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Mitochondria fission

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https://www.readbyqxmd.com/read/29775559/mechanosensitivity-of-mitochondr-ial-large-conductance-calcium-activated-potassium-channels
#1
Agnieszka Walewska, Bogusz Kulawiak, Adam Szewczyk, Piotr Koprowski
Potassium channels have been discovered in the inner mitochondrial membrane of various cells. These channels can regulate the mitochondrial membrane potential, the matrix volume, respiration and reactive species generation. Therefore, it is believed that their activation is cytoprotective in various tissues. In our study, the single-channel activity of a large-conductance calcium-activated potassium channel (mitoBKCa ) was measured by the patch-clamp technique on mitoplasts derived from mitochondria isolated from human glioma U-87 MG cells...
May 15, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29772718/ectromelia-virus-affects-mitochondrial-network-morphology-distribution-and-physiology-in-murine-fibroblasts-and-macrophage-cell-line
#2
Karolina P Gregorczyk, Zbigniew Wyżewski, Joanna Szczepanowska, Felix N Toka, Matylda B Mielcarska, Magdalena Bossowska-Nowicka, Małgorzata Gieryńska, Anna Boratyńska-Jasińska, Justyna Struzik, Marek G Niemiałtowski, Lidia Szulc-Dąbrowska
Mitochondria are multifunctional organelles that participate in numerous processes in response to viral infection, but they are also a target for viruses. The aim of this study was to define subcellular events leading to alterations in mitochondrial morphology and function during infection with ectromelia virus (ECTV). We used two different cell lines and a combination of immunofluorescence techniques, confocal and electron microscopy, and flow cytometry to address subcellular changes following infection. Early in infection of L929 fibroblasts and RAW 264...
May 16, 2018: Viruses
https://www.readbyqxmd.com/read/29768044/cocl2-induces-apoptosis-via-ros-dependent-pathway-and-drp1-mediated-mitochondria-fission-in-the-periodontal-ligament-stem-cells
#3
Yuting He, Xueqi Gan, Ling Zhang, Beilei Liu, Zhuoli Zhu, Tao Li, Junfei Zhu, Junsheng Chen, Haiyang Yu
Oxygen deficiency is associated with various oral diseases, including chronic periodontitis, age-related alveolar bone loss and mechanical stress-linked cell injury from orthodontic appliances. Nevertheless, our understanding of the impact of hypoxia on periodontal tissues and its biochemical mechanism is still rudimentary. The purpose of this research was to elucidate the effects of hypoxia on the apoptosis of human periodontal ligament stem cells (PDLSCs) in vitro and the underlying mechanism. Herein, we showed that CoCl2 triggered cell dysfunction in human PDLSCs in a concentration-dependent manner and resulted in cell apoptosis and oxidative stress overproduction and accumulation in PDLSCs...
May 16, 2018: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29760744/mst1-regulates-post-infarction-cardiac-injury-through-the-jnk-drp1-mitochondrial-fission-pathway
#4
Xisong Wang, Qing Song
Background: Post-infarction cardiac injury is closely associated with cardiac remodeling and heart dysfunction. Mammalian STE20-like kinase 1 (Mst1), a regulator of cellular apoptosis, is involved in cardiac remodeling in post-infarction heart, but the mechanisms remain poorly defined. We aimed to explore the role of Mst1 in regulating chronic post-infarction cardiac injury, with a focus on mitochondrial homoeostasis. Methods: Wild-type (WT) and Mst1-knockout mice were as the cardiac myocardial infarction model...
2018: Cellular & Molecular Biology Letters
https://www.readbyqxmd.com/read/29749475/mir-125a-induces-apoptosis-metabolism-disorder-and-migrationimpairment-in-pancreatic-cancer-cells-by-targeting-mfn2-related-mitochondrial-fission
#5
Lichao Pan, Lin Zhou, Weijia Yin, Jia Bai, Rong Liu
Mitochondrial fission is important for the development and progression of pancreatic cancer (PC). However, little is known regarding its role in pancreatic cancer apoptosis, metabolism and migration. In the current study, the mechanism by which mitochondrial fission modifies the biological characteristics of PC was explored. MicroRNA‑125a (miR‑125a) had the ability to inhibit mitochondrial fission and contributed to cellular survival. Suppressed mitochondrial fission led to a reduction in mitochondrial debris, preserved the mitochondrial membrane potential, inhibited mitochondrial permeability transition pore opening, ablated cytochrome c leakage into the cytoplasm and reduced the pro‑apoptotic protein contents, finally blocking mitochondria related apoptosis pathways...
April 26, 2018: International Journal of Oncology
https://www.readbyqxmd.com/read/29748634/gene-by-environment-interactions-that-disrupt-mitochondrial-homeostasis-cause-neurodegeneration-in-c-elegans-parkinson-s-models
#6
Hanna Kim, Rylee J Perentis, Guy A Caldwell, Kim A Caldwell
Parkinson's disease (PD) is a complex multifactorial disorder where environmental factors interact with genetic susceptibility. Accumulating evidence suggests that mitochondria have a central role in the progression of neurodegeneration in sporadic and/or genetic forms of PD. We previously reported that exposure to a secondary metabolite from the soil bacterium, Streptomyces venezuelae, results in age- and dose-dependent dopaminergic (DA) neurodegeneration in Caenorhabditis elegans and human SH-SY5Y neurons...
May 10, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29744594/nr4a1-aggravates-the-cardiac-microvascular-ischemia-reperfusion-injury-through-suppressing-fundc1-mediated-mitophagy-and-promoting-mff-required-mitochondrial-fission-by-ck2%C3%AE
#7
Hao Zhou, Jin Wang, Pingjun Zhu, Hong Zhu, Sam Toan, Shunying Hu, Jun Ren, Yundai Chen
Mitochondrial fission and mitophagy are considered key processes involved in the pathogenesis of cardiac microvascular ischemia reperfusion (IR) injury although the upstream regulatory mechanism for fission and mitophagy still remains unclear. Herein, we reported that NR4A1 was significantly upregulated following cardiac microvascular IR injury, and its level was positively correlated with microvascular collapse, endothelial cellular apoptosis and mitochondrial damage. However, NR4A1-knockout mice exhibited resistance against the acute microvascular injury and mitochondrial dysfunction compared with the wild-type mice...
May 9, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29743663/drp-1-mediated-apoptosis-induces-muscle-degeneration-in-dystrophin-mutants
#8
Charlotte Scholtes, Stéphanie Bellemin, Edwige Martin, Maïté Carre-Pierrat, Bertrand Mollereau, Kathrin Gieseler, Ludivine Walter
Mitochondria are double-membrane subcellular organelles with highly conserved metabolic functions including ATP production. Mitochondria shapes change continually through the combined actions of fission and fusion events rendering mitochondrial network very dynamic. Mitochondria are largely implicated in pathologies and mitochondrial dynamics is often disrupted upon muscle degeneration in various models. Currently, the exact roles of mitochondria in the molecular mechanisms that lead to muscle degeneration remain poorly understood...
May 9, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29742430/manipulation-of-mitochondria-dynamics-reveals-separate-roles-for-form-and-function-in-mitochondria-distribution
#9
Tatiana Trevisan, Diana Pendin, Aldo Montagna, Sergio Bova, Anna Maria Ghelli, Andrea Daga
Mitochondria shape is controlled by membrane fusion and fission mediated by mitofusins, Opa1, and Drp1, whereas mitochondrial motility relies on microtubule motors. These processes govern mitochondria subcellular distribution, whose defects are emphasized in neurons because of their polarized structure. We have studied how perturbation of the fusion/fission balance affects mitochondria distribution in Drosophila axons. Knockdown of Marf or Opa1 resulted in progressive loss of distal mitochondria and in a distinct oxidative phosphorylation and membrane potential deficit...
May 8, 2018: Cell Reports
https://www.readbyqxmd.com/read/29721922/mitochondria-potential-targets-for-protection-in-age-related-macular-degeneration
#10
Emily E Brown, Alfred S Lewin, John D Ash
Age-related macular degeneration (AMD) is the leading cause of blindness in older adults in developed countries. The molecular mechanisms of disease pathogenesis remain poorly understood; however, evidence suggests that mitochondrial dysfunction may contribute to the progression of the disease. Studies have shown that mitochondrial DNA lesions are increased in the retinal pigment epithelium (RPE) of human patients with the disease and that the number of these lesions increases with disease severity. Additionally, microscopy of human RPE from patients with dry AMD shows severe disruptions in mitochondrial inner and outer membrane structure, mitochondrial size, and mitochondrial cellular organization...
2018: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29721168/recruitment-of-mitofusin-2-into-lipid-rafts-drives-mitochondria-fusion-induced-by-mdivi-1
#11
Laura Ciarlo, Rosa Vona, Valeria Manganelli, Lucrezia Gambardella, Carla Raggi, Matteo Marconi, Walter Malorni, Maurizio Sorice, Tina Garofalo, Paola Matarrese
The regulation of the mitochondrial dynamics and the balance between fusion and fission processes are crucial for the health and fate of the cell. Mitochondrial fusion and fission machinery is controlled by key proteins such as mitofusins, OPA-1 and several further molecules. In the present work we investigated the implication of lipid rafts in mitochondrial fusion induced by Mdivi-1. Our results underscore the possible implication of lipid "rafts" in mitochondrial morphogenetic changes and their homeostasis...
April 10, 2018: Oncotarget
https://www.readbyqxmd.com/read/29710722/mitochondrial-dysfunction-as-a-predictor-and-driver-of-alzheimer-s-disease-like-pathology-in-oxys-rats
#12
Mikhail A Tyumentsev, Natalia A Stefanova, Natalia A Muraleva, Yulia V Rumyantseva, Elena Kiseleva, Valentin A Vavilin, Nataliya G Kolosova
Growing evidence suggests that mitochondrial dysfunction is an early event in sporadic Alzheimer's disease (AD), but the impact of mitochondrial dysfunction on the transition from healthy aging to AD remains elusive. Here we estimated the influence of mitochondrial dysfunction on the initiation of AD signs in OXYS rats, which simulate key characteristics of sporadic AD. We assessed the mitochondrial ultrastructure of pyramidal neurons of the hippocampus at the age preceding the development (age 20 days), during manifestation (4-5 months), and at the well-pronounced stages (18-24 months) of the AD-like pathology in OXYS rats...
April 27, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29709476/different-mitochondrial-fragmentation-after-irradiation-with-x-rays-and-carbon-ions-in-hela-cells-and-its-influence-on-cellular-apoptosis
#13
Xiaodong Jin, Feifei Li, Bingtao Liu, Xiaogang Zheng, Hongbin Li, Fei Ye, Weiqiang Chen, Qiang Li
Although mitochondria are known to play an important role in radiation-induced cellular damage, the mechanisms by which ionizing radiation modulates mitochondrial dynamics are largely unknown. In this study, human cervical carcinoma cell line HeLa was used to demonstrate the different modes of mitochondrial network in response to different quality radiations such as low linear energy transfer (LET) X-rays and high-LET carbon ions. Mitochondria fragmented into punctate and clustered ones upon carbon ion irradiation in a dose- and LET-dependent manner, which was associated with apoptotic cell death...
April 27, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29707607/analysis-of-mitochondrial-structure-in-the-body-wall-muscle-of-caenorhabditis-elegans
#14
Shaarika Sarasija, Kenneth R Norman
Mitochondrial function is altered in various pathologies, highlighting the crucial role mitochondria plays in maintaining cellular homeostasis. Mitochondrial structure undergoes constant fission and fusion in response to changing cellular environment. Due to this, analyzing mitochondrial structure could provide insight into the physiological state of the cell. In this protocol, we describe a method to analyze mitochondrial structure in body wall muscles in the nematode Caenorhabditis elegans, using both transgenic and dye-based approaches...
April 5, 2018: Bio-protocol
https://www.readbyqxmd.com/read/29705815/pancreatic-%C3%AE-cells-overexpressing-hiapp-impaired-mitophagy-and-unbalanced-mitochondrial-dynamics
#15
Miriam García Hernández, Ana García Aguilar, Jesús Burillo, Raquel Gómez Oca, Maria Antonietta Manca, Ana Novials, Gema Alcarraz-Vizan, Carlos Guillén, Manuel Benito
Human islet amyloid polypeptide (hIAPP), or amylin, has the tendency to aggregate into insoluble amyloid fibrils, a typical feature of islets from type 2 diabetes individuals. Thus, we investigated comparatively the impact of hIAPP on key pathways involved in pancreatic beta survival. INS1E-hIAPP cells present a hyperactivation of MTORC1 and an inhibition of autophagy signaling, those cells showing an increase in cell size. Resveratrol, a MTORC1 inhibitor, can reverse TSC2 degradation that occurs in INS1E-hIAPP cells and diminished MTORC1 hyperactivation with concomitant autophagy stimulation...
April 29, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29694881/miro-1-determines-mitochondrial-shape-transition-upon-gpcr-activation-and-ca-2-stress
#16
Neeharika Nemani, Edmund Carvalho, Dhanendra Tomar, Zhiwei Dong, Andrea Ketschek, Sarah L Breves, Fabián Jaña, Alison M Worth, Julie Heffler, Palaniappan Palaniappan, Aparna Tripathi, Ramasamy Subbiah, Massimo F Riitano, Ajay Seelam, Thomas Manfred, Kie Itoh, Shuxia Meng, Hiromi Sesaki, William J Craigen, Sudarsan Rajan, Santhanam Shanmughapriya, Jeffrey Caplan, Benjamin L Prosser, Donald L Gill, Peter B Stathopulos, Gianluca Gallo, David C Chan, Prashant Mishra, Muniswamy Madesh
Mitochondria shape cytosolic calcium ([Ca2+ ]c ) transients and utilize the mitochondrial Ca2+ ([Ca2+ ]m ) in exchange for bioenergetics output. Conversely, dysregulated [Ca2+ ]c causes [Ca2+ ]m overload and induces permeability transition pore and cell death. Ablation of MCU-mediated Ca2+ uptake exhibited elevated [Ca2+ ]c and failed to prevent stress-induced cell death. The mechanisms for these effects remain elusive. Here, we report that mitochondria undergo a cytosolic Ca2+ -induced shape change that is distinct from mitochondrial fission and swelling...
April 24, 2018: Cell Reports
https://www.readbyqxmd.com/read/29694336/a-role-for-the-gdap1-gene-in-the-molecular-pathogenesis-of-charcot%C3%A2-marie%C3%A2-tooth-disease
#17
Weronika Rzepnikowska, Andrzej Kochański
In 2002 a series of mutations in the GDAP1 gene were reported in patients suffering from Charcot‑Marie‑Tooth disease manifesting as early-onset, progressive distal‑muscle wasting and weakness. The molecular etiology of Charcot‑Marie‑Tooth ‑GDAP1 disease has been elucidated but its pathogenesis remains unclear, especially given the seemingly contradictory function of the GDAP1 protein. Expression of GDAP1 is observed almost exclusively in neuronal cells, however, the GDAP1 protein is present in mitochondria, where it plays a role in fission, a ubiquitous process occurring in all cells...
2018: Acta Neurobiologiae Experimentalis
https://www.readbyqxmd.com/read/29684364/inhibition-of-mitochondrial-fission-preserves-photoreceptors-after-retinal-detachment
#18
Xiangjun She, Xinmin Lu, Tong Li, Junran Sun, Jian Liang, Yuanqi Zhai, Shiqi Yang, Qing Gu, Fang Wei, Hong Zhu, Fenghua Wang, Xueting Luo, Xiaodong Sun
Photoreceptor degeneration is a leading cause of visual impairment worldwide. Separation of neurosensory retina from the underlying retinal pigment epithelium is a prominent feature preceding photoreceptor degeneration in a variety of retinal diseases. Although ophthalmic surgeries have been well developed to restore retinal structures, post-op patients usually experience progressive photoreceptor degeneration and irreversible vision loss that is incurable at present. Previous studies point to a critical role of mitochondria-mediated apoptotic pathway in photoreceptor degeneration, but the upstream triggers remain largely unexplored...
April 20, 2018: American Journal of Pathology
https://www.readbyqxmd.com/read/29682760/protective-role-of-parkin-in-skeletal-muscle-contractile-and-mitochondrial-function
#19
Gilles Gouspillou, Richard Godin, Jérome Piquereau, Martin Picard, Mahroo Mofarrahi, Jasmin Mathew, Fennigje M Purves-Smith, Nicolas Sgarioto, Russell T Hepple, Yan Burelle, Sabah Na Hussain
KEY POINTS SUMMARY: Parkin, an E3 ubiquitin ligase encoded by the Park2 gene, has been implicated in the regulation of mitophagy, a quality control process whereby defective mitochondria are degraded. The exact physiological significance of Parkin in regulating mitochondrial function and contractility in skeletal muscle remains largely unexplored. Using Park2-/- mice, we show that Parkin ablation causes a decrease in muscle specific force, a severe decrease in mitochondrial respiration, mitochondrial uncoupling and an increased susceptibility to opening of the permeability transition pore...
April 22, 2018: Journal of Physiology
https://www.readbyqxmd.com/read/29673648/s6-kinase-1-plays-a-key-role-in-mitochondrial-morphology-and-cellular-energy-flow
#20
Quangdon Tran, Jae-Hun Jung, Jisoo Park, Hyunji Lee, Youngeun Hong, Hyeonjeong Cho, Minhee Kim, Sungjin Park, So-Hee Kwon, Seon-Hwan Kim, George Thomas, Kwang Pyo Kim, Myung-Haing Cho, Jongsun Park
Mitochondrial morphology, which is associated with changes in metabolism, cell cycle, cell development and cell death, is tightly regulated by the balance between fusion and fission. In this study, we found that S6 kinase 1 (S6K1) contributes to mitochondrial dynamics, homeostasis and function. Mouse embryo fibroblasts lacking S6K1 (S6K1-KO MEFs) exhibited more fragmented mitochondria and a higher level of Dynamin related protein 1 (Drp1) and active Drp1 (pS616) in both whole cell extracts and mitochondrial fraction...
April 16, 2018: Cellular Signalling
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