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https://www.readbyqxmd.com/read/29768513/increased-mitochondrial-fission-is-critical-for-hypoxia-induced-pancreatic-beta-cell-death
#1
Da Zhang, Yanfang Liu, Yao Tang, Xiaofeng Wang, Zhichao Li, Rui Li, Zhenyu Ti, Weidong Gao, Jigang Bai, Yi Lv
Hypoxia-mediated pancreatic beta cell death is one of the main causes of pancreatic beta celldeath, which leads to the loss of functional pancreatic beta cell mass and type 1 diabetes andtype 2 diabetes.However, the molecular mechanisms that control life and death of pancreatic beta cells remain poorly understood. Here we showed that mitochondrial fission was strongly induced in pancreatic beta cellsmainly due to an elevation of DRP1S616 phosphorylation through HIF-1αactivation and subsequent DRP1 mitochondrial translocation...
2018: PloS One
https://www.readbyqxmd.com/read/29768044/cocl2-induces-apoptosis-via-ros-dependent-pathway-and-drp1-mediated-mitochondria-fission-in-the-periodontal-ligament-stem-cells
#2
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
#3
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/29744667/vagus-nerve-stimulation-exerts-cardioprotection-against-myocardial-ischemia-reperfusion-injury-predominantly-through-its-efferent-vagal-fibers
#4
Watthana Nuntaphum, Wanpitak Pongkan, Suwakon Wongjaikam, Savitree Thummasorn, Pongpan Tanajak, Juthamas Khamseekaew, Kannaporn Intachai, Siriporn C Chattipakorn, Nipon Chattipakorn, Krekwit Shinlapawittayatorn
Vagus nerve stimulation (VNS) has been shown to exert cardioprotection against myocardial ischemia/reperfusion (I/R) injury. However, whether the cardioprotection of VNS is mainly due to direct activation through its ipsilateral efferent fibers (motor) rather than indirect effects mediated by the afferent fibers (sensory) have not been clearly understood. We hypothesized that VNS exerts cardioprotection predominantly through its efferent vagal fibers. Thirty swine (30-35 kg) were randomized into five groups: I/R no VNS (I/R), and left mid-cervical VNS with both vagal trunks intact (LC-VNS), with left vagus nerve transection (LtVNX), with right vagus nerve transection (RtVNX) and with atropine pretreatment (Atropine), respectively...
May 9, 2018: Basic Research in Cardiology
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
#5
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/29742430/manipulation-of-mitochondria-dynamics-reveals-separate-roles-for-form-and-function-in-mitochondria-distribution
#6
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/29727016/metabolic-stress-dependent-regulation-of-the-mitochondrial-biogenic-molecular-response-to-high-intensity-exercise-in-human-skeletal-muscle
#7
M Fiorenza, T P Gunnarsson, M Hostrup, F M Iaia, F Schena, H Pilegaard, J Bangsbo
KEY POINTS: Low-volume high-intensity exercise training promotes muscle mitochondrial adaptations that resemble the ones associated with high-volume moderate-intensity exercise training. These training-induced mitochondrial adaptations stem from the cumulative effects of transient transcriptional responses to each acute exercise bout. However, whether metabolic stress is a key mediator of the acute molecular responses to high-intensity exercise is still incompletely understood. Herein we show that, by comparing different work-matched low-volume high-intensity exercise protocols, more marked metabolic perturbations were associated with enhanced mitochondrial biogenesis-related muscle mRNA responses...
May 4, 2018: Journal of Physiology
https://www.readbyqxmd.com/read/29726929/impaired-mitochondrial-dynamics-underlie-axonal-defects-in-hereditary-spastic-paraplegias
#8
Kyle Denton, Yongchao Mou, Chong-Chong Xu, Dhruvi Shah, Jaerak Chang, Craig Blackstone, Xue-Jun Li
Mechanisms by which long corticospinal axons degenerate in hereditary spastic paraplegia (HSP) are largely unknown. Here, we have generated induced pluripotent stem cells (iPSCs) from patients with two autosomal recessive forms of HSP, SPG15 and SPG48, which are caused by mutations in the ZFYVE26 and AP5Z1 genes encoding proteins in the same complex, the spastizin and AP5Z1 proteins, respectively. In patient iPSC-derived telencephalic glutamatergic and midbrain dopaminergic neurons, neurite number, length and branching are significantly reduced, recapitulating disease-specific phenotypes...
May 2, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29725013/iron-overload-promotes-mitochondrial-fragmentation-in-mesenchymal-stromal-cells-from-myelodysplastic-syndrome-patients-through-activation-of-the-ampk-mff-drp1-pathway
#9
Qingqing Zheng, Youshan Zhao, Juan Guo, Sida Zhao, Chengming Fei, Chao Xiao, Dong Wu, Lingyun Wu, Xiao Li, Chunkang Chang
Iron overload (IO) has been reported to contribute to mesenchymal stromal cell (MSC) damage, but the precise mechanism has yet to be clearly elucidated. In this study, we found that IO increased cell apoptosis and lowered cell viability in MSCs, accompanied by extensive mitochondrial fragmentation and autophagy enhancement. All these effects were reactive oxygen species (ROS) dependent. In MSCs with IO, the ATP concentrations were significantly reduced due to high ROS levels and low electron respiratory chain complex (ETC) II/III activity...
May 3, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29710722/mitochondrial-dysfunction-as-a-predictor-and-driver-of-alzheimer-s-disease-like-pathology-in-oxys-rats
#10
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
#11
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/29704468/renal-ischemia-reperfusion-induced-mitophagy-protects-against-renal-dysfunction-via-drp1-dependent-pathway
#12
Nan Li, Hengjin Wang, Chunming Jiang, Miao Zhang
Autophagy is upregulated under stress conditions to degrade superfluous proteins and recycle damaged organelles including damaged mitochondria. However, the occurrence of mitochondrial autophagy and its contribution remain to be elucidated during renal ischemia/reperfusion injury (IRI). In this study, mitophagosomes and engulfed mitochondria were frequently observed by electron microscopy after renal IRI vs. control. Meanwhile, the increase of lipidated microtubule associated protein light chain 3 (LC3-II) and decrease of mitochondrial proteins were detected by western blot, suggesting the presence of mitophagy...
April 25, 2018: Experimental Cell Research
https://www.readbyqxmd.com/read/29701781/mutant-app-and-amyloid-beta-induced-defective-autophagy-mitophagy-mitochondrial-structural-and-functional-changes-and-synaptic-damage-in-hippocampal-neurons-from-alzheimer-s-disease
#13
P Hemachandra Reddy, XiangLin Yin, Maria Manczak, Subodh Kumar, Pradeepkiran Jangampalli Adi, Murali Vijayan, Arubala P Reddy
The purpose of our study was to determine the toxic effects of hippocampal mutant APP and amyloid beta (Aβ) in human mutant APP (mAPP) cDNA transfected with primary mouse hippocampal neurons (HT22). Hippocampal tissues are the best source of studying learning and memory functions in patients with Alzheimer's disease (AD) and healthy controls. However, investigating immortalized hippocampal neurons that express AD proteins provide an excellent opportunity for drug testing. Using quantitative RT-PCR, immunoblotting & immunofluorescence, and transmission electron microscopy, we assessed mRNA and protein levels of synaptic, autophagy, mitophagy, mitochondrial dynamics, biogenesis, dendritic protein MAP2, and assessed mitochondrial number and length in mAPP-HT22 cells that express Swedish/Indiana mutations...
April 25, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29694914/the-origin-of-gskip-a-multifaceted-regulatory-factor-in-the-mammalian-wnt-pathway
#14
Chia-Hua Chou, Ming-Chang Yang, Bo-Xiu Hsiao, Yin-Hsuan Wang, Hsin-Fu Liu, Shean-Jaw Chiou, Yu-Chung Chuang, Chia-Ning Yang, Ann-Shung Lieu, Joon-Khim Loh, Shen-Long Howng, An-Kuo Chou, Chao-Neng Tseng, Jiin-Tsuey Cheng, Yi-Ren Hong
GSK3β interacting protein (GSKIP) is a naturally occurring negative regulator of GSK3β and retains both the Protein Kinase A Regulatory subunit binding (PKA-RII) domain and GSK3β interacting domain. Of these two domains, we found that PKA-RII is required for forming a working complex comprising PKA/GSKIP/GSK3β/Drp1 to influence phosphorylation of Drp1 Ser637. In this study, bioinformatics and experimental explorations re-analyzing GSKIP's biofunctions suggest that the evolutionarily conserved Domain of Unknown Function (DUF727) is an ancestral prototype of GSKIP in prokaryotes, and acquired the C-terminal GSK3β binding site (tail) in invertebrates except for Saccharomyces spp...
April 22, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29687234/ros-as-regulators-of-mitochondrial-dynamics-in-neurons
#15
REVIEW
Carolina Cid-Castro, Diego Rolando Hernández-Espinosa, Julio Morán
Mitochondrial dynamics is a complex process, which involves the fission and fusion of mitochondrial outer and inner membranes. These processes organize the mitochondrial size and morphology, as well as their localization throughout the cells. In the last two decades, it has become a spotlight due to their importance in the pathophysiological processes, particularly in neurological diseases. It is known that Drp1, mitofusin 1 and 2, and Opa1 constitute the core of proteins that coordinate this intricate and dynamic process...
April 23, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/29684364/inhibition-of-mitochondrial-fission-preserves-photoreceptors-after-retinal-detachment
#16
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
#17
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/29682689/effect-evaluation-of-methylprednisolone-plus-mitochondrial-division-inhibitor-1-on-spinal-cord-injury-rats
#18
Xu-Gui Chen, Li-Hua Chen, Ru-Xiang Xu, Hong-Tian Zhang
PURPOSE: To investigate the combination effect of methylprednisolone (MP) and mitochondrial division inhibitor-1 (Mdivi-1) on the neurological function recovery of rat spinal cord injury (SCI) model. METHODS: The weight-drop method was used to establish the rat SCI model; then, rats were randomized into sham group, SCI group, MP group, Mdivi-1 group and MP+Mdivi-1 group. Motor function scores were quantified to evaluate locomotor ability; HE staining was used to assess spinal cord histopathology; tissue water content, oxidative stress, tissue mitochondrial function, neurons apoptosis, and apoptosis-related protein expression were detected...
April 23, 2018: Child's Nervous System: ChNS: Official Journal of the International Society for Pediatric Neurosurgery
https://www.readbyqxmd.com/read/29673648/s6-kinase-1-plays-a-key-role-in-mitochondrial-morphology-and-cellular-energy-flow
#19
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
https://www.readbyqxmd.com/read/29673589/intracellular-calcium-is-a-rheostat-for-the-sting-signaling-pathway
#20
Dohyeong Kwon, Hiromi Sesaki, Suk-Jo Kang
Stimulator of IFN genes (STING) is essential for the DNA-sensing innate immune pathway. Recently, evidence is emerging that suggests STING also plays important roles in autoimmunity, cancer therapy, and senescence. Although a multitude of post-translational modifications that regulate the STING pathway have been discovered, the cellular events that guide STING translocation remain unclear. Here, we show, paradoxically, that both BAPTA-AM-mediated calcium depletion and ionomycin-induced calcium elevation suppress STING translocation and STING-mediated IFN-β production...
April 16, 2018: Biochemical and Biophysical Research Communications
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