Chin, Chur
    • Journal of Korean Neurosurgical Society
    • /
    • v.42 no.6
    • /
    • pp.470-474
    • /
    • 2007
  • Objective : The brain is dependent on glucose as an energy source. Intricate homeostatic mechanisms have been implicated in maintaining the blood glucose concentration in the brain. The aim of this study is to find the way to identify the metabolic proteins regulating the glucose in rat hypothalamus. Methods : In this study, we analysed the secretome from rat hypothalamus in vivo. We introduced 500 nM of insulin into the rat hypothalamus. The chromatographic patterns of the secretome were identified, after which Mass Spectrometry-Mass Spectrometry (MS-MS) analysis was performed. Results : In Liquid Chromatography-Mass Spectrometry (LC-MS) analysis, 60 proteins were identified in the secretome. Among them, 8 novel proteins were unveiled and were associated with the energy metabolism of insulin signaling in mitochondria of rat hypothalamic neuron. Nineteen other proteins have unknown functions. These ligands were confirmed to be secreting from the rat hypothalmus on insulin signaling by western blotting. Conclusion : The hypothalamus is the master endocrine gland responsible for the regulation of various physiological and metabolic processes. Proteomics using LC-MS analysis offer a efficient means for generating a comprehensive analysis of hypothalamic protein expression by insulin signaling.

The cellular basis of dendrite pathology in neurodegenerative diseases

  • Kweon, Jung Hyun;Kim, Sunhong;Lee, Sung Bae
    • BMB Reports
    • /
    • v.50 no.1
    • /
    • pp.5-11
    • /
    • 2017
  • One of the characteristics of the neurons that distinguishes them from other cells is their complex and polarized structure consisting of dendrites, cell body, and axon. The complexity and diversity of dendrites are particularly well recognized, and accumulating evidences suggest that the alterations in the dendrite structure are associated with many neurodegenerative diseases. Given the importance of the proper dendritic structures for neuronal functions, the dendrite pathology appears to have crucial contribution to the pathogenesis of neurodegenerative diseases. Nonetheless, the cellular and molecular basis of dendritic changes in the neurodegenerative diseases remains largely elusive. Previous studies in normal condition have revealed that several cellular components, such as local cytoskeletal structures and organelles located locally in dendrites, play crucial roles in dendrite growth. By reviewing what has been unveiled to date regarding dendrite growth in terms of these local cellular components, we aim to provide an insight to categorize the potential cellular basis that can be applied to the dendrite pathology manifested in many neurodegenerative diseases.

Effects of Sea Tangle (Laminaria japonica) and Fucoidan Components on Chronic Degenerative Diseases (만성퇴행성 질환에 미치는 다시마(Laminaria japonica)와 후코이단 성분의 영향)

  • 최진호;김대익;박수현;김동우;이종수;유종현;정유섭
    • Journal of Life Science
    • /
    • v.9 no.4
    • /
    • pp.430-438
    • /
    • 1999
  • This study was designed to investigate the effects of sea tangle (Laminaria japonica) extract and fucoidan components on chronic degenerative diseases. Sprague-Dawley(SD) male rats (210$\pm$5g) were fed experimental diets: Dasi-Ex group: dasima extract powder of 4.0% added to control diet; Fuco-I, II and III groups: fucoidan powder of 1, 2 and 3% added to Dasi-Ex group for 45 days. Triglyceride (TG) levels in serum were significantly lower (10~15%) in Fuco-I, II and III groups compared with control group. Total cholesterol levels were significantly decreased (7~10% and 15~ 35%) in brain mitochondria and microsomes of Fuco-II and III group compared with control group. LDL-cholesterol levels were remarkably decreased (20~30%) in Dasi-Ex and Fuco-I, II, III groups, but HDL-cholesterol levels were significantly increased (10~12%) in Fuco-II and III groups only compared with control group. The ratios of HDL/total cholesterol resulted in a marked increase (3 5~55%) in Dasi-Ex and Fuco-I, II, III groups, but atherogenic indices were remakably decreased (40~50%) in Dasi-Ex and Fuco-I, II, III groups compared with control group. Membrane fluidities were remarkably increased (45~70% and 38~42%, respectively) in brain mitochondria and microsomes of Fuco-II and III groups compared with control group. Administrations of fucoidan added to dasima effectively decreased TG, total and LDL-cholesterol, and atherogenic index, while also effectively increased HDL-cholesterol, HDL/total cholesterol ratio, and membrane fluidity, suggesting chronic degenerative diseases were very effectively prevented by the administration of fucoidan component.

  • PDF

Role of Oxidative Stress and Mitochondria in Parkinson's Disease

  • Jin, Son-Hyeung
    • Proceedings of the Korean Society of Applied Pharmacology
    • /
    • 2007.04a
    • /
    • pp.147-153
    • /
    • 2007
  • Central to developing new treatment strategies for late onset sporadic Parkinson's disease (PD) and early onset familial PD is resolving the enigma of the specific vulnerability exhibited by substantia nigra dopamine (DA) neurons despite multiple risk factors. Neuropathological evidence from both human and experimental models of PD firmly supports a significant role for oxidative stress (OS) and mitochondrial dysfunction in the death of nigral DA neurons. Largely unknown are the genes underlying selective susceptibility of nigral DA neuron to OS and mitochondrial dysfunction and how they effect nigral DA cell death. To overcome the paucity of nigral DA neurons as well as the dilution effect of non-DA cells in brain tissues, we have developed wild type DA cell line model, SN4741 and mutant DJ-1 (-/-) DA cells, appropriate for microarray analysis and differential mitochondrial proteomics. Mutations in the DJ-1 gene (PARK7), localized in cytoplasm and mitochondria, cause autosomal recessive early onset PD. Through microarray analysis using SN4741 cells followed by validation tests, we have identified a novel phylogenically conserved neuroprotective gene, Oxi-a, which is specifically expressed in DA neurons. The knockdown of the gene dramatically increased vulnerability to as. Importantly as down-regulated the expression level of the gene and recovery of its expression via transient transfection exerted significant neuroprotection against as insult. We also have identified altered expression of mitochondrial proteins and other familial PD genes in DJ-1 (-/-) mutant cells by differential mitochondrial proteomics. In DJ-1 (-/-) cells the knockdown of the other familial PD genes (Parkin and PINK1) dramatically increased susceptibility to as. Thus, further functional characterization of the Oxi-$\alpha$ gene family and the mitochondrial alteration in the DJ-1 (-/-) cell model will provide the rationale for the neuroprotective therapy against both sporadic and familial PD.

  • PDF