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https://www.readbyqxmd.com/read/29618819/advanced-maturation-of-human-cardiac-tissue-grown-from-pluripotent-stem-cells
#1
Kacey Ronaldson-Bouchard, Stephen P Ma, Keith Yeager, Timothy Chen, LouJin Song, Dario Sirabella, Kumi Morikawa, Diogo Teles, Masayuki Yazawa, Gordana Vunjak-Novakovic
Cardiac tissues generated from human induced pluripotent stem cells (iPSCs) can serve as platforms for patient-specific studies of physiology and disease1-6 . However, the predictive power of these models is presently limited by the immature state of the cells1, 2, 5, 6 . Here we show that this fundamental limitation can be overcome if cardiac tissues are formed from early-stage iPSC-derived cardiomyocytes soon after the initiation of spontaneous contractions and are subjected to physical conditioning with increasing intensity over time...
April 4, 2018: Nature
https://www.readbyqxmd.com/read/29615920/redox-aspects-of-chaperones-in-cardiac-function
#2
REVIEW
Claudia Penna, Matteo Sorge, Saveria Femminò, Pasquale Pagliaro, Mara Brancaccio
Molecular chaperones are stress proteins that allow the correct folding or unfolding as well as the assembly or disassembly of macromolecular cellular components. Changes in expression and post-translational modifications of chaperones have been linked to a number of age- and stress-related diseases including cancer, neurodegeneration, and cardiovascular diseases. Redox sensible post-translational modifications, such as S-nitrosylation, glutathionylation and phosphorylation of chaperone proteins have been reported...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29607874/astraglaus-polysaccharide-protects-diabetic-cardiomyopathy-by-activating-nrg1-erbb-pathway
#3
Xiao Chang, Kang Lu, Ling Wang, Min Lv, Wenjun Fu
Diabetic cardiomyopathy (DCM) is one of the main cardiac complications among diabetic patients. According to previous studies, the pathogenesis of DCM is associated with oxidative stress, apoptosis and proliferation of local cardiac cells. It showed, NRG1 can improve the function of mitochondria, and thereby, increasing proliferation and decreasing apoptosis of cardiac muscle cell via ErbB/AKT signaling, also, exert antioxidative function. Besides, NRG1/ErbB pathway was impaired in the DCM model which suggested this signaling played key role in DCM...
April 2, 2018: Bioscience Trends
https://www.readbyqxmd.com/read/29605530/zinc-improves-mitochondrial-respiratory-function-and-prevents-mitochondrial-ros-generation-at-reperfusion-by-phosphorylating-stat3-at-ser-727
#4
Ge Zhang, Mingwei Sheng, Jiannan Wang, Tianming Teng, Yuemin Sun, Qing Yang, Zhelong Xu
Serine 727 (Ser727 ) phosphorylation of STAT3 plays a role in the regulation of mitochondrial respiration. This study aimed to test if zinc could regulate mitochondrial respiration through phosphorylation of STAT3 at Ser727 in the setting of ischemia/reperfusion in the heart. Under normoxic conditions, treatment of isolated rat hearts with ZnCl2 increased cytosolic STAT3 phosphorylation at Ser727 followed by phospho-STAT3 translocation to mitochondria. In isolated rat hearts subjected to 30 min regional ischemia followed by 20 min of reperfusion, ZnCl2 given 5 min before the onset of reperfusion also increased mitochondrial phospho-STAT3...
March 29, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29590644/acetylation-of-gata4-on-lysine-residue-k313-promotes-osteoblastic-cells-growth
#5
Wenjun You, Lijuan Song, Kun Wang
BACKGROUND/AIMS: GATA4, a protein related to osteoblast differentiation and mineralization, whose acetylation is essential for cardiac defects. Here, we aimed to explore the functional impacts of GATA4 acetylation on osteoporosis (OS). METHODS: GATA4 acetylation in hFOB1.19 and 293T cells was detected after exposure of HDAC inhibitors (TSA and SAHA). Co-immunoprecipitation was conducted to determine which HATs and HDACs was involved in the modulation of GATA4 acetylation/deacetylation, and to identify the acetylation site...
March 22, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29576852/zp2495-protects-against-myocardial-ischemia-reperfusion-injury-in-diabetic-mice-through-improvement-of-cardiac-metabolism-and-mitochondrial-function-the-possible-involvement-of-ampk-foxo3a-signal-pathway
#6
Shuang Li, Hao Wu, Dong Han, Mingming Zhang, Na Li, Weihua Yu, Dongdong Sun, Zhongchan Sun, Sai Ma, Erhe Gao, Congye Li, Min Shen, Feng Cao
Coronary heart disease patients with type 2 diabetes were subject to higher vulnerability for cardiac ischemia-reperfusion (I/R) injury. This study was designed to evaluate the impact of ZP2495 (a glucagon-GLP-1 dual-agonist) on cardiac function and energy metabolism after myocardial I/R injury in db/db mice with a focus on mitochondrial function. C57BLKS/J-lepr+ /lepr+ (BKS) and db/db mice received 4-week treatment of glucagon, ZP131 (GLP-1 receptor agonist), or ZP2495, followed by cardiac I/R injury. The results showed that cardiac function, cardiac glucose metabolism, cardiomyocyte apoptosis, cardiac mitochondrial morphology, and energetic transition were improved or ameliorated by ZP2495 to a greater extent than that of glucagon and ZP131...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29575479/increasing-autophagy-and-blocking-nrf2-suppress-laminopathy-induced-age-dependent-cardiac-dysfunction-and-shortened-lifespan
#7
Shruti Bhide, Adriana S Trujillo, Maureen T O'Connor, Grant H Young, Diane E Cryderman, Sahaana Chandran, Mastaneh Nikravesh, Lori L Wallrath, Girish C Melkani
Mutations in the human LMNA gene cause a collection of diseases known as laminopathies. These include myocardial diseases that exhibit age-dependent penetrance of dysrhythmias and heart failure. The LMNA gene encodes A-type lamins, intermediate filaments that support nuclear structure and organize the genome. Mechanisms by which mutant lamins cause age-dependent heart defects are not well understood. To address this issue, we modeled human disease-causing mutations in the Drosophila melanogaster Lamin C gene and expressed mutant Lamin C exclusively in the heart...
March 25, 2018: Aging Cell
https://www.readbyqxmd.com/read/29575122/melatonin-prevents-drp1-mediated-mitochondrial-fission-in-diabetic-hearts-through-sirt1-pgc1%C3%AE-pathway
#8
Mingge Ding, Na Feng, Daishi Tang, Jiahao Feng, Zeyang Li, Min Jia, Zhenhua Liu, Xiaoming Gu, Yuemin Wang, Feng Fu, Jianming Pei
Myocardial contractile dysfunction is associated with an increase in mitochondrial fission in patients with diabetes. However, whether mitochondrial fission directly promotes diabetes-induced cardiac dysfunction is still unknown. Melatonin exerts a substantial influence on the regulation of mitochondrial fission/fusion. This study investigated whether melatonin protects against diabetes-induced cardiac dysfunction via regulation of mitochondrial fission/fusion and explored its underlying mechanisms. Here, we show that melatonin prevented diabetes-induced cardiac dysfunction by inhibiting dynamin-related protein 1 (Drp1)-mediated mitochondrial fission...
March 25, 2018: Journal of Pineal Research
https://www.readbyqxmd.com/read/29547569/melatonin-balance-the-autophagy-and-apoptosis-by-regulating-ucp2-in-the-lps-induced-cardiomyopathy
#9
Pan Pan, Hongmin Zhang, Longxiang Su, Xiaoting Wang, Dawei Liu
To explore the mechanism of mitochondrial uncoupling protein 2 (UCP2) mediating the protective of melatonin when septic cardiomyopathy. UCP2 knocked out mice and cardiomyocytes were used to study the effect of melatonin in response to LPS. Indicators of myocardial and mitochondria injury including mitochondrial membrane potential, mitochondrial permeability transition pore, calcium loading, ROS, and ATP detection were assessed. In addition cell viability and apoptosis as well as autophagy-associated proteins were evaluated...
March 16, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/29544373/mitochondria-regulate-cardiac-contraction-through-atp-dependent-and-atp-independent-mechanisms
#10
Kexin Wang, Yang Xu, Qiong Sun, Jiangang Long, Jiankang Liu, Jian Ding
The multipurpose organelle mitochondria play an essential role(s) in controlling cardiac muscle contraction. Mitochondria, not only function as the powerhouses and the energy source of myocytes, but also modulate intracellular Ca2+ homeostasis, the production of intermediary metabolites/reactive oxygen species (ROS), and other cellular processes. Those molecular events can substantially influence myocardial contraction. Mitochondrial dysfunction is usually associated with cardiac remodeling, and is the causal factor of heart contraction defects in many cases...
March 16, 2018: Free Radical Research
https://www.readbyqxmd.com/read/29540794/pathogenesis-of-cardiac-ischemia-reperfusion-injury-is-associated-with-ck2%C3%AE-disturbed-mitochondrial-homeostasis-via-suppression-of-fundc1-related-mitophagy
#11
Hao Zhou, Pingjun Zhu, Jin Wang, Hong Zhu, Jun Ren, Yundai Chen
Disturbed mitochondrial homeostasis contributes to the pathogenesis of cardiac ischemia reperfusion (IR) injury, although the underlying mechanism remains elusive. Here, we demonstrated that casein kinase 2α (CK2α) was upregulated following acute cardiac IR injury. Increased CK2α was shown to be instrumental to mitochondrial damage, cardiomyocyte death, infarction area expansion and cardiac dysfunction, whereas cardiac-specific CK2α knockout (CK2αCKO ) mice were protected against IR injury and mitochondrial damage...
March 14, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29540486/coenzyme-a-mediated-degradation-of-pyruvate-dehydrogenase-kinase-4-promotes-cardiac-metabolic-flexibility-after-high-fat-feeding-in-mice
#12
Christopher Schafer, Zachary T Young, Catherine A Makarewich, Abdallah Elnwasany, Caroline S Kinter, Michael Kinter, Luke I Szweda
Cardiac energy is produced primarily by oxidation of fatty acids and glucose, with the relative contributions of each nutrient being sensitive to changes in substrate availability and energetic demand. A major contributor to cardiac metabolic flexibility is pyruvate dehydrogenase (PDH) which converts glucose-derived pyruvate to acetyl-CoA within the mitochondria. PDH is inhibited by phosphorylation dependent on the competing activities of pyruvate dehydrogenase kinases (PDK1-4) and phosphatases (PDP1-2). A single high-fat meal increases cardiac PDK4 content and subsequently inhibits PDH activity, reducing pyruvate utilization when abundant fatty acids are available...
March 14, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29536431/translational-application-of-measuring-mitochondrial-functions-in-blood-cells-obtained-from-patients-with-acute-poisoning
#13
David H Jang, Utsha G Khatri, Anita Mudan, Jennifer S Love, Shawn Owiredu, David M Eckmann
It is conservatively estimated that 5,000 deaths per year and 20,000 injuries in the USA are due to poisonings caused by chemical exposures (e.g., carbon monoxide, cyanide, hydrogen sulfide, phosphides) that are cellular inhibitors. These chemical agents result in mitochondrial inhibition resulting in cardiac arrest and/or shock. These cellular inhibitors have multi-organ effects, but cardiovascular collapse is the primary cause of death marked by hypotension, lactic acidosis, and cardiac arrest. The mitochondria play a central role in cellular metabolism where oxygen consumption through the electron transport system is tightly coupled to ATP production and regulated by metabolic demands...
March 13, 2018: Journal of Medical Toxicology: Official Journal of the American College of Medical Toxicology
https://www.readbyqxmd.com/read/29515442/ginkgolide-c-alleviates-myocardial-ischemia-reperfusion-induced-inflammatory-injury-via-inhibition-of-cd40-nf-%C3%AE%C2%BAb-pathway
#14
Rui Zhang, Dan Han, Zhenyu Li, Chengwu Shen, Yahui Zhang, Jun Li, Genquan Yan, Shasha Li, Bo Hu, Jiangbing Li, Ping Liu
Increasing evidence shows that inflammation plays a vital role in the occurrence and development of ischemia/reperfusion (I/R). Suppression of excessive inflammation can ameliorate impaired cardiac function, which shows therapeutic potential for clinical treatment of myocardial ischemia/reperfusion (MI/R) diseases. In this study, we investigated whether Ginkgolide C (GC), a potent anti-inflammatory flavone, extenuated MI/R injury through inhibition of inflammation. In vivo , rats with the occlusion of the left anterior descending (LAD) coronary artery were applied to mimic MI/R injury...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29511093/mitochondrial-dna-as-an-inflammatory-mediator-in-cardiovascular-diseases
#15
REVIEW
Hiroyuki Nakayama, Kinya Otsu
Mitochondria play a central role in multiple cellular functions, including energy production, calcium homeostasis, and cell death. Currently, growing evidence indicates the vital roles of mitochondria in triggering and maintaining inflammation. Chronic inflammation without microbial infection - termed sterile inflammation - is strongly involved in the development of heart failure. Sterile inflammation is triggered by the activation of pattern recognition receptors (PRRs) that sense endogenous ligands called damage-associated molecular patterns (DAMPs)...
March 6, 2018: Biochemical Journal
https://www.readbyqxmd.com/read/29509881/over-expression-of-mitochondrial-creatine-kinase-in-the-murine-heart-improves-functional-recovery-and-protects-against-injury-following-ischaemia-reperfusion
#16
Hannah J Whittington, Philip J Ostrowski, Debra J McAndrew, Fang Cao, Andrew Shaw, Thomas R Eykyn, Hannah Lake, Jack Tyler, Jurgen E Schneider, Stefan Neubauer, Sevasti Zervou, Craig A Lygate
Aims: Mitochondrial creatine kinase (MtCK) couples ATP production via oxidative phosphorylation to phosphocreatine in the cytosol, which acts as a mobile energy store available for regeneration of ATP at times of high demand. We hypothesised that elevating MtCK would be beneficial in ischaemia-reperfusion (I/R) injury. Methods and Results: Mice were created overexpressing the sarcomeric MtCK gene with αMHC promoter at the Rosa26 locus (MtCK-OE) and compared with wild-type (WT) littermates...
March 2, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29481798/first-description-of-a-novel-mitochondrial-mutation-in-the-mt-ti-gene-associated-with-multiple-mitochondrial-dna-deletion-and-depletion-in-family-with-severe-dilated-mitochondrial-cardiomyopathy
#17
Olfa Alila-Fersi, Mouna Tabebi, Marwa Maalej, Neila Belguith, Leila Keskes, Emna Mkaouar-Rebai, Faiza Fakhfakh
Mitochondria are essential for early cardiac development and impaired mitochondrial function was described associated with heart diseases such as hypertrophic or dilated mitochondrial cardiomyopathy. In this study, we report a family including two individuals with severe dilated mitochondrial cardiomyopathy. The whole mitochondrial genome screening showed the presence of several variations and a novel homoplasmic mutation m.4318-4322delC in the MT-TI gene shared by the two patients and their mother and leading to a disruption of the tRNAIle secondary structure...
February 23, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29477758/an-automated-workflow-for-segmenting-single-adult-cardiac-cells-from-large-volume-serial-block-face-scanning-electron-microscopy-data
#18
Akter Hussain, Shouryadipta Ghosh, Siavash Beikoghli Kalkhoran, Derek J Hausenloy, Eric Hanssen, Vijay Rajagopal
This paper presents a new algorithm to automatically segment the myofibrils, mitochondria and nuclei within single adult cardiac cells that are part of a large serial-block-face scanning electron microscopy (SBF-SEM) dataset. The algorithm only requires a set of manually drawn contours that roughly demarcate the cell boundary at routine slice intervals (every 50th , for example). The algorithm correctly classified pixels within the single cell with 97% accuracy when compared to manual segmentations. One entire cell and the partial volumes of two cells were segmented...
February 22, 2018: Journal of Structural Biology
https://www.readbyqxmd.com/read/29476646/metabolite-accumulation-in-vlcad-deficiency-markedly-disrupts-mitochondrial-bioenergetics-and-ca-2-homeostasis-in-the-heart
#19
Cristiane Cecatto, Alexandre Umpierrez Amaral, Janaína Camacho da Silva, Alessandro Wajner, Mariana de Oliveira Vargas Schimit, Lucas Henrique Rodrigues da Silva, Simone Magagnin Wajner, Ângela Zanatta, Roger Frigério Castilho, Moacir Wajner
We studied the effects of the major long-chain fatty acids accumulating in very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency, namely cis-5-tetradecenoic acid (Cis-5) and myristic acid (Myr), on important mitochondrial functions in isolated mitochondria from heart, cardiac fibers of juvenile rats and cardiomyocytes. Cis-5 and Myr at pathological concentrations markedly reduced mitochondrial membrane potential (ΔΨm), matrix NAD(P)H pool, Ca2+ retention capacity, ADP- (state 3) and CCCP-stimulated (uncoupled) respiration and ATP generation...
February 24, 2018: FEBS Journal
https://www.readbyqxmd.com/read/29459772/monoamine-oxidase-dependent-endoplasmic-reticulum-mitochondria-dysfunction-and-mast-cell-degranulation-lead-to-adverse-cardiac-remodeling-in-diabetes
#20
Soni Deshwal, Marleen Forkink, Chou-Hui Hu, Guido Buonincontri, Salvatore Antonucci, Moises Di Sante, Michael P Murphy, Nazareno Paolocci, Daria Mochly-Rosen, Thomas Krieg, Fabio Di Lisa, Nina Kaludercic
Monoamine oxidase (MAO) inhibitors ameliorate contractile function in diabetic animals, but the mechanisms remain unknown. Equally elusive is the interplay between the cardiomyocyte alterations induced by hyperglycemia and the accompanying inflammation. Here we show that exposure of primary cardiomyocytes to high glucose and pro-inflammatory stimuli leads to MAO-dependent increase in reactive oxygen species that causes permeability transition pore opening and mitochondrial dysfunction. These events occur upstream of endoplasmic reticulum (ER) stress and are abolished by the MAO inhibitor pargyline, highlighting the role of these flavoenzymes in the ER/mitochondria cross-talk...
February 19, 2018: Cell Death and Differentiation
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