A5088387320- Muscle Physiology and Disorders
- Ion channel regulation and function
- Cardiomyopathy and Myosin Studies
- Cardiac electrophysiology and arrhythmias
- Genetic Neurodegenerative Diseases
- Mitochondrial Function and Pathology
- Cellular transport and secretion
- Adipose Tissue and Metabolism
- Nuclear Structure and Function
- Exercise and Physiological Responses
- Ion Channels and Receptors
- Neuroscience and Neural Engineering
- RNA Interference and Gene Delivery
- Neurobiology and Insect Physiology Research
- Viral Infections and Immunology Research
- Skin and Cellular Biology Research
- Signaling Pathways in Disease
- RNA Research and Splicing
- Cellular Mechanics and Interactions
- interferon and immune responses
- Caveolin-1 and cellular processes
- Inflammatory Myopathies and Dermatomyositis
- Muscle activation and electromyography studies
- Cell death mechanisms and regulation
- Cardiac Ischemia and Reperfusion
University of Kentucky
2024-2025
The Ohio State University
2015-2024
The Ohio State University Wexner Medical Center
2012-2024
Lung Institute
2014-2023
Oregon State University
2020
Johnson University
2006-2017
Ohio University
2017
Noah's Path
2014-2015
American College of Surgeons
2015
TRIM edicine (United States)
2010-2014
Ultrastructural studies have previously suggested potential association of intermediate filaments (IFs) with mitochondria. Thus, we investigated mitochondrial distribution and function in muscle lacking the IF protein desmin. Immunostaining skeletal tissue sections, as well histochemical staining for marker enzymes cytochrome C oxidase succinate dehydrogenase, demonstrate abnormal accumulation subsarcolemmal clumps mitochondria predominantly slow twitch desmin-null mice. observation cardiac...
Defective membrane repair can contribute to the progression of muscular dystrophy. Although mutations in caveolin-3 (Cav3) and dysferlin are linked dystrophy human patients, molecular mechanism underlying functional interplay between Cav3 muscle physiology disease has not been fully resolved. We recently discovered that mitsugumin 53 (MG53), a muscle-specific TRIM (Tri-partite motif) family protein (TRIM72), contributes intracellular vesicle trafficking is an essential component machinery...
Recombinant human MG53 protein can increase membrane repair after injury in cells and reduce pathology animal models of muscle muscular dystrophy.
Background— Ischemic heart disease is the greatest cause of death in Western countries. The deleterious effects cardiac ischemia are ameliorated by ischemic preconditioning (IPC), which transient protects against subsequent severe ischemia/reperfusion injury. IPC activates multiple signaling pathways, including reperfusion injury salvage kinase pathway (mainly PI3K-Akt-glycogen synthase kinase-3β [GSK3β] and ERK1/2) survivor activating factor enhancement involving activation JAK-STAT3 axis....
Unrepaired cardiomyocyte membrane injury causes irreplaceable cell loss, leading to myocardial fibrosis and eventually heart failure. However, the cellular molecular mechanisms of cardiac repair are largely unknown. MG53, a newly identified striated muscle-specific protein, is involved in skeletal muscle repair. But role MG53 has not been determined.We sought investigate whether mediates cardiomyocytes and, if so, mechanism underlying MG53-mediated cardiomyocytes. Moreover, we determined...
Highlights•Development of a mouse model pancreatic adenocarcinoma (PDA)-induced cachexia•Model develops progressive wasting associated with advancing pancreas pathology•Induction cachexia in adult KPP mice models tissue loss PDA cancer patients•Gene ontology cachectic muscles from resembles that patientsSummaryCachexia is syndrome characterized by pronounced skeletal muscle loss. In cancer, increased morbidity and mortality decreased treatment tolerance. Although advances have been made...
It is difficult to achieve minimally invasive injectable cell delivery while maintaining high retention and animal survival for in vivo stem therapy of myocardial infarction. Here we show that pluripotent aggregates pre-differentiated into the early cardiac lineage encapsulated a biocompatible biodegradable micromatrix, are suitable delivery. This method significantly improves injected cells by more than six-fold compared with conventional practice injecting single cells, effectively...
One of the hallmarks cardiomyopathy and heart failure is pronounced progressive cardiomyocyte death. Understanding mechanisms involved in cell death a topic great interest for treatment cardiac disease. Mice null desmin, muscle-specific member intermediate filament gene family, develop characterized by extensive death, fibrosis, calcification, eventual failure. The earliest ultrastructural defects are observed mitochondria. In present study, we have demonstrated that these mitochondrial...
Reduced homeostatic capacity for intracellular Ca2+ ([Ca2+]i) movement may underlie the progression of sarcopenia and contractile dysfunction during muscle aging. We report two alterations to homeostasis in skeletal that are associated with sparks, which elemental units release from sarcoplasmic reticulum, silent under resting conditions young muscle, yet activate a dynamic manner upon deformation membrane structures. The nature sparks appears be lost aged muscle. Using repetitive voltage...
Membrane recycling and remodeling contribute to multiple cellular functions, including cell fusion events during myogenesis. We have identified a tripartite motif (TRIM72) family member protein named MG53 defined its role in mediating the dynamic process of membrane exocytosis striated muscle. is muscle-specific that contains TRIM at amino terminus SPRY carboxyl terminus. Live imaging green fluorescent protein-MG53 construct cultured myoblasts showed although no transmembrane segment it...
Background— Junctophilin-2 (JPH2), a protein expressed in the junctional membrane complex, is necessary for proper intracellular calcium (Ca 2+ ) signaling cardiac myocytes. Downregulation of JPH2 expression model hypertrophy was recently associated with defective coupling between plasmalemmal L-type Ca channels and sarcoplasmic reticular ryanodine receptors. However, it remains unclear whether altered patients hypertrophic cardiomyopathy (HCM). In addition, effects downregulation on...
Plasma membrane repair is an essential process for maintenance of homeostasis at the cellular and tissue levels, whereas compromised capacity contributes to degenerative human diseases. Our recent studies show that MG53 muscle repair, defects in function are linked muscular dystrophy cardiac dysfunction. Here we report polymerase I transcript release factor (PTRF), a gene known regulate caveolae structure, indispensable component machinery. PTRF acts as docking protein during potentially by...
A novel coaxial electrospray technology is developed to generate microcapsules with a hydrogel shell of alginate and an aqueous liquid core living cells using two fluids in one step. Approximately 50 murine embryonic stem (ES) encapsulated the high viability (92.3 ± 2.9%) can proliferate form single ES cell aggregate 128.9 17.4 μm each microcapsule within 7 days. Quantitative analyses gene protein expression indicate that cultured miniaturized 3D core-shell have significantly higher...
Muscular dystrophies (MDs) are caused by genetic mutations in over 30 different genes, many of which encode for proteins essential the integrity muscle cell structure and membrane. Their deficiencies cause vulnerable to mechanical biochemical damages, leading membrane leakage, dystrophic pathology, eventual loss cells. Recent studies report that MG53, a muscle-specific TRIM-family protein, plays an role sarcolemmal repair. Here, we show systemic delivery overexpression human MG53 gene...
Defective coupling between sarcoplasmic reticulum and mitochondria during control of intracellular Ca2+ signaling has been implicated in the progression neuromuscular diseases. Our previous study showed that skeletal muscles derived from an amyotrophic lateral sclerosis (ALS) mouse model displayed segmental loss mitochondrial function was coupled with elevated uncontrolled release activity. The localized defect ALS muscle allows for examination contribution to removal excitation-contraction...