A5083348278- Autophagy in Disease and Therapy
- Cardiac Fibrosis and Remodeling
- Cardiac electrophysiology and arrhythmias
- Mitochondrial Function and Pathology
- Signaling Pathways in Disease
- Ion channel regulation and function
- Cardiac Ischemia and Reperfusion
- Cardiovascular Function and Risk Factors
- Melanoma and MAPK Pathways
- Adipose Tissue and Metabolism
- Redox biology and oxidative stress
- Endoplasmic Reticulum Stress and Disease
- Calpain Protease Function and Regulation
- Heat shock proteins research
- Immune Response and Inflammation
- Receptor Mechanisms and Signaling
- Cardiomyopathy and Myosin Studies
- Iron Metabolism and Disorders
- Atherosclerosis and Cardiovascular Diseases
- RNA regulation and disease
- Hormonal Regulation and Hypertension
- Nuclear Receptors and Signaling
- Metabolism, Diabetes, and Cancer
- T-cell and B-cell Immunology
- Cell death mechanisms and regulation
National Cerebral and Cardiovascular Center
2015-2025
Matsumoto Livestock Hygiene Service Center
2025
British Heart Foundation
2015-2024
King's College London
2015-2024
Osaka University
2010-2024
National Hospital Organization Hokkaido Medical Center
2017
Cincinnati Children's Hospital Medical Center
2017
Howard Hughes Medical Institute
2017
University of Cincinnati
2017
University of Washington
2017
Malignant hyperthermia (MH) causes neurological, liver, and kidney damage death in humans major economic losses the swine industry. A single point mutation porcine gene for skeletal muscle ryanodine receptor ( ryr1 ) was found to be correlated with MH five breeds of lean, heavily muscled swine. Haplotyping suggests that all has a common origin. Assuming this is causal MH, development noninvasive diagnostic test will provide basis elimination or its controlled inclusion breeding programs.
We have cloned cDNAs encoding the rabbit and human forms of Ca2+ release channel sarcoplasmic reticulum. The cDNA encodes a protein 5032 amino acids, with molecular weight 563,584, which is made without an NH2-terminal signal sequence. Amino acid substitutions between sequences were noted in 163 positions deletions or insertions eight regions accounted for additional sequence differences two proteins. Analysis indicates that 10 potential transmembrane COOH-terminal fifth molecule additional,...
We have cloned and sequenced cDNA encoding the Ca2+ release channel (ryanodine receptor) of rabbit cardiac muscle sarcoplasmic reticulum. The cDNA, 16,532 base pairs in length, encodes a protein 4,969 amino acids with Mr 564,711. deduced acid sequence is 66% identical that skeletal ryanodine receptor, but analysis predicted secondary structures hydropathy plots suggests two isoforms exhibit same topology both transmembrane cytoplasmic domains. A potential ATP binding domain was identified at...
The gap junction protein connexin-43 is normally located at the intercalated discs of cardiac myocytes, and it plays a critical role in synchronization their contraction. mechanism by which localized within myocytes unknown. However, localization likely involves an interaction with cytoskeleton; immunofluorescence microscopy showed that specifically colocalizes cytoskeletal proteins ZO-1 α-spectrin. In transfected HEK293 cells, immunoprecipitation experiments using coexpressed epitope-tagged...
AbstractConstitutive autophagy is important for control of the quality proteins and organelles to maintain cell function. Damaged accumulate in aged organs. We have previously reported that cardiac-specific Atg5 (autophagy-related gene 5)-deficient mice, which was floxed out early embryogenesis, were born normally, showed normal cardiac function structure up 10 weeks old. In present study, determine longer-term consequences Atg5-deficiency heart, we monitored Atg5-deficient mice further 12...
Abstract Damaged mitochondria are removed by mitophagy. Although Atg32 is essential for mitophagy in yeast, no homologue has been identified mammalian cells. Here, we show that Bcl-2-like protein 13 (Bcl2-L-13) induces mitochondrial fragmentation and First, hypothesized unidentified receptors would share molecular features of Atg32. By screening the public database homologues, identify Bcl2-L-13. Bcl2-L-13 binds to LC3 through WXXI motif HEK293 In Bcl2-L-13, BH domains important...
Fibroblasts, which are the most numerous cell type in heart, interact with cardiomyocytes vitro and affect their function; however, they considered to play a secondary role cardiac hypertrophy failure. Here we have shown that fibroblasts essential for protective hypertrophic myocardial responses pressure overload vivo mice. Haploinsufficiency of transcription factor–encoding gene Krüppel-like factor 5 (Klf5) suppressed fibrosis elicited by moderate-intensity overload, whereas...
In the heart, acute injury induces a fibrotic healing response that generates collagen-rich scarring is at first protective but if inappropriately sustained can worsen heart disease. The process initiated by cytokines, neuroendocrine effectors, and mechanical strain promote resident fibroblast differentiation into contractile extracellular matrix-producing myofibroblasts. mitogen-activated protein kinase p38α (Mapk14 gene) known to influence cardiac response, its direct role in orchestrating...
In some patients with type 2 diabetes mellitus (DM) without hypertension, cardiac hypertrophy and attenuated function are observed, this insult is termed diabetic cardiomyopathy. To date, microRNA (miRNAs or miR) functions in cardiomyopathy remain to be elucidated.To clarify the of miRNAs involved caused by DM.C57BL/6 mice were fed a high-fat diet (HFD) for 20 weeks, which induced obesity DM. miRNA microarray analyses real-time polymerase chain reaction revealed that miR-451 levels...
Epidemiologic investigations have shown that exercise reduces morbidity and mortality from coronary artery disease. In this study, using a rat model, we attempted to determine whether can reduce ischemic injury the heart elucidate mechanism for cardioprotective effect of exercise. Results showed significantly reduced magnitude myocardial infarction in biphasic manner. The time course cardioprotection resembled change manganese superoxide dismutase (Mn-SOD) activity. administration antisense...
Background — Recently, reactive oxygen species (ROS) have emerged as important molecules in cardiac hypertrophy. However, the ROS-dependent signal transduction mechanism remains to be elucidated. In this study, we examined role of an ROS-sensitive transcriptional factor, NF-κB, and a mitogen-activated protein kinase kinase, apoptosis signal-regulating 1 (ASK1), G-protein–coupled receptor (GPCR) agonist (angiotensin II, endothelin-1, phenylephrine)-induced hypertrophy isolated rat neonatal...
The molecular mechanism for the transition from cardiac hypertrophy, an adaptive response to biomechanical stress, heart failure is poorly understood. mitogen-activated protein kinase p38alpha a key component of stress pathways in various types cells. In this study, we attempted explore vivo physiological functions hearts. First, generated mice with floxed alleles and crossbred them expressing Cre recombinase under control alpha-myosin heavy-chain promoter obtain cardiac-specific knockout...