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https://www.readbyqxmd.com/read/28727070/short-term-heat-stress-causes-altered-intracellular-signaling-in-oxidative-skeletal-muscle
#1
S Ganesan, C M Summers, S C Pearce, N K Gabler, R J Valentine, L H Baumgard, R P Rhoads, J T Selsby
Heat stress (HS) causes morbidities and mortalities, in part by inducing organ-specific injury and dysfunction. Further, HS markedly reduces farm animal productivity, and this is especially true for lean tissue accretion. The purpose of this investigation was to determine the extent to which short-term HS caused muscle dysfunction in skeletal muscle. We have previously found increased free radical injury in skeletal muscle following 24 h of HS. Thus, we hypothesized that HS would lead to apoptosis, autophagy, and decreased mitochondrial content in skeletal muscle...
June 2017: Journal of Animal Science
https://www.readbyqxmd.com/read/28713932/human-trypsin-inhibitor-reduces-the-apoptosis-of-lipopolysaccharide%C3%A2-induced-human-kidney%C3%A2-2-cells-by-promoting-mitochondrial-fusion
#2
Ning Liu, Zhiyi Jiang, Yongjun Liu, Yao Nie, Juan Chen, Bin Ouyang, Xiangdong Guan, Minying Chen
Imbalance in mitochondrial fusion/fission is one of the mechanisms leading to sepsis‑induced mitochondrial dysfunction and cell apoptosis. The present study examined the effects of human trypsin inhibitor (UTI), a well‑known antioxidant and anti‑inflammatory substance, on mitochondrial dynamics and cell apoptosis in lipopolysaccharide (LPS)‑induced human kidney‑2 (HK‑2) cells. The HK‑2 cells were incubated for 24 h either with LPS (800 ng/ml) or LPS (800 ng/ml) mixed with UTI (250 U/ml). Cell viability was assessed using a3‑(4,5‑dimethyl‑2‑thiazolyl)‑2, 5‑diphenyl‑2‑H‑tetrazolium bromide assay...
July 5, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28705612/cardiac-mitochondrial-dynamics-mir-mediated-regulation-during-cardiac-injury
#3
Anusha Sivakumar, Ramasamy Subbiah, Rekha Balakrishnan, Jeyaprakash Rajendhran
Mitochondrial integrity is indispensable for cardiac health. With the advent of modern imaging technologies, mitochondrial motility and dynamics within the cell are extensively studied. Terminally differentiated and well-structured cardiomyocytes depict little mitochondrial division and fusion, questioning the contribution of mitochondrial fusion proteins (Mitofusin 1/2 and Optic Atrophy 1 protein) and fission factors (Dynamin-like protein 1 and mitochondrial fission 1 protein) in cardiomyocyte homeostasis...
July 10, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28684211/age-related-accumulation-of-phosphorylated-mitofusin-2-protein-in-retinal-ganglion-cells-correlates-with-glaucoma-progression
#4
Mary P Nivison, Nolan G Ericson, Virginia M Green, Jason H Bielas, Jean S Campbell, Philip J Horner
Dysregulation of axonal bioenergetics is likely a key mechanism in the initiation and progression of age-related neurodegenerative diseases. Glaucoma is a quintessential neurodegenerative disorder characterized by progressive deterioration of the optic nerve (ON) and eventual death of retinal ganglion cells (RGCs). Age and elevation of intraocular pressure are key risk factors in glaucoma, but the common early hallmarks of decreased axonal transport and increased bioenergetic vulnerability likely underlie disease initiation...
July 3, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28677814/involvement-of-mitochondrial-dynamics-in-the-antineoplastic-activity-of-cisplatin-in-murine-leukemia-l1210-cells
#5
Xiao-Jian Han, Sheng-Lan Shi, Yong-Fang Wei, Li-Ping Jiang, Miao-Yu Guo, Hong-Li Wu, Yu-Ying Wan
Leukemia is a type of hematopoietic stem cell malignant cloned disease with high mortality. Cisplatin-based chemotherapy is one of the most common treatments for leukemia. Similar to other chemotherapeutic agents, cisplatin resistance has become a serious issue in cancer therapy. In the present study, we investigated the role of mitochondrial dynamics in the antineoplastic activity of cisplatin in murine leukemia L1210 cells. Firstly, the L1210 cell line resistant to cisplatin (L1210/DDP) was established. Compared to its parental cell line, the IC50 value of cisplatin in the L1210/DDP cells was increased 10-fold...
August 2017: Oncology Reports
https://www.readbyqxmd.com/read/28672961/salidroside-inhibits-high-glucose-induced-proliferation-of-vascular-smooth-muscle-cells-via-inhibiting-mitochondrial-fission-and-oxidative-stress
#6
Xinyu Zhuang, Alimujiang Maimaitijiang, Yong Li, Haiming Shi, Xiaofei Jiang
The mitochondria are highly dynamic organelles, carefully maintaining network homeostasis by regulating mitochondrial fusion and fission. Mitochondrial dynamics are involved in the regulation of a variety of pathophysiological processes, including cell proliferation. Oxidative stress serves an important role in the remodeling of arterial vascular tissue in diabetic patients by affecting the proliferation of vascular smooth muscle cells (VSMCs). Salidroside is the primary active component of Rhodiola rosea and has been demonstrated to be an antioxidant with cardio- and vascular-protective effects, in addition to improving glucose metabolism...
July 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28669827/mitochondria-elongation-is-mediated-through-sirt1-mediated-mfn1-stabilization
#7
Nguyen Thi Kim Oanh, Yong-Yea Park, Hyeseong Cho
Mitochondria are highly dynamic organelles that change size and morphology by fusing together or dividing through fission. In response to cellular cues, signaling cascades may post-translationally modify mitochondria-shaping proteins, which lead to a change in mitochondria morphology. Here we show that nicotinamide (NAM), an inhibitor of sirtuin deacetylases, promotes degradation of mitochondria fusion protein mitofusin 1 (MFN1), suggesting that acetylation status of MFN1 is important for its protein stability...
June 29, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28666985/keratins-regulate-%C3%AE-cell-mitochondrial-morphology-motility-and-homeostasis
#8
Jonas S G Silvander, Sofie M Kvarnström, Angeli Kumari-Ilieva, Anup Shrestha, Catharina M Alam, Diana M Toivola
Loss of the epithelial intermediate filament protein keratin 8 (K8) in murine β-cells leads to irregular insulin vesicles and decreased insulin levels. Because mitochondria are central in glucose-stimulated insulin secretion, the relationship between keratins and β-cell mitochondrial function and morphology was investigated. β-cells in murine K8 knockout (K8(-/-)) islets of Langerhans have increased numbers of mitochondria, which are rounder and have diffuse cristae, as seen by electron microscopy. The mitochondrial network in primary cultured K8(-/-) β-cells is more fragmented compared with K8(+/+) mitochondria, correlating with decreased levels of mitofusin 2 and the mitofusin 2- and keratin-binding protein trichoplein...
June 30, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28626117/physiological-roles-of-mitochondria-and-mitofusins-on-ca-2-signaling-in-smooth-muscles
#9
Hisao Yamamura, Yoshiaki Suzuki, Yuji Imaizumi
No abstract text is available yet for this article.
2017: Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
https://www.readbyqxmd.com/read/28608965/hydrogen-sulphide-modulating-mitochondrial-morphology-to-promote-mitophagy-in-endothelial-cells-under-high-glucose-and-high-palmitate
#10
Ning Liu, Jichao Wu, Linxue Zhang, Zhaopeng Gao, Yu Sun, Miao Yu, Yajun Zhao, Shiyun Dong, Fanghao Lu, Weihua Zhang
Endothelial cell dysfunction is one of the main reasons for type II diabetes vascular complications. Hydrogen sulphide (H2 S) has antioxidative effect, but its regulation on mitochondrial dynamics and mitophagy in aortic endothelial cells under hyperglycaemia and hyperlipidaemia is unclear. Rat aortic endothelial cells (RAECs) were treated with 40 mM glucose and 200 μM palmitate to imitate endothelium under hyperglycaemia and hyperlipidaemia, and 100 μM NaHS was used as an exogenous H2 S donor. Firstly, we demonstrated that high glucose and palmitate decreased H2 S production and CSE expression in RAECs...
June 13, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28607589/overexpression-of-mitochondrial-gtpase-mfn2-represents-a-negative-prognostic-marker-in-human-gastric-cancer-and-its-inhibition-exerts-anti-cancer-effects
#11
Chia-Lang Fang, Ding-Ping Sun, Han-Kun Chen, Chih-Chan Lin, Shih-Ting Hung, Yih-Huei Uen, Kai-Yuan Lin
Background: As one of the most common malignancies in the world, little is known about the molecular mechanism underlying gastric cancer (GC) and its progression. In this study, we aimed to investigate the clinical impact of the mitochondrial GTPase mitofusin 2 (MFN2) in GC. Methods: Immunohistochemistry was used to examine the expression levels of MFN2 in gastric tissues obtained from 141 patients with GC. The correlations between MFN2 protein level and clinicopathologic parameters, as well as the significance of MFN2 protein level for overall and disease-free survival were assessed...
2017: Journal of Cancer
https://www.readbyqxmd.com/read/28607491/an-ubiquitin-dependent-balance-between-mitofusin-turnover-and-fatty-acids-desaturation-regulates-mitochondrial-fusion
#12
Laetitia Cavellini, Julie Meurisse, Justin Findinier, Zoi Erpapazoglou, Naïma Belgareh-Touzé, Allan M Weissman, Mickael M Cohen
Mitochondrial integrity relies on homotypic fusion between adjacent outer membranes, which is mediated by large GTPases called mitofusins. The regulation of this process remains nonetheless elusive. Here, we report a crosstalk between the ubiquitin protease Ubp2 and the ubiquitin ligases Mdm30 and Rsp5 that modulates mitochondrial fusion. Ubp2 is an antagonist of Rsp5, which promotes synthesis of the fatty acids desaturase Ole1. We show that Ubp2 also counteracts Mdm30-mediated turnover of the yeast mitofusin Fzo1 and that Mdm30 targets Ubp2 for degradation thereby inducing Rsp5-mediated desaturation of fatty acids...
June 13, 2017: Nature Communications
https://www.readbyqxmd.com/read/28603693/cancer-untethering-mitochondria-from-the-endoplasmic-reticulum
#13
REVIEW
Maria Sol Herrera-Cruz, Thomas Simmen
Following the discovery of the mitochondria-associated membrane (MAM) as a hub for lipid metabolism in 1990 and its description as one of the first examples for membrane contact sites at the turn of the century, the past decade has seen the emergence of this structure as a potential regulator of cancer growth and metabolism. The mechanistic basis for this hypothesis is that the MAM accommodates flux of Ca(2+) from the endoplasmic reticulum (ER) to mitochondria. This flux then determines mitochondrial ATP production, known to be low in many tumors as part of the Warburg effect...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28602957/mitochondrial-dynamics-signaling-is-shifted-toward-fusion-in-muscles-of-very-old-hip-fractured-patients-results-from-the-sarcopenia-in-hip-fracture-shift-exploratory-study
#14
Anna Picca, Riccardo Calvani, Maria Lorenzi, Amerigo Menghi, Marco Galli, Raffaele Vitiello, Francesco Randisi, Roberto Bernabei, Francesco Landi, Emanuele Marzetti
BACKGROUND: Mitochondrial quality control (MQC) is crucial for maintaining mitochondrial fitness. We investigated MQC signaling in muscle of old hip-fractured patients. METHODS: Twenty-three patients, enrolled in the Sarcopenia in HIp FracTure (SHIFT) study, were categorized into old (OL; n=8) and very old groups (VOL; n=15) using 85years as the cut-off. The expression of a set of MQC signaling proteins was assayed in vastus lateralis muscle biopsies. RESULTS: The content of lysosome-associated membrane protein 2, microtubule-associated protein 1 light chain 3B, optic atrophy protein 1, fission protein 1 (Fis1), peroxisome proliferator-activated receptor-γ coactivator-1α, and forkhead box O3 was unvaried between groups...
June 7, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28593577/mir-125a-regulates-mitochondrial-homeostasis-through-targeting-mitofusin-1-to-control-hypoxic-pulmonary-vascular-remodeling
#15
Cui Ma, Chen Zhang, Mingfei Ma, Lixin Zhang, Linlin Zhang, Fengying Zhang, Yingli Chen, Fangyuan Cao, Minghui Li, Guangtian Wang, Tingting Shen, Hongmin Yao, Yumei Liu, Zhenwei Pan, Shasha Song, Daling Zhu
Abnormal pulmonary arterial smooth muscle cells (PASMCs) proliferation is an important pathological process in hypoxic pulmonary arterial hypertension. Mitochondrial dynamics and quality control have a central role in the maintenance of the cell proliferation-apoptosis balance. However, the molecular mechanism is still unknown. We used hypoxic animal models, cell biology, and molecular biology to determine the effect of mitofusin 1 (Mfn1) on hypoxia-mediated PASMCs mitochondrial homeostasis. We found that Mfn1 expression was increased in hypoxia, which was crucial for hypoxia-induced mitochondrial dysfunction and smooth muscle cell proliferation as well as hypoxia-stimulated cell-cycle transition from the G0/G1 phase to S phase...
June 7, 2017: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/28591639/mitochondrial-dynamics-mediated-by-mitofusin-1-is-required-for-pomc-neuron-glucose-sensing-and-insulin-release-control
#16
Sara Ramírez, Alicia G Gómez-Valadés, Marc Schneeberger, Luis Varela, Roberta Haddad-Tóvolli, Jordi Altirriba, Eduard Noguera, Anne Drougard, Álvaro Flores-Martínez, Mónica Imbernón, Iñigo Chivite, Macarena Pozo, Andrés Vidal-Itriago, Ainhoa Garcia, Sara Cervantes, Rosa Gasa, Ruben Nogueiras, Pau Gama-Pérez, Pablo M Garcia-Roves, David A Cano, Claude Knauf, Joan-Marc Servitja, Tamas L Horvath, Ramon Gomis, Antonio Zorzano, Marc Claret
Proopiomelanocortin (POMC) neurons are critical sensors of nutrient availability implicated in energy balance and glucose metabolism control. However, the precise mechanisms underlying nutrient sensing in POMC neurons remain incompletely understood. We show that mitochondrial dynamics mediated by Mitofusin 1 (MFN1) in POMC neurons couple nutrient sensing with systemic glucose metabolism. Mice lacking MFN1 in POMC neurons exhibited defective mitochondrial architecture remodeling and attenuated hypothalamic gene expression programs during the fast-to-fed transition...
June 6, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28587902/involvement-of-charcot-marie-tooth-disease-gene-mitofusin-2-expression-in-paclitaxel-induced-mechanical-allodynia-in-rats
#17
Yuta Yamashita, Keiichi Irie, Akane Kochi, Nami Kimura, Toshinobu Hayashi, Koichi Matsuo, Takayuki Myose, Kazunori Sano, Takafumi Nakano, Yumi Takase, Yoshihiko Nakamura, Tomomitsu Satho, Kenji Mishima, Kenichi Mishima
Paclitaxel induces peripheral neuropathy, which is dose-limiting and results in loss of quality of life. Therefore, the prevention and treatment of paclitaxel-induced peripheral neuropathy are major concerns in clinical cancer therapy. However, the detailed mechanisms have not been fully elucidated. It has recently been reported that allelic variability in the Charcot-Marie-Tooth disease (CMT) genes, mitofusin 2 (MFN2), Rho guanine nucleotide exchange factor 10 (ARHGEF10), and periaxin (PRX), affected paclitaxel-induced peripheral neuropathy in clinical cases...
July 13, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28539410/leishmania-donovani-restricts-mitochondrial-dynamics-to-enhance-mirnp-stability-and-target-rna-repression-in-host-macrophages
#18
Yogaditya Chakrabarty, Suvendra N Bhattacharyya
MicroRNAs (miRNAs), the tiny regulatory RNAs, form complexes with Argonaute (Ago) proteins and inhibit gene expression in metazoan cells. While studying parasite-invaded macrophages, we identify a unique mode of gene regulation in which the parasite Leishmania donovani (Ld) causes mitochondrial depolarization, reduces mitochondrial dynamics, and restricts turnover of cellular microRNA ribonucleoprotein (miRNP) complexes in infected host cells. This leads to increased stability of miRNPs along with elevated levels of Ago2-bound cytokine mRNA in Ld-infected macrophages...
July 15, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/28539390/mfn2-deletion-in-brown-adipose-tissue-protects-from-insulin-resistance-and-impairs-thermogenesis
#19
Kiana Mahdaviani, Ilan Y Benador, Shi Su, Raffi A Gharakhanian, Linsey Stiles, Kyle M Trudeau, Maria Cardamone, Violeta Enríquez-Zarralanga, Eleni Ritou, Tamar Aprahamian, Marcus F Oliveira, Barbara E Corkey, Valentina Perissi, Marc Liesa, Orian S Shirihai
BAT-controlled thermogenic activity is thought to be required for its capacity to prevent the development of insulin resistance. This hypothesis predicts that mediators of thermogenesis may help prevent diet-induced insulin resistance. We report that the mitochondrial fusion protein Mitofusin 2 (Mfn2) in BAT is essential for cold-stimulated thermogenesis, but promotes insulin resistance in obese mice. Mfn2 deletion in mice through Ucp1-cre (BAT-Mfn2-KO) causes BAT lipohypertrophy and cold intolerance. Surprisingly however, deletion of Mfn2 in mice fed a high fat diet (HFD) results in improved insulin sensitivity and resistance to obesity, while impaired cold-stimulated thermogenesis is maintained...
May 24, 2017: EMBO Reports
https://www.readbyqxmd.com/read/28539389/let-s-burn-whatever-you-have-mitofusin-2-metabolically-re-wires-brown-adipose-tissue
#20
Marcel Scheideler, Stephan Herzig
No abstract text is available yet for this article.
May 24, 2017: EMBO Reports
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