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Alzheimer's disease(AD)and Parkinson's disease(PD)are common neurodegenerative diseases that seriously threaten the health of the elderly, involving various abnormalities in physiology and metabolism including the impairment of mitochondrial function, Ca 2+ homeostasis deregulation, oxidative stress, aggregation of misfolded proteins, autophagy and inflammation.However, mechanisms underlying the pathogenesis of these diseases have not been clearly elucidated, thus impeding advances in their treatment.In recent years, it has been found that mitochondria-associated endoplasmic reticulum membranes(MAM)play an important role in the development of AD and PD and exert their effects by regulating the functions of mitochondria and endoplasmic reticula.This article reviews studies of the past decade related to the effects of MAM on AD and PD, aiming to generate insights for exploring the constituent proteins of MAM and the molecular mechanisms of AD and PD via endoplasmic reticulum-mitochondria Ca 2+ transport and ER stress regulated by MAM.
ABSTRACT
BACKGROUND: High-intensity exercise can induce the depolymerization and/or degradation of tubulin in the skeletal muscle. According to the close relation with the mitochondria, tubulin may influence mitochondrial movement track and molecular motor, thereby varying the movement and distribution of mitochondria. OBJECTIVE: To observe the effect of high-intensity exercise on α-tubulin, MAP4, Miro1 and mitochondrial ultrastructures, analyze their sequential changes and further explore whether tubular depolymerization regulates the movement and distribution of mitochondria via Miro1. METHODS: Fifty-six Sprague-Dawley rats were divided into control (n=8) and exercise (n=48) groups. The rats in the exercise group ran on the treadmill ( -16°, 20 m/minute) for 90 minutes, and the soleus samples were removed immediately, 6, 12, 24, 48 and 72 hours after exercise (n=8 each time point). The expression levels of α-tubulin, MAP4 and Miro1 were detected by western blot assay, and the ultrastructural changes of mitochondria were observed under transmission electron microscope. RESULTS AND CONCLUSION: The expression level of α-tubulin was decreased significantly at 6 and 12 hours after exercise. The expression level of MAP4 was increased significantly at 6, 12, 48 and 72 hours after exercise. The expression level of Miro1 was increased firstly at 6 and 12 hours after exercise, and decreased at 72 hours after exercise. In the control group, the paired mitochondria were arranged on the both sides of Z line, and few appeared in the myolemma. Mitochondria began to accumulate in the myolemma immediately and 6 hours after exercise; the number achieved the peak at 12 hours, reduced at 24 and 48 hours, and returned to normal at 72 hours. These results suggest that high-intensity exercise can induce the depolymerization of microtubules in the skeletal muscle, thus regulating the movement and distribution of mitochondria via Miro1.
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BACKGROUND:Heavy load exercises can induce the ultrastructural changes in the skeletal muscle by the depolymerization and/or degradation of tubulin in the skeletal muscle, thereby lessening contraction activities of the skeletal muscle. OBJECTIVE:To observe the effects of heavy load exercise and acupuncture on tubulin levels, and to analyze their roles and mechanisms in skeletal muscle injury and repair. METHODS:138 male Sprague-Dawley rats aged 8 weeks were randomly divided into acute exercise group (n=114) and long-term exercise group (n=24). The acute exercise group included four subgroups:sedentary group (n=6), exercise group (n=36), acupunctured group (n=36) and exercise plus acupuncture group (n=36). In the acute exercise experiment, rats were acupunctured after a medium-large intensity downhil running. Rat’s soleus samples were taken immediately, 6, 12, 24, 48 and 72 hours after exercise and/or acupuncture. In the long-term exercise experiment, rats underwent exercise and acupuncture for 3 weeks, and rat’s soleus samples were col ected at 24 hours after the last training. Expressions ofα-tubulin and microtubule-associated protein 4 (MAP4) in the soleus were detected by western blot assay. RESULTS AND CONCLUSION:After acute exercise, expression ofα-tubulin and MAP4 was up-or down-regulated transiently. After acute exercise combined with acupuncture, the protein expressions ofα-tubulin and MAP4 changed slightly. However, the long-term exercise induced an increase inα-tubulin protein expression, while a significant decrease in MAP4 protein expression. It was worth noting that acupuncture treatment reduced long-term exercise-induced variations of MAP4 expression. These results suggest that the heavy load exercise can induce the depolymerization of tubulins in the skeletal muscle, and acupuncture may relieve this effect.
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Objective To explore the effects of an acute exercise on the contractile protein degradation and 26S proteasome activity in skeletal muscle.Methods Thirty-six male Sprague-Dawley rats were randomly divided into 6 groups,each group consisted of 6 rats.They were killed respectively at rest,immediately after half an hour of exercise(running on the treadmill at 25m/min,5% grade),and 1 hour,2h and 6h after one hour exercise.The 3-methylhistidine(3-MH)content,26S proteasome activity and C2 subunit mRNA expression in rat gastrocnemius muscle were detected.Resuits(1)3-MH content increased immediately and 6 hours after exercise,and reached its peak level immediately after half an hour of exercise(P<0.01).(2)26S proteasome activity increased immediately after half an hour of exercise and 6 hours after exercise(P<0.05).(3)Expression of 26S proteasome C2 subunit mRNA Was lower than baseline during and after exercise,but increased sharply 6 hours after exercise(P<0.01).Conclusion The increase in 26S proteasome activity regulated by subunits gene after exercise could enhance skeletal muscle contractile protein degradation
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Lamin A,which is an important skeleton protein in the cell nucleus,can play an important role in maintaining the morphological structures of the cells.This article summarizes the location of LMNA gene in the chromosome,the shape and the structum of lamin A protein;the different diseases of the body which result from the mutations and deletions of LMNA gene in different sites;the differentiation functions of myoblast in which lamin A is involved:degradation of lamin A that may be promoted by Caspase-6;theexpression of lamin Athatmay bepromoted by NFAT5.
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Fiber type of skeletal muscle and its multiple and specialized protein isoform are the structure and molecular basis of the skeletal muscle's function and adaptability.Myosin heavy chain(MHC)isoform,as the factor determinating the type of the skeletal muscle to be fast or slow one,has become molecular biomarker of muscle fiber type and adaptability.Exercise may lead to the transform between myosin subtypes.This article reviewed not only the relation between myosin heavy chain and muscle fiber type of skeletal muscle,but also the influences of different motor patterns' on the transform of skeletal muscle fiber MHC isoform.