A5071424209- Muscle Physiology and Disorders
- Adipose Tissue and Metabolism
- Exercise and Physiological Responses
- Mitochondrial Function and Pathology
- Fatty Acid Research and Health
- Genetic Neurodegenerative Diseases
- Respiratory Support and Mechanisms
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Muscle activation and electromyography studies
- Muscle metabolism and nutrition
- Genetics, Aging, and Longevity in Model Organisms
- Congenital Diaphragmatic Hernia Studies
- Neurogenetic and Muscular Disorders Research
- Cardiovascular and exercise physiology
- Sports injuries and prevention
- Tendon Structure and Treatment
- Nerve injury and regeneration
- Sports Performance and Training
- Mesenchymal stem cell research
- Telomeres, Telomerase, and Senescence
- Nutrition and Health in Aging
- Amyotrophic Lateral Sclerosis Research
- Coenzyme Q10 studies and effects
- Cholesterol and Lipid Metabolism
- Photoreceptor and optogenetics research
University of Michigan–Ann Arbor
2015-2025
Michigan Medicine
2024
King's College Hospital
2024
Michigan United
2023
Pennington Biomedical Research Center
2020
Laboratoire d’immunologie intégrative du cancer
2008-2020
Louisiana State University
2020
The University of Texas Health Science Center at San Antonio
2013
Jackson Laboratory
2012
Agricultural Research Service
1987-1999
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTCarotenoid Content of Thermally Processed Tomato-Based Food ProductsLinda H. Tonucci, Joanne M. Holden, Gary R. Beecher, Frederick Khachik, Carol S. Davis, and Generose MulokoziCite this: J. Agric. Chem. 1995, 43, 3, 579–586Publication Date (Print):March 1, 1995Publication History Published online1 May 2002Published inissue 1 March 1995https://pubs.acs.org/doi/10.1021/jf00051a005https://doi.org/10.1021/jf00051a005research-articleACS...
The inherited motor neuron disease spinal muscular atrophy (SMA) is caused by deficient expression of survival (SMN) protein and results in severe muscle weakness. In SMA mice, synaptic dysfunction both neuromuscular junctions (NMJs) central sensorimotor synapses precedes cell death. To address whether this due to SMN deficiency neurons, muscle, or both, we generated three lines conditional mice with tissue-specific increases expression. All showed increased survival, weights, improved...
Transforming growth factor-beta (TGF-β) is a well-known regulator of fibrosis and inflammation in many tissues. During embryonic development, TGF-β signaling induces expression the transcription factor scleraxis, which promotes fibroblast proliferation collagen synthesis tendons. In skeletal muscle, has been shown to induce atrophy fibrosis, but effect on muscle contractility scleraxis atrogin-1, an important atrophy, were not known.We treated muscles from mice with measured force...
Abstract Exercise is among the most effective interventions for age-associated mobility decline and metabolic dysregulation. Although long-term endurance exercise promotes insulin sensitivity expands respiratory capacity, genetic components pathways mediating benefits of have remained elusive. Here, we show that Sestrins, a family evolutionarily conserved exercise-inducible proteins, are critical mediators benefits. In both fly mouse models, ablation Sestrins prevents organisms from...
Volumetric muscle loss (VML) overwhelms the innate regenerative capacity of mammalian skeletal (SkM), leading to numerous disabilities and reduced quality life. Immune cells are critical responders injury guide tissue resident stem cell– progenitor-mediated myogenic repair. However, how immune cell infiltration intercellular communication networks with altered following VML drive pathological outcomes remains underexplored. Herein, we contrast cellular molecular mechanisms injuries that...
Objective: The paper addresses the degree to which attainment of status as an elite athlete in different sports ameliorates known age-related losses skeletal muscle structure and function. Design: retrospective design, based on comparisons published data former masters athletes control subjects, assessed ameliorated changes Setting: Institutional. Participants: Elite male athletes. Interventions: Participation selected individual team sports. Main Outcome Measurements: Strength, power,...
Abstract The lipid composition of margarines from stores in selected locations the U.S. is reported. lipids determined include fatty acids, tocopherols and major plant sterols. Data are included for isomeric octadecenoic acids (14 isomers or groups isomers) four octadecadienoic common partially hydrogenated vegetable fats, insofar as these separable by capillary gas chromatography. Amounts individual found oil margarines, spreads, imitation diet were: palmitate, 8.49 to 13.17% (normalized...
Deletion of copper-zinc superoxide dismutase (CuZnSOD) in Sod1(-/-) mice leads to accelerated loss muscle mass and force during aging, but the losses do not occur with muscle-specific deletion CuZnSOD. To determine role motor neurons decline, we generated transgenic which CuZnSOD was expressed under control synapsin 1 promoter (SynTgSod1(-/-) mice). SynTgSod1(-/-) brain, spinal cord, peripheral nerve, other tissues. Sciatic nerve content ~20% that mice, no reduction or isometric observed...
An association between oxidative stress and muscle atrophy weakness in vivo is supported by elevated damage accelerated loss of mass force with aging CuZn-superoxide dismutase-deficient (Sod1(-/-)) mice. The purpose was to determine the basis for low specific (N/cm(2)) gastrocnemius muscles Sod1(-/-) mice establish extent which structural functional changes resemble those associated normal aging. We tested hypothesis that due functionally denervated fibers comparing forces during nerve...
We have previously shown that deletion of CuZnSOD in mice (Sod1–/– mice) leads to accelerated loss muscle mass and contractile force during aging. To dissect the relative roles skeletal motor neurons this process, we used a Cre-Lox targeted approach establish muscle-specific Sod1-knockout (mKO) mouse determine whether is sufficient cause atrophy. Surprisingly, mKO maintain masses at or above those wild-type control up 18 mo age. In contrast, maximum isometric specific measured gastrocnemius...
Respiratory dysfunction is a common complication of obesity, conferring cardiovascular morbidity and increased mortality often necessitating mechanical ventilatory support. While impaired lung expansion in the setting adipose mass reduced central response to hypercapnia have been implicated as pathophysiological drivers, impact obesity on respiratory muscles—in particular, diaphragm—has not investigated detail. Here, we demonstrate that chronic high-fat diet (HFD) feeding impairs diaphragm...
Specialized proresolving mediators (SPMs) actively limit inflammation and expedite its resolution by modulating leukocyte recruitment function. Here we profiled intramuscular lipid via liquid chromatography-tandem mass spectrometry–based metabolipidomics following myofiber injury investigated the potential role of SPMs in skeletal muscle repair. Both proinflammatory eicosanoids increased damage induced either injection barium chloride or synergist ablation–induced functional overload. Daily...
Our previous studies showed that adult (8 month) mice lacking CuZn-superoxide dismutase (CuZnSOD, Sod1KO mice) have neuromuscular changes resulting in dramatic accelerated muscle atrophy and weakness mimics age-related sarcopenia. We further shown loss of CuZnSOD targeted to skeletal alone results only mild no atrophy. In this study, we deletion specifically neurons (nSod1KO determined the effect on mass weakness. The nSod1KO show a significant activity protein level brain spinal cord but...
A lysosome activator ameliorates muscular dystrophies.
Abstract Specialized pro‐resolving mediators actively limit inflammation and support tissue regeneration, but their role in age‐related muscle dysfunction has not been explored. We profiled the mediator lipidome of aging via liquid chromatography‐tandem mass spectrometry tested whether treatment with resolvin D1 (RvD1) could rejuvenate regenerative ability aged muscle. Aged mice displayed chronic this was associated a basal deficiency 8‐oxo‐RvD1, E3, maresin 1, as well many anti‐inflammatory...
SUMMARY Tendinopathy is a tendon disorder that caused by the failure to self-repair and has many pathological characteristics such as disorganized ECM decreased cell viability. We have identified possible target combat these changes, AMPK, an energy stress sensor was shown maintain intracellular homeostasis. Through bulk RNA-sequencing of healthy tendinopathic tendons from humans we novel finding downregulation AMPK signaling in samples which suggests plays role Our studies utilizing...
The molecular mechanisms behind aging-related declines in muscle function are not well understood, but the growth factor myostatin (MSTN) appears to play an important role this process. Additionally, epidemiological studies have identified a positive correlation between skeletal mass and longevity. Given of regulating size, longevity, we tested hypotheses that deficiency would protect oldest-old mice (28–30 months old) from loss size contractility, extend maximum lifespan mice. We found...
Key points Myostatin is an important regulator of muscle mass and a potential therapeutic target for the treatment diseases injuries that result in atrophy. Targeted genetic mutations myostatin have been generated mice, spontaneous loss‐of‐function reported several species. The impact deficiency on structure function muscles has well described but not other We report creation model rats using zinc finger nuclease technology. main findings study are inactivation results increases without...
Abstract Whole-body knock-out of Cu,Zn superoxide dismutase (Sod1KO) results in accelerated, age-related loss muscle mass and function associated with neuromuscular junction (NMJ) breakdown similar to sarcopenia. In order determine whether altered redox motor neurons underlies this phenotype, an inducible neuron-specific deletion Sod1 (i-mnSod1KO) was compared wild-type (WT) mice different ages (adult, mid-age, old) whole-body Sod1KO mice. Nerve oxidative damage, neuron numbers structural...
The glycosylation of dystroglycan is required for its function as a high-affinity laminin receptor, and loss results in congenital muscular dystrophy. purpose this study was to investigate the functional defects slow- fast-twitch muscles glycosylation-deficient Large myd mice. While partial alteration heterozygous myd/+ mice not sufficient alter muscle function, homozygous myd/myd demonstrated marked reduction specific force both soleus extensor digitorum longus (EDL) muscles. Although EDL...
Skeletal muscle suffers atrophy and weakness with aging. Denervation, oxidative stress, mitochondrial dysfunction are all proposed as contributors to age-associated loss, but connections between these factors have not been established. We examined contractility, function, intracellular calcium transients (ICTs) in muscles of mice throughout the life span define their sequential relationships. performed same measures analyzed neuromuscular junction (NMJ) morphology postnatal deletion neuronal...
Aging results in the progressive accumulation of senescent cells tissues that display loss proliferative capacity and acquire a senescence-associated secretory phenotype (SASP). The tumor suppressor, p16 INK4A , which slows progression cell cycle, is highly expressed most removal p16-expressing has been shown to be beneficial tissue health. Although much work done assess effects cellular senescence on variety different organs, little known about skeletal muscle whether reducing load would...