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Jing Wu, Shuangying Hao, Xiao-Ru Sun, Hui Zhang, Huihui Li, Hongting Zhao, Mu-Huo Ji, Jian-Jun Yang, Kuanyu Li
Mitochondria are supposed to be involved in the early pathogenesis of general anesthesia (GA)-induced neurotoxicity and long-term cognitive deficits in developing brains. However, effective pharmacologic agents targeted on mitochondria during GA exposure are lacking. This study explores the protective effects of mitochondrion-targeted antioxidant elamipretide (SS-31) on mitochondrial morphogenesis and cognition in developing rats exposed to isoflurane. Rat pups at postnatal day (PND) 7 were exposed to 1.5% isoflurane for 6 h following intraperitoneal administration of elamipretide or vehicle with 30 min interval...
2017: Frontiers in Cellular Neuroscience
Hao Zhao, Yan-Jun Liu, Zong-Rui Liu, Dong-Dong Tang, Xiao-Wen Chen, Yi-Hua Chen, Ru-Ning Zhou, Si-Qi Chen, Hong-Xin Niu
Oxidative stress aggravates renal fibrosis, a pathway involved in almost all forms of chronic kidney disease (CKD). However, the underlying mechanism involved in the pathogenesis of renal oxidative stress has not been completely elucidated. In this study, we explored the role and mechanism of hypochlorite-modified albumin (HOCl-alb) in mediating oxidative stress and fibrotic response in a remnant-kidney rat model. Five-sixths nephrectomy (5/6 NX) was performed on the rats and then the animals were randomly assigned to intravenous treatment with either vehicle alone, or HOCl-rat serum albumin (RSA) in the presence or absence of SS-31 (administered intraperitoneally)...
June 5, 2017: European Journal of Pharmacology
Mariya T Sweetwyne, Jeffrey W Pippin, Diana G Eng, Kelly L Hudkins, Ying Ann Chiao, Matthew D Campbell, David J Marcinek, Charles E Alpers, Hazel H Szeto, Peter S Rabinovitch, Stuart J Shankland
Although age-associated changes in kidney glomerular architecture have been described in mice and man, the mechanisms are unknown. It is unclear if these changes can be prevented or even reversed by systemic therapies administered at advanced age. Using light microscopy and transmission electron microscopy, our results showed glomerulosclerosis with injury to mitochondria in glomerular epithelial cells in mice aged 26 months (equivalent to a 79-year-old human). To test the hypothesis that reducing mitochondrial damage in late age would result in lowered glomerulosclerosis, we administered the mitochondrial targeted peptide, SS-31, to aged mice...
May 2017: Kidney International
Hazel H Szeto, Shaoyi Liu, Yi Soong, Surya V Seshan, Leona Cohen-Gould, Viacheslav Manichev, Leonard C Feldman, Torgny Gustafsson
The innate immune system has been implicated in both AKI and CKD. Damaged mitochondria release danger molecules, such as reactive oxygen species, DNA, and cardiolipin, which can cause NLRP3 inflammasome activation and upregulation of IL-18 and IL-1β It is not known if mitochondrial damage persists long after ischemia to sustain chronic inflammasome activation. We conducted a 9-month study in Sprague-Dawley rats after 45 minutes of bilateral renal ischemia. We detected glomerular and peritubular capillary rarefaction, macrophage infiltration, and fibrosis at 1 month...
May 2017: Journal of the American Society of Nephrology: JASN
Takahiko Imai, Keisuke Mishiro, Toshinori Takagi, Aoi Isono, Hideko Nagasawa, Kazuhiro Tsuruma, Masamitsu Shimazawa, Hideaki Hara
Mitochondria play a key role in cell survival by perfoming functions such as adenosine tri-phosphate (ATP) synthesis, regulation of apoptotic cell death, calcium storage. Hypoxic conditions induce mitochondrial dysfunction, which leads to endothelial injury in cerebral ischemia. Functional disorders include the following: collapse of mitochondrial membrane potential, reduction of ATP synthesis, and generation of reactive oxygen species (ROS). Bendavia, a novel tetra-peptide, has been reported to restrict the uncoupling of the mitochondrial membrane chain, protect the synthesis of ATP, and inhibit ROS generation...
November 17, 2016: Current Neurovascular Research
Hazel H Szeto, Shaoyi Liu, Yi Soong, Nazia Alam, Glen T Prusky, Surya V Seshan
Obesity is a major risk factor for the development of chronic kidney disease, even independent of its association with hypertension, diabetes, and dyslipidemia. The primary pathologic finding of obesity-related kidney disease is glomerulopathy, with glomerular hypertrophy, mesangial matrix expansion, and focal segmental glomerulosclerosis. Proposed mechanisms leading to renal pathology include abnormal lipid metabolism, lipotoxicity, inhibition of AMP kinase, and endoplasmic reticulum stress. Here we report dramatic changes in mitochondrial structure in glomerular endothelial cells, podocytes, and proximal tubular epithelial cells after 28 weeks of a high-fat diet in C57BL/6 mice...
November 2016: Kidney International
Yu Pang, Chao Wang, Ling Yu
Glaucoma is the second leading cause of irreversible blindness and a neurodegenerative disease with a complex pathogenesis. Increasing evidence suggests that oxidative stress and mitochondrial dysfunction have crucial roles in most neurodegenerative diseases such as glaucoma. The conventional clinical treatment for glaucoma is lowering the intraocular pressure (IOP). Some patients have normal IOP, whereas other patients appear to obtain adequate control of IOP after filtration surgery or medication. However, these patients still experience progressive visual field loss...
2015: Medical Hypothesis, Discovery and Innovation in Ophthalmology
M C W Schoenell, C L Alberton, C L Tiggemann, M Noll, R Costa, N S Santos, L F M Kruel
This study aims to analyze the neuromuscular adaptations of sedentary young women between water-based resistance training performed with single and multiple sets. 66 women (24.72±4.33 years old) were randomly divided into 2 training groups: SS (single set of 30 s) and MS (3 sets of 30 s). Both groups performed 2 sessions per week for 10 weeks. One repetition maximal test (1RM), muscle endurance test (maximal repetitions at 60% 1RM) and muscle power test (squat and countermovement jump performance) were evaluated at pre- and post-training...
September 2016: International Journal of Sports Medicine
Leonie G M Wijermars, Alexander F Schaapherder, Dorottya K de Vries, Lars Verschuren, Rob C I Wüst, Sarantos Kostidis, Oleg A Mayboroda, Frans Prins, Jan Ringers, Jörgen Bierau, Jaap A Bakker, Teake Kooistra, Jan H N Lindeman
Delayed graft function (DGF) following kidney transplantation affects long-term graft function and survival and is considered a manifestation of ischemia reperfusion injury. Preclinical studies characterize metabolic defects resulting from mitochondrial damage as primary driver of ischemia reperfusion injury. In a comprehensive approach that included sequential establishment of postreperfusion arteriovenous concentration differences over the human graft, metabolomic and genomic analysis in tissue biopsies taken before and after reperfusion, we tested whether the preclinical observations translate to the context of clinical DGF...
July 2016: Kidney International
Jae Hyo Park, Gil Su Jang, Hyung Yoon Kim, Ki Hwan Seok, Hee Jae Chae, Sol Kyu Lee, Seung Ki Joo
Realizing a low-temperature polycrystalline-silicon (LTPS) thin-film transistor (TFT) with sub-kT/q subthreshold slope (SS) is significantly important to the development of next generation active-matrix organic-light emitting diode displays. This is the first time a sub-kT/q SS (31.44 mV/dec) incorporated with a LTPS-TFT with polycrystalline-Pb(Zr,Ti)O3 (PZT)/ZrTiO4 (ZTO) gate dielectrics has been demonstrated. The sub-kT/q SS was observed in the weak inversion region at -0.5 V showing ultra-low operating voltage with the highest mobility (250...
April 21, 2016: Scientific Reports
Hung-I Lu, Tien-Hung Huang, Pei-Hsun Sung, Yung-Lung Chen, Sarah Chua, Han-Yan Chai, Sheng-Ying Chung, Chu-Feng Liu, Cheuk-Kwan Sun, Hsueh-Wen Chang, Yen-Yi Zhen, Fan-Yen Lee, Hon-Kan Yip
AIM: Antioxidant peptide SS-31 is a class of cell-permeable small peptides, which selectively resides on the inner mitochondrial membrane and possesses intrinsic mitochondrial protective capacities. In this study we investigated the therapeutic effects of antioxidant peptide SS-31 on transverse aortic constriction (TAC)-induced pulmonary arterial hypertension (PAH) in a murine model. METHODS: Adult male mice were divided into 3 groups: sham-operated mice, TAC mice, and TAC+SS-31 mice that underwent TAC surgery and received SS-31 (2 mg/d, ip) for 60 d...
May 2016: Acta Pharmacologica Sinica
Jing Wu, Mingqiang Zhang, Huihui Li, Xiaoru Sun, Shuangying Hao, Muhuo Ji, Jianjun Yang, Kuanyu Li
Mitochondrial dysfunction has been linked to the earliest pathogenesis of isoflurane-induced cognitive impairments in developing or aging mammalian brain. However, its molecular mechanism is poorly understood and a pharmacologic treatment to rapidly reverse mitochondrial dysfunction is lacking. Fifteen-month-old male C57BL/6 mice were exposed to isoflurane for two hours following intraperitoneal administration of mitochondrion-targeted peptide SS-31 or vehicle with 30min interval. The hippocampus was immediately removed for biochemical assays and mitochondria isolation after inhalation...
May 15, 2016: Behavioural Brain Research
Yanjuan Hou, Shuangcheng Li, Ming Wu, Jinying Wei, Yunzhuo Ren, Chunyang Du, Haijiang Wu, Caili Han, Huijun Duan, Yonghong Shi
Oxidative stress is implicated in the pathogenesis of diabetic kidney injury. SS-31 is a mitochondria-targeted tetrapeptide that can scavenge reactive oxygen species (ROS). Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience. CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk...
March 15, 2016: American Journal of Physiology. Renal Physiology
Caterina Constantinou, Yiorgos Apidianakis, Nikolaos Psychogios, Valeria Righi, Michael N Mindrinos, Nadeem Khan, Harold M Swartz, Hazel H Szeto, Ronald G Tompkins, Laurence G Rahme, A Aria Tzika
Trauma is the most common cause of mortality among individuals aged between 1 and 44 years and the third leading cause of mortality overall in the US. In this study, we examined the effects of trauma on the expression of genes in Drosophila melanogaster, a useful model for investigating genetics and physiology. After trauma was induced by a non-lethal needle puncture of the thorax, we observed the differential expression of genes encoding for mitochondrial uncoupling proteins, as well as those encoding for apoptosis-related and insulin signaling-related proteins, thus indicating muscle functional dysregulation...
February 2016: International Journal of Molecular Medicine
Shuangying Hao, Jiajie Ji, Hongting Zhao, Longcheng Shang, Jing Wu, Huihui Li, Tong Qiao, Kuanyu Li
Foam cell formation as a result of imbalance of modified cholesterol influx and efflux by macrophages is a key to the occurrence and development of atherosclerosis. Oxidative stress is thought to be involved in the pathogenesis of atherosclerosis. SS-31 is a member of the Szeto-Schiller (SS) peptides shown to specifically target the inner mitochondrial membrane to scavenge reactive oxygen species. In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264...
2015: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
Jing Wu, Huihui Li, Xiaoru Sun, Hui Zhang, Shuangying Hao, Muhuo Ji, Jianjun Yang, Kuanyu Li
Isoflurane possesses neurotoxicity and can induce cognitive deficits, particularly in aging mammals. Mitochondrial reactive oxygen species (mtROS) have been linked to the early pathogenesis of this disorder. However, the role of mtROS remains to be evaluated due to a lack of targeted method to treat mtROS. Here, we determined in aging mice the effects of the mitochondrion-targeted antioxidant SS-31, on cognitive deficits induced by isoflurane, a general inhalation anesthetic. We further investigated the possible mechanisms underlying the effects of SS-31 on hippocampal neuro-inflammation and apoptosis...
2015: PloS One
Adam P Lightfoot, Giorgos K Sakellariou, Gareth A Nye, Francis McArdle, Malcolm J Jackson, Richard D Griffiths, Anne McArdle
TNF-α is a key inflammatory mediator and is proposed to induce transcriptional responses via the mitochondrial generation of Reactive Oxygen Species (ROS). The aim of this study was to determine the effect of TNF-α on the production of myokines by skeletal muscle. Significant increases were seen in the release of IL-6, MCP-1/CCL2, RANTES/CCL5 and KC/CXCL1 and this release was inhibited by treatment with Brefeldin A, suggesting a golgi-mediated release of cytokines by muscle cells. An increase was also seen in superoxide in response to treatment with TNF-α, which was localised to the mitochondria and this was also associated with activation of NF-κB...
December 2015: Redox Biology
Alexander G Nickel, Albrecht von Hardenberg, Mathias Hohl, Joachim R Löffler, Michael Kohlhaas, Janne Becker, Jan-Christian Reil, Andrey Kazakov, Julia Bonnekoh, Moritz Stadelmaier, Sarah-Lena Puhl, Michael Wagner, Ivan Bogeski, Sonia Cortassa, Reinhard Kappl, Bastian Pasieka, Michael Lafontaine, C Roy D Lancaster, Thomas S Blacker, Andrew R Hall, Michael R Duchen, Lars Kästner, Peter Lipp, Tanja Zeller, Christian Müller, Andreas Knopp, Ulrich Laufs, Michael Böhm, Markus Hoth, Christoph Maack
Mitochondrial reactive oxygen species (ROS) play a central role in most aging-related diseases. ROS are produced at the respiratory chain that demands NADH for electron transport and are eliminated by enzymes that require NADPH. The nicotinamide nucleotide transhydrogenase (Nnt) is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH. Here, we show that pathological metabolic demand reverses the direction of the Nnt, consuming NADPH to support NADH and ATP production, but at the cost of NADPH-linked antioxidative capacity...
September 1, 2015: Cell Metabolism
Camila Nunes Carvalho, Rodrigo Feliciano do Carmo, Angela Luzia Pinto Duarte, Alessandra Albuquerque Tavares Carvalho, Jair Carneiro Leão, Luiz Alcino Gueiros
OBJECTIVE: The aim of this study was to evaluate the influence of Th17 polymorphisms on the susceptibility or severity of rheumatoid arthritis (RA) and Sjögren's syndrome (SS). MATERIALS AND METHODS: The study sample comprised 206 individuals of both genders divided into three groups: exclusive rheumatoid arthritis (RA-100 patients), rheumatoid arthritis and Sjögren's syndrome (RA/SS-31 patients), and healthy controls (C-75 individuals). All the individuals were submitted to clinical evaluation, unstimulated sialometry, and Schirmer test; some patients with RA were also submitted to minor salivary gland biopsy for definition of SS diagnosis...
April 2016: Clinical Oral Investigations
Guoming Li, Jing Wu, Renqi Li, Dong Yuan, Yunxia Fan, Jianjun Yang, Muhuo Ji, Sihai Zhu
Oxidative stress causes mitochondrial impairment, the failure of energy production, and consequent organ dysfunctions. The aim of the present study was to investigate the potential therapeutic effects of mitochondrial antioxidant SS-31 on sepsis-induced organ dysfunctions and to explore the possible mechanism. Sepsis was induced by cecal ligation and puncture. Immediately and at 5 h after the operation, SS-31 (5 mg/kg) or vehicle was administered intraperitoneally. The levels of organ dysfunctions, malondialdehyde, superoxide dismutase, proinflammatory cytokines, pulmonary wet-to-dry weight ratio, myeloperoxidase activity, histological scores, nuclear factor kappa B p65, inducible nitric oxide synthase, reactive oxygen species, adenosine triphosphate, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells were assessed at the indicated time points...
February 2016: Inflammation
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