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Mitochondria cAMP

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https://www.readbyqxmd.com/read/28395332/acetamiprid-inhibits-testosterone-synthesis-by-affecting-the-mitochondrial-function-and-cytoplasmic-adenosine-triphosphate-production-in-rat-leydig-cells%C3%A2
#1
Deying Kong, Jidong Zhang, Xiaohui Hou, Shibin Zhang, Jun Tan, Yuanshou Chen, Weirong Yang, Junwei Zeng, Yong Han, Xiaohong Liu, Delin Xu, Renlian Cai
The insecticide acetamiprid is used to control noxious agricultural pests. However, it can cause mammalian toxicity. We evaluated the reproductive toxicity of acetamiprid in adult male Sprague Dawley rats. Rats were given oral acetamiprid alone or with vitamin E for 35 days. Rat plasma testosterone concentration and sperm quality decreased significantly as the levels of luteinizing hormone (LH) increased after exposure. At the same time, acetamiprid increased malondialdehyde and nitric oxide (NO) levels of Leydig cells...
January 1, 2017: Biology of Reproduction
https://www.readbyqxmd.com/read/28387563/curcumin-upregulates-antioxidant-defense-lon-protease-and-heat-shock-protein-70-under-hyperglycemic-conditions-in-human-hepatoma-cells
#2
Shivona Gounden, Anil Chuturgoon
Sirtuin 3 (SIRT3) regulates mitochondrial antioxidant (AO) defense and improves mitochondrial disorders. Curcumin protects mitochondria; however, the mechanisms need investigation. We postulated that curcumin increases AO defense under hyperglycemic conditions in HepG2 cells through SIRT3-mediated mechanisms. Cell viability was determined in HepG2 cells cultured with 5 mM glucose, 19.9 mM mannitol, vehicle control, 10 mM glucose, and 30 mM glucose in the absence or presence of curcumin for 24 h. SIRT3, nuclear factor-kappa B (NF-κB), heat-shock protein 70 (Hsp70), and Lon protein expressions were determined using western blot...
April 7, 2017: Journal of Medicinal Food
https://www.readbyqxmd.com/read/28351484/hypocapnic-hypothesis-of-leigh-disease
#3
Ewa Pronicka
Leigh syndrome (LS) is a neurogenetic disorder of children caused by mutations in at least 75 genes which impair mitochondrial bioenergetics. The changes have typical localization in basal ganglia and brainstem, and typical histological picture of spongiform appearance, vascular proliferation and gliosis. ATP deprivation, free radicals and lactate accumulation are suspected to be the causes. Hypocapnic hypothesis proposed in the paper questions the energy deprivation as the mechanism of LS. We assume that the primary harmful factor is hypocapnia (decrease in pCO2) and respiratory alkalosis (increase in pH) due to hyperventilation, permanent or in response to stress...
April 2017: Medical Hypotheses
https://www.readbyqxmd.com/read/28336949/induction-of-apoptosis-and-ganoderic-acid-biosynthesis-by-camp-signaling-in-ganoderma-lucidum
#4
Bang-Jau You, Ni Tien, Miin-Huey Lee, Bo-Ying Bao, Yih-Shyuan Wu, Tsung-Chi Hu, Hong-Zin Lee
Apoptosis is an essential physiological process that controls many important biological functions. However, apoptosis signaling in relation to secondary metabolite biosynthesis in plants and fungi remains a mystery. The fungus Ganoderma lucidum is a popular herbal medicine worldwide, but the biosynthetic regulation of its active ingredients (ganoderic acids, GAs) is poorly understood. We investigated the role of 3',5'-cyclic adenosine monophosphate (cAMP) signaling in fungal apoptosis and GA biosynthesis in G...
March 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28254846/rhoa-inhibits-the-hypoxia-induced-apoptosis-and-mitochondrial-dysfunction-in-chondrocytes-via-positively-regulating-the-creb-phosphorylation
#5
Kai Zhang, Dianming Jiang
Chondrocytes which are embedded within the growth-plate or the intervertebral discare sensitive to environmental stresses, such as inflammation and hypoxia. However, little is known about the molecular signaling pathways underlining the hypoxia-induced mitochondrial dysfunction and apoptosis in chondrocytes. In this study, we firstly examined the hypoxia-induced apoptosis, mitochondrial dysfunction and the activation of cAMP response element-binding protein (CREB) signaling in human chondrocyte cell line, C28/I2, and then investigated the regulatory role of RhoA, a well-recognized apoptosis suppressor, in such process, with gain-of-function strategy...
March 2, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28202681/components-of-the-mitochondrial-camp-signalosome
#6
REVIEW
Stefania Monterisi, Manuela Zaccolo
3'-5'-Cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signalling is activated by different extracellular stimuli and mediates many diverse processes within the same cell. It is now well established that in order to translate into the appropriate cellular function multiple extracellular inputs, which may act simultaneously on the same cell, the cAMP/PKA signalling pathway is compartmentalised. Multimolecular complexes are organised at specific subcellular sites to generate spatially confined signalosomes, which include effectors, modulators and targets of the pathway...
February 8, 2017: Biochemical Society Transactions
https://www.readbyqxmd.com/read/28096195/the-multifunctional-mitochondrial-epac1-controls-myocardial-cell-death
#7
Loubina Fazal, Marion Laudette, Sílvia Paula-Gomes, Sandrine Pons, Caroline Conte, Florence Tortosa, Pierre Sicard, Yannis Sainte-Marie, Malik Bisserier, Olivier Lairez, Alexandre Lucas, Jérôme Roy, Bijan Ghaleh, Jeremy Fauconnier, Jeanne Mialet-Perez, Frank Lezoualc'h
RATIONALE: Although the second messenger cyclic AMP (cAMP) is physiologically beneficial in the heart, it largely contributes to cardiac disease progression when dysregulated. Current evidence suggests that cAMP is produced within mitochondria. However, mitochondrial cAMP signaling and its involvement in cardiac pathophysiology are far from being understood. OBJECTIVE: To investigate the role of mitochondrial exchange protein directly activated by cAMP 1 (MitEpac1) in ischemia/reperfusion (I/R) injury...
January 17, 2017: Circulation Research
https://www.readbyqxmd.com/read/27890624/mitochondrial-camp-prevents-apoptosis-modulating-sirt3-protein-level-and-opa1-processing-in-cardiac-myoblast-cells
#8
Anna Signorile, Arcangela Santeramo, Grazia Tamma, Tommaso Pellegrino, Susanna D'Oria, Paolo Lattanzio, Domenico De Rasmo
Mitochondria, responding to a wide variety of signals, including oxidative stress, are critical in regulating apoptosis that plays a key role in the pathogenesis of a variety of cardiovascular diseases. A number of mitochondrial proteins and pathways have been found to be involved in the mitochondrial dependent apoptosis mechanism, such as optic atrophy 1 (OPA1), sirtuin 3 (Sirt3), deacetylase enzyme and cAMP signal. In the present work we report a network among OPA1, Sirt3 and cAMP in ROS-dependent apoptosis...
February 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27862857/casticin-induced-apoptotic-cell-death-and-altered-associated-gene-expression-in-human-colon-cancer-colo-205-cells
#9
Hung-Sheng Shang, Jia-You Liu, Hsu-Feng Lu, Han-Sun Chiang, Chia-Hain Lin, Ann Chen, Yuh-Feng Lin, Jing-Gung Chung
Casticin, a polymethoxyflavone, derived from natural plant Fructus Viticis exhibits biological activities including anti-cancer characteristics. The anti-cancer and alter gene expression of casticin on human colon cancer cells and the underlying mechanisms were investigated. Flow cytometric assay was used to measure viable cell, cell cycle and sub-G1 phase, reactive oxygen species (ROS) and Ca(2+) productions, level of mitochondria membrane potential (ΔΨm ) and caspase activity. Western blotting assay was used to detect expression of protein level associated with cell death...
November 14, 2016: Environmental Toxicology
https://www.readbyqxmd.com/read/27836641/2-3-cyclic-nucleotide-3-phosphodiesterase-as-a-messenger-of-protection-of-the-mitochondrial-function-during-melatonin-treatment-in-aging
#10
Yulia Baburina, Irina Odinokova, Tamara Azarashvili, Vladimir Akatov, John J Lemasters, Olga Krestinina
The process of aging is considered to be tightly related to mitochondrial dysfunction. One of the causes of aging is an increased sensitivity to the induction of mitochondrial permeability transition pore (mPTP) opening in the inner membrane of mitochondria. Melatonin, a natural antioxidant, is a hormone produced by the pineal gland. The role of melatonin whose level decreases with aging is well understood. In the present study, we demonstrated that long-term treatment of aged rats with melatonin improved the functional state of mitochondria; thus, the Ca(2+) capacity was enhanced and mitochondrial swelling was deaccelerated in mitochondria...
January 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27815506/plasma-membrane-origin-of-the-steroidogenic-pool-of-cholesterol-used-in-hormone-induced-acute-steroid-formation-in-leydig-cells
#11
Sathvika Venugopal, Daniel Benjamin Martinez-Arguelles, Seimia Chebbi, Françoise Hullin-Matsuda, Toshihide Kobayashi, Vassilios Papadopoulos
Hormone-sensitive acute steroid biosynthesis requires trafficking of cholesterol from intracellular sources to the inner mitochondrial membrane. The precise location of the intracellular cholesterol and its transport mechanism are uncertain. Perfringolysin O, produced by Clostridium perfringens, binds cholesterol. Its fourth domain (D4) retains cholesterol-binding properties but not cytotoxicity. We transfected steroidogenic MA-10 cells of mouse Leydig cell tumors with the mCherry-D4 plasmid. Tagged D4 with fluorescent proteins enabled us to track cholesterol...
December 9, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27649969/epac2-rap1-signaling-regulates-reactive-oxygen-species-production-and-susceptibility-to-cardiac-arrhythmias
#12
Zhaokang Yang, Hannah M Kirton, Moza Al-Owais, Jérôme Thireau, Sylvain Richard, Chris Peers, Derek S Steele
AIMS: In the heart, β1-adrenergic signaling involves cyclic adenosine monophosphate (cAMP) acting via both protein kinase-A (PKA) and exchange protein directly activated by cAMP (Epac): a guanine nucleotide exchange factor for the small GTPase Rap1. Inhibition of Epac-Rap1 signaling has been proposed as a therapeutic strategy for both cancer and cardiovascular disease. However, previous work suggests that impaired Rap1 signaling may have detrimental effects on cardiac function. The aim of the present study was to investigate the influence of Epac2-Rap1 signaling on the heart using both in vivo and in vitro approaches...
October 27, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/27531991/regulation-of-star-by-the-n-terminal-domain-and-coinduction-of-sik1-and-tis11b-znf36l1-in-single-cells
#13
Jinwoo Lee, Tiegang Tong, Haichuan Duan, Yee Hoon Foong, Ibrahim Musaitif, Takeshi Yamazaki, Colin Jefcoate
The cholesterol transfer function of steroidogenic acute regulatory protein (StAR) is uniquely integrated into adrenal cells, with mRNA translation and protein kinase A (PKA) phosphorylation occurring at the mitochondrial outer membrane (OMM). The StAR C-terminal cholesterol-binding domain (CBD) initiates mitochondrial intermembrane contacts to rapidly direct cholesterol to Cyp11a1 in the inner membrane (IMM). The conserved StAR N-terminal regulatory domain (NTD) includes a leader sequence targeting the CBD to OMM complexes that initiate cholesterol transfer...
2016: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/27521960/a-single-cell-level-measurement-of-star-expression-and-activity-in-adrenal-cells
#14
Jinwoo Lee, Takeshi Yamazaki, Hui Dong, Colin Jefcoate
The Steroidogenic acute regulatory protein (StAR) directs mitochondrial cholesterol uptake through a C-terminal cholesterol binding domain (CBD) and a 62 amino acid N-terminal regulatory domain (NTD) that contains an import sequence and conserved sites for inner membrane metalloproteases. Deletion of the NTD prevents mitochondrial import while maintaining steroidogenesis but with compromised cholesterol homeostasis. The rapid StAR-mediated cholesterol transfer in adrenal cells depends on concerted mRNA translation, p37 StAR phosphorylation and controlled NTD cleavage...
August 10, 2016: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/27503834/epigenetics-and-nutrition-related-epidemics-of-metabolic-diseases-current-perspectives-and-challenges
#15
REVIEW
Anna Hernández-Aguilera, Salvador Fernández-Arroyo, Elisabet Cuyàs, Fedra Luciano-Mateo, Noemi Cabre, Jordi Camps, Jose Lopez-Miranda, Javier A Menendez, Jorge Joven
We live in a world fascinated by the relationship between disease and nutritional disequilibrium. The subtle and slow effects of chronic nutrient toxicity are a major public health concern. Since food is potentially important for the development of "metabolic memory", there is a need for more information on the type of nutrients causing adverse or toxic effects. We now know that metabolic alterations produced by excessive intake of some nutrients, drugs and chemicals directly impact epigenetic regulation. We envision that understanding how metabolic pathways are coordinated by environmental and genetic factors will provide novel insights for the treatment of metabolic diseases...
October 2016: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/27485212/acute-upregulation-of-neuronal-mitochondrial-type-1-cannabinoid-receptor-and-it-s-role-in-metabolic-defects-and-neuronal-apoptosis-after-tbi
#16
Zhen Xu, Xiao-Ai Lv, Qun Dai, Yu-Qing Ge, Jie Xu
Metabolic defects and neuronal apoptosis initiated by traumatic brain injury (TBI) contribute to subsequent neurodegeneration. They are all regulated by mechanisms centered around mitochondrion. Type-1 cannabinoid receptor (CB1) is a G-protein coupled receptor (GPCR) enriched on neuronal plasma membrane. Recent evidences point to the substantial presence of CB1 receptors on neuronal mitochondrial outer membranes (mtCB1) and the activation of mtCB1 influences aerobic respiration via inhibiting mitochondrial cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/complex I pathway...
2016: Molecular Brain
https://www.readbyqxmd.com/read/27459537/glp-1-ra-corrects-mitochondrial-labile-iron-accumulation-and-improves-%C3%AE-cell-function-in-type-2-wolfram-syndrome
#17
Liron Danielpur, Yang-Sung Sohn, Ola Karmi, Chen Fogel, Adar Zinger, Abdulsalam Abu-Libdeh, Tal Israeli, Yael Riahi, Orit Pappo, Ruth Birk, David H Zangen, Ron Mittler, Zvi-Ioav Cabantchik, Erol Cerasi, Rachel Nechushtai, Gil Leibowitz
CONTEXT: Type 2 Wolfram syndrome (T2-WFS) is a neuronal and β-cell degenerative disorder caused by mutations in the CISD2 gene. The mechanisms underlying β-cell dysfunction in T2-WFS are not known, and treatments that effectively improve diabetes in this context are lacking. OBJECTIVE: Unraveling the mechanisms of β-cell dysfunction in T2-WFS and the effects of treatment with GLP-1 receptor agonist (GLP-1-RA). DESIGN AND SETTING: A case report and in vitro mechanistic studies...
October 2016: Journal of Clinical Endocrinology and Metabolism
https://www.readbyqxmd.com/read/27412728/mitochondrial-oxidative-phosphorylation-system-oxphos-deficits-in-schizophrenia-possible-interactions-with-cellular-processes
#18
Oded Bergman, Dorit Ben-Shachar
Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate molecules by the oxidative phosphorylation system (OXPHOS). Linked to numerous signaling pathways and cellular functions, mitochondria, and OXPHOS in particular, are involved in neuronal development, connectivity, plasticity, and differentiation. Impairments in a variety of mitochondrial functions have been described in different general and psychiatric disorders, including schizophrenia (SCZ), a severe, chronic, debilitating illness that heavily affects the lives of patients and their families...
August 2016: Canadian Journal of Psychiatry. Revue Canadienne de Psychiatrie
https://www.readbyqxmd.com/read/27409833/hypoxia-mediated-alterations-and-their-role-in-the-her-2-neuregulated-creb-status-and-localization
#19
André Steven, Sandra Leisz, Katharina Sychra, Bernhard Hiebl, Claudia Wickenhauser, Dimitrios Mougiakakos, Rolf Kiessling, Carsten Denkert, Barbara Seliger
The cAMP-responsive element-binding protein (CREB) is involved in the tumorigenicity of HER-2/neu-overexpressing murine and human tumor cells, but a link between the HER-2/neu-mediated CREB activation, its posttranslational modification and localization and changes in the cellular metabolism, due to an altered (tumor) microenvironment remains to be established. The present study demonstrated that shRNA-mediated silencing of CREB in HER-2/neu-transformed cells resulted in decreased tumor formation, which was associated with reduced angiogenesis, but increased necrotic and hypoxic areas in the tumor...
August 9, 2016: Oncotarget
https://www.readbyqxmd.com/read/27351024/etiologies-of-sperm-oxidative-stress
#20
REVIEW
Parvin Sabeti, Soheila Pourmasumi, Tahereh Rahiminia, Fatemeh Akyash, Ali Reza Talebi
Sperm is particularly susceptible to reactive oxygen species (ROS) during critical phases of spermiogenesis. However, the level of seminal ROS is restricted by seminal antioxidants which have beneficial effects on sperm parameters and developmental potentials. Mitochondria and sperm plasma membrane are two major sites of ROS generation in sperm cells. Besides, leukocytes including polymer phonuclear (PMN) leukocytes and macrophages produce broad category of molecules including oxygen free radicals, non-radical species and reactive nitrogen species...
April 2016: International Journal of Reproductive Biomedicine (Yazd, Iran)
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