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https://www.readbyqxmd.com/read/27893424/accumulated-promoter-methylation-as-a-potential-biomarker-for-esophageal-cancer
#1
Xianzhen Peng, Hengchuan Xue, Lingshuang Lü, Peiyi Shi, Jianping Wang, Jianming Wang
We performed a two-stage molecular epidemiological study to explore DNA methylation profiles for potential biomarkers of esophageal squamous cell carcinoma (ESCC) in a Chinese population. Infinium Methylation 450K BeadChip was used to identify genes with differentially methylated CpG sites. Sixteen candidate genes were validated by sequencing 1160 CpG sites in their promoter regions using the Illumina MiSeq platform. When excluding sites with negative changes, 10 genes (BNIP3, BRCA1, CCND1, CDKN2A, HTATIP2, ITGAV, NFKB1, PIK3R1, PRDM16 and PTX3) showed significantly different methylation levels among cancer lesions, remote normal-appearing tissues, and healthy controls...
November 22, 2016: Oncotarget
https://www.readbyqxmd.com/read/27886395/popdc1-bves-functions-in-the-preservation-of-cardiomyocyte-viability-while-affecting-rac1-activity-and-bnip3-expression
#2
Kliminski Vitaly, Uziel Orit, Kessler-Icekson Gania
The Popeye domain containing1, also called Bves (Popdc1/Bves), is a transmembrane protein that functions in muscle regeneration, heart rate regulation, hypoxia tolerance, and ischemia preconditioning. The expression of Popdc1/Bves is elevated in cardiomyocytes maintained in serum free defined medium. We hypothesized that Popdc1/Bves is important for cardiomyocyte survival under the stress of serum deprivation and investigated the mechanisms involved. A deficit in Popdc1/Bves, achieved by siRNA-mediated gene silencing, results in cardiomyocyte injury and death, upregulation of the pro-apoptotic protein Bcl-2/adenovirus E1B 19-kDa interacting protein3 (Bnip3), as well as reduction in Rac1-GTPase activity and in Akt phosphorylation...
November 25, 2016: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/27864279/nutrition-deficiency-promotes-apoptosis-of-cartilage-endplate-stem-cells-in-a-caspase-independent-manner-partially-through-upregulating-bnip3
#3
Zhiliang He, Luqiao Pu, Chao Yuan, Min Jia, Jian Wang
Nutrition deficiency is reported to induce apoptosis of chondrocytes and degeneration of cartilage endplate (CEP) in rabbit. Cartilage endplate stem cells (CESCs) are important for the integrity of structure and function of CEP. Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3) has been reported to regulate apoptosis, autophagy, and cytoprotection. In this study, we aimed to determine whether nutrition deficiency induces apoptosis of CESCs, and whether or not the BNIP3-related pathway is activated in CESCs during nutrition deficiency...
November 17, 2016: Acta Biochimica et Biophysica Sinica
https://www.readbyqxmd.com/read/27862640/long-non-coding-rna-malat1-functions-as-a-mediator-in-cardioprotective-effects-of-fentanyl-in-myocardial-ischemia-reperfusion-injury
#4
Zhi-Hui Zhao, Wei Hao, Qing-Tao Meng, Xiao-Bing Du, Shao-Qing Lei, Zhong-Yuan Xia
Long non-coding (lncRNA) MALAT1 can be increased by hypoxia or ischemic limbs. Also downregulation of MALAT1 contributes to reduction of cardiomyocyte apoptosis. However, the functional involvement of MALAT1 in myocardial ischemia-reperfusion (I/R) injury has not been defined. This study investigated the functional involvement of lncRNA-MALAT1 in cardioprotective effects of fentanyl. HL-1, a cardiac muscle cell line from the AT-1 mouse atrial cardiomyocyte tumor lineage, was pre-treated with fentanyl and generated cell model of hypoxia-reoxygenation (H/R)...
November 9, 2016: Cell Biology International
https://www.readbyqxmd.com/read/27861891/opa1-haploinsufficiency-induces-a-bnip3-dependent-decrease-in-mitophagy-in-neurons-relevance-to-dominant-optic-atrophy
#5
Manon Moulis, Aurélie Millet, Marlène Daloyau, Marie-Christine Miquel, Brice Ronsin, Bernd Wissinger, Laetitia Arnauné-Pelloquin, Pascale Belenguer
Dominant Optic Atrophy (DOA) is due to mutations in the mitochondrial protein OPA1. The disease principally affects retinal ganglion cells, whose axons degenerate leading to vision impairments, and sometimes other neuronal phenotypes. The exact mechanisms underlying DOA pathogenesis are not known. We previously demonstrated that the main role of OPA1, as a mitochondrial fusogenic and anti-apoptotic protein, are inhibited by interaction with the stress inducible pro-apoptotic BNIP3 protein. Because BNIP3 was recently reported to participate in autophagy and mitophagy, we tested the involvement of these processes in DOA pathogenesis...
November 10, 2016: Journal of Neurochemistry
https://www.readbyqxmd.com/read/27858285/the-role-of-hypoxia-inducible-factor-1-in-mild-cognitive-impairment
#6
REVIEW
Osigbemhe Iyalomhe, Sabina Swierczek, Ngozi Enwerem, Yuanxiu Chen, Monica O Adedeji, Joanne Allard, Oyonumo Ntekim, Sheree Johnson, Kakra Hughes, Philip Kurian, Thomas O Obisesan
Neuroinflammation and reactive oxygen species are thought to mediate the pathogenesis of Alzheimer's disease (AD), suggesting that mild cognitive impairment (MCI), a prodromal stage of AD, may be driven by similar insults. Several studies document that hypoxia-inducible factor 1 (HIF-1) is neuroprotective in the setting of neuronal insults, since this transcription factor drives the expression of critical genes that diminish neuronal cell death. HIF-1 facilitates glycolysis and glucose metabolism, thus helping to generate reductive equivalents of NADH/NADPH that counter oxidative stress...
November 17, 2016: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/27837193/intact-initiation-of-autophagy-and-mitochondrial-fission-by-acute-exercise-in-skeletal-muscle-of-patientswith-type-2-diabetes
#7
Rikke Kruse, Andreas J T Pedersen, Jonas M Kristensen, Stine J Petersson, Jørgen F P Wojtaszewski, Kurt Højlund
AIMS: Type 2 diabetes (T2D) is characterized by insulin resistance, mitochondrial dysregulation, and, in some studies, exercise resistance in skeletal muscle. Regulation of autophagy and mitochondrial dynamics during exercise and recovery is important for skeletal muscle homeostasis, and these responses may be altered in T2D. MATERIALS AND METHODS: We examined the effect of acute exercise on markers of autophagy and mitochondrial fusion and fission in skeletal muscle biopsies from patients with T2D (n=13) and weight-matched controls (n=14) before, immediately after and 3h after an acute bout of exercise...
November 11, 2016: Clinical Science (1979-)
https://www.readbyqxmd.com/read/27807188/autophagy-induction-results-in-enhanced-anoikis-resistance-in-models-of-peritoneal-disease
#8
James L Chen, Jason David, Douglas Cook-Spaeth, Sydney Casey, David Cohen, Karuppaiyah Selvendiran, Tanios Bekaii-Saab, John Hays
: Peritoneal carcinomatosis and peritoneal sarcomatosis (PC/PS) is a potential complication of nearly all solid tumors and results in profoundly increased morbidity and mortality. Despite the ubiquity of PC/PS, there are no clinically relevant targeted therapies for either its treatment or prevention. To identify potential therapies, we developed in vitro models of PC/PS using tumor cell lines and patient-derived spheroids (PDS) that recapitulate anoikis resistance and spheroid proliferation across multiple cancer types...
November 2, 2016: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/27800505/fifteen-days-of-3-200-m-simulated-hypoxia-marginally-regulates-markers-for-protein-synthesis-and-degradation-in-human-skeletal-muscle
#9
Gommaar D'Hulst, Alessandra Ferri, Damien Naslain, Luc Bertrand, Sandrine Horman, Marc Francaux, David J Bishop, Louise Deldicque
Chronic hypoxia leads to muscle atrophy. The molecular mechanisms responsible for this phenomenon are not well defined in vivo. We sought to determine how chronic hypoxia regulates molecular markers of protein synthesis and degradation in human skeletal muscle and whether these regulations were related to the regulation of the hypoxia-inducible factor (HIF) pathway. Eight young male subjects lived in a normobaric hypoxic hotel (FiO2 14.1%, 3,200 m) for 15 days in well-controlled conditions for nutrition and physical activity...
2016: Hypoxia
https://www.readbyqxmd.com/read/27787518/glioblastoma-hypoxia-and-autophagy-a-survival-prone-m%C3%A3-nage-%C3%A3-trois
#10
REVIEW
Soha Jawhari, Marie-Hélène Ratinaud, Mireille Verdier
Glioblastoma multiforme is the most common and the most aggressive primary brain tumor. It is characterized by a high degree of hypoxia and also by a remarkable resistance to therapy because of its adaptation capabilities that include autophagy. This degradation process allows the recycling of cellular components, leading to the formation of metabolic precursors and production of adenosine triphosphate. Hypoxia can induce autophagy through the activation of several autophagy-related proteins such as BNIP3, AMPK, REDD1, PML, and the unfolded protein response-related transcription factors ATF4 and CHOP...
October 27, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27783443/bnip3-promotes-the-motility-and-migration-of-keratinocyte-under-hypoxia
#11
Junhui Zhang, Dongxia Zhang, Tiantian Yan, Xupin Jiang, Can Zhang, Liping Zhao, Lingfei Li, Di Tang, Qiong Zhang, Jiezhi Jia, Jiaping Zhang, Yuesheng Huang
The migration of keratinocytes from wound margins plays a critical role in the re-epithelialization of skin wounds. Hypoxia occurs immediately after injury and acts as an early stimulus to initiate the healing processes. Although our previous studies have revealed that hypoxia promotes keratinocyte migration, the precise mechanisms involved remain unclear. Here, we found that BNIP3 expression was up-regulated in hypoxic keratinocytes, and BNIP3 silencing suppressed hypoxia-induced cell migration. Additionally, hypoxia activated the FAK pathway through up-regulation of BNIP3, while FAK inhibition attenuated hypoxic keratinocyte migration...
October 26, 2016: Experimental Dermatology
https://www.readbyqxmd.com/read/27746856/coordinated-upregulation-of-mitochondrial-biogenesis-and-autophagy-in-breast-cancer-cells-the-role-of-dynamin-related-protein-1-and-implication-for-breast-cancer-treatment
#12
Peng Zou, Longhua Liu, Louise D Zheng, Kyle K Payne, Masoud H Manjili, Michael O Idowu, Jinfeng Zhang, Eva M Schmelz, Zhiyong Cheng
Overactive mitochondrial fission was shown to promote cell transformation and tumor growth. It remains elusive how mitochondrial quality is regulated in such conditions. Here, we show that upregulation of mitochondrial fission protein, dynamin related protein-1 (Drp1), was accompanied with increased mitochondrial biogenesis markers (PGC1α, NRF1, and Tfam) in breast cancer cells. However, mitochondrial number was reduced, which was associated with lower mitochondrial oxidative capacity in breast cancer cells...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27738772/the-cardioprotective-effect-of-dihydromyricetin-prevents-ischemia-reperfusion-induced-apoptosis-in-vivo-and-in-vitro-via-the-pi3k-akt-and-hif-1%C3%AE-signaling-pathways
#13
Shasha Liu, Qidi Ai, Kai Feng, Yubing Li, Xiang Liu
Reperfusion therapy is widely used to treat acute myocardial infarction (AMI). However, further injury to the heart induced by rapidly initiating reperfusion is often encountered in clinical practice. A lack of pharmacological strategies in clinics limits the prognosis of patients with myocardial ischemia-reperfusion injury (MIRI). Dihydromyricetin (DMY) is one of the most abundant components in vine tea, commonly known as the tender stems and leaves of Ampelopsis grossedentata. The aim of this study was to evaluate the cardioprotection of DMY against myocardial ischemia-reperfusion (I/R) injury and to further investigate the underlying mechanism...
December 2016: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/27694219/foxo3a-regulates-bnip3-and-modulates-mitochondrial-calcium-dynamics-and-function-in-cardiac-stress
#14
Antoine H Chaanine, Erik Kohlbrenner, Scott I Gamb, Adam J Guenzel, Katherine Klaus, Ahmed U Fayyaz, K Sreekumaran Nair, Roger J Hajjar, Margaret M Redfield
The forkhead box O3a (FOXO3a) transcription factor has been shown to regulate glucose metabolism, muscle atrophy, and cell death in postmitotic cells. Its role in regulation of mitochondrial and myocardial function is not well studied. Based on previous work, we hypothesized that FOXO3a, through BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 (BNIP3), modulates mitochondrial morphology and function in heart failure (HF). We modulated the FOXO3a-BNIP3 pathway in normal and phenylephrine (PE)-stressed adult cardiomyocytes (ACM) in vitro and developed a cardiotropic adeno-associated virus serotype 9 encoding dominant-negative FOXO3a (AAV9...
December 1, 2016: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/27677502/protein-coingestion-with-alcohol-following-strenuous-exercise-attenuates-alcohol-induced-intramyocellular-apoptosis-and-inhibition-of-autophagy
#15
William J Smiles, Evelyn B Parr, Vernon G Coffey, Orly Lacham-Kaplan, John A Hawley, Donny M Camera
Alcohol ingestion decreases post-exercise rates of muscle protein synthesis, but the mechanism(s) (e.g., increased protein breakdown) underlying this observation are unknown. Autophagy is an intracellular "recycling" system required for homeostatic substrate and organelle turnover; its dysregulation may provoke apoptosis and lead to muscle atrophy. We investigated the acute effects of alcohol ingestion on autophagic cell signaling responses to a bout of concurrent (combined resistance- and endurance-based) exercise...
September 27, 2016: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/27608954/knockout-of-programmed-cell-death-5-pdcd5-gene-attenuates-neuron-injury-after-middle-cerebral-artery-occlusion-in-mice
#16
Jianfei Lu, Zhao Jiang, Yingyu Chen, Changman Zhou, Chunhua Chen
Loss of von Hippel-Lindau tumor suppressor protein (VHL) or hypoxia results in nuclear relocalization of PDCD5 and subsequent mouse double minute 2 homolog (Mdm2) degradation. Thus, VHL may involved in the PDCD5 mediated apoptosis and autophagy after MCAO. In the present study, using PDCD5 knockout (PDCD5(-/-)) mice, we aimed to demonstrate that knockout of PDCD5 gene could protect the brain from ischemic injury by inhibiting the PDCD5-VHL pathway. 24h post MCAO surgery, PDCD5 gene knockout mice presented obvious improved brain blood flow, improved neurological behavior and decreased cerebral infarction compared with wild type mice...
November 1, 2016: Brain Research
https://www.readbyqxmd.com/read/27604425/gemcitabine-induced-autophagy-protects-human-lung-cancer-cells-from-apoptotic-death
#17
Hui-Mei Wu, Li-Jie Shao, Zi-Feng Jiang, Rong-Yu Liu
PURPOSE: Gemcitabine has been used as a therapeutic drug combined with cisplatin for the treatment of lung cancer patients. However, the prognosis is poor due to acquired resistance. Accumulating studies have revealed that autophagy may contribute to the drug resistance. Therefore, the present study is aimed to clarify the mechanisms underlying gemcitabine-acquired resistance. METHODS: SPC-A1 and A549 cells were incubated with gemcitabine followed by assessment of cell viability with MTT assays...
September 7, 2016: Lung
https://www.readbyqxmd.com/read/27592257/armillaridin-induces-autophagy-associated-cell-death-in-human-chronic-myelogenous-leukemia-k562-cells
#18
Wen-Han Chang, Huey-Lan Huang, Wei-Pang Huang, Chien-Chih Chen, Yu-Jen Chen
Armillaridin (AM) is an aromatic ester compound isolated from Armillaria mellea. Treatment with AM markedly reduced the viability of human chronic myelogenous leukemia K562, chronic erythroleukemia HEL 92.1.7, and acute monoblastic leukemia U937 cells, but not normal human monocytes, in a dose- and time-dependent manner. Treatment of K562 cells with AM caused changes characteristic of autophagy. Only a small amount of AM-treated K562 cells exhibited apoptosis. By contrast, AM treatment resulted in extensive apoptotic features in U937 and HEL 92...
September 3, 2016: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/27567705/rna-sequence-analyses-of-r-moj-dm-treated-cells-txnip-is-required-to-induce-apoptosis-of-sk-mel-28
#19
Terri D McBride, U Andrew, Nicko Ly, Julio G Soto
RNA sequencing of untreated and r-Moj-DM treated SK-Mel-28 cells was performed after 6 h, to begin unraveling the apoptotic pathway induced by r-Moj-DM. Bioinformatic analyses of RNA sequencing data yielded 40 genes that were differentially expressed. Nine genes were upregulated and 31 were downregulated. qRT-PCR was used to validate differential expression of 13 genes with known survival or apoptotic-inducing activities. Expression of BNiP3, IGFBP3, PTPSF, Prune 2, TGF-ß, and TXNIP were compared from cells treated with r-Moj-DN (a strong apoptotic inducer) or r-Moj-DA (a non-apoptotic inducer) for 1 h, 2 h, 4 h, and 6 h after treatment...
October 2016: Toxicon: Official Journal of the International Society on Toxinology
https://www.readbyqxmd.com/read/27567590/long-term-treatment-with-nicotinamide-induces-glucose-intolerance-and-skeletal-muscle-lipotoxicity-in-normal-chow-fed-mice-compared-to-diet-induced-obesity
#20
Zhengtang Qi, Jie Xia, Xiangli Xue, Qiang He, Liu Ji, Shuzhe Ding
Nicotinamide (NAM), or vitamin B3, is an essential coenzyme for ATP synthesis and an inhibitor of sirtuin 1. Recently, conflicting results were reported regarding the treatment of NAM in type 2 diabetes and obesity. The aim of this study was to determine whether and how long-term treatment with NAM at lower dose would affect insulin sensitivity in mice fed chow diet. We treated mice with NAM (100 mg/kg/day) and normal chow for 8 weeks. Strikingly, NAM induced glucose intolerance and skeletal muscle lipid accumulation in nonobese mice...
October 2016: Journal of Nutritional Biochemistry
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