Exercise-Induced MicroRNA Regulation in the Mice Nervous System is Maintained after Activity Cessation

MicroRNA ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Andrea Carvalho ◽  
Sonia Zanon ◽  
Guilherme Lucas
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Soleus Muscle ◽  
Expression Profiles ◽  
Ventral Horn ◽  
Synaptic Function ◽  
Microrna Regulation ◽  
Exercise Maintenance ◽  
Spinal Cord Dorsal ◽  
Exercise Induced

Background: Physical exercise can improve synaptic function and protect the nervous system against many diseases by altering gene regulation. MicroRNAs (miRs) have emerged as vital regulators of gene expression and protein synthesis not only in the muscular system, but also in the brain. Objective: Here we investigated whether exercise-induced miRs expression in the nervous and muscular systems is activity-dependent or it remain regulated even after exercise cessation. Methods: The expression profile of miR-1, -16, and -206 was monitored by RT-PCR in the dorsal root ganglion, in the spinal cord dorsal and ventral horn, and in the soleus muscle of mice after 5 weeks of swimming training and after swimming exercise followed by 4 weeks of sedentary conditions. Control animals consisted of mice that swan daily for 30s during the 5-weeks training period, returning to the non-swimming activity for additional 4 weeks. Results: After exercise, miR-1 was upregulated in all tissues investigated. However, the upregulation of miR-1 continued significantly high in both aspects of the spinal cord, and in the soleus muscle. The expression profiles of miR-16, and -206 were increased only in the nervous system. However, miR-16 upregulation persisted in the DRG and in the spinal cord after exercise interruption, whereas miR-206 continued upregulated only in the spinal cord ventral horn. Conclusion: Exercise training can cause long-lasting changes in the expression of miRs independently of exercise maintenance. Spatial and temporal expression of miRs is to some extent dependent on this activity. The data raised a new conceptual hypothesis on the biogenesis of miRs indicating that long-lasting and systematic exercise can potentially cause irreversible miR regulation after activity cessation.

scholarly journals Transcriptome assessment of the Pompe (Gaa−/−) mouse spinal cord indicates widespread neuropathology

2016 ◽  
Vol 48 (11) ◽  
pp. 785-794 ◽  
Author(s):  
S. M. F. Turner ◽  
D. J. Falk ◽  
B. J. Byrne ◽  
D. D. Fuller
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Cell Death ◽  
Nervous System ◽  
Pompe Disease ◽  
Gene Array ◽  
Synaptic Function ◽  
Motor Dysfunction ◽  
Molecular Signature ◽  
Cervical Cord

Pompe disease, caused by deficiency of acid alpha-glucosidase (GAA), leads to widespread glycogen accumulation and profound neuromuscular impairments. There has been controversy, however, regarding the role of central nervous system pathology in Pompe motor dysfunction. We hypothesized that absence of GAA protein causes progressive activation of neuropathological signaling, including pathways associated with cell death. To test this hypothesis, genomic data (Affymetrix Mouse Gene Array 2.0ST) from the midcervical spinal cord in 6 and 16 mo old Pompe ( Gaa −/−) mice were evaluated (Broad Institute Molecular Signature Database), along with spinal cord histology. The midcervical cord was selected because it contains phrenic motoneurons, and phrenic-diaphragm dysfunction is prominent in Pompe disease. Several clinically important themes for the neurologic etiology of Pompe disease emerged from this unbiased genomic assessment. First, pathways associated with cell death were strongly upregulated as Gaa −/− mice aged, and motoneuron apoptosis was histologically verified. Second, proinflammatory signaling was dramatically upregulated in the Gaa −/− spinal cord. Third, many signal transduction pathways in the Gaa −/− cervical cord were altered in a manner suggestive of impaired synaptic function. Notably, glutamatergic signaling pathways were downregulated, as were “synaptic plasticity pathways” including genes related to neuroplasticity. Fourth, many genes and pathways related to cellular metabolism are dysregulated. Collectively, the data unequivocally confirm that systemic absence of GAA induces a complex neuropathological cascade in the spinal cord. Most importantly, the results indicate that Pompe is a neurodegenerative condition, and this underscores the need for early therapeutic intervention capable of targeting the central nervous system.

Exercise-induced gene expression in soleus muscle is dependent on time after spinal cord injury in rats

2003 ◽  
Vol 29 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Esther E. Dupont-Versteegden ◽  
John D. Houlé ◽  
Richard A. Dennis ◽  
Junming Zhang ◽  
Micheal Knox ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Soleus Muscle ◽  
Cord Injury ◽  
Exercise Induced

c-fos proto-oncogene expression in the nervous system during mouse development

1989 ◽  
Vol 9 (5) ◽  
pp. 2269-2272
Author(s):  
J F Caubet
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
In Situ Hybridization ◽  
Dorsal Root ◽  
Olfactory Lobe ◽  
Mouse Development ◽  
Fos Protein ◽  
Spinal Cord Dorsal ◽  
Late Stages

I show, by in situ hybridization, that c-fos is expressed in the nervous system during mouse development. This expression was found to be restricted to specific regions at late stages of development (day 16 postcoitum), particularly to the spinal cord, dorsal root ganglia, and olfactory lobe. The c-fos protein may play a role in the maturation of these structures by activating specific genes.

scholarly journals Reactive Astrocytes in Central Nervous System Injury: Subgroup and Potential Therapy

2021 ◽  
Vol 15 ◽  
Author(s):  
GuiLian Yu ◽  
Ying Zhang ◽  
Bin Ning
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Phenotypic Diversity ◽  
Expression Profiles ◽  
Reactive Astrocytes ◽  
Cns Injury ◽  
Cord Injury

Traumatic central nervous system (CNS) injury, which includes both traumatic brain injury (TBI) and spinal cord injury (SCI), is associated with irreversible loss of neurological function and high medical care costs. Currently, no effective treatment exists to improve the prognosis of patients. Astrocytes comprise the largest population of glial cells in the CNS and, with the advancements in the field of neurology, are increasingly recognized as having key functions in both the brain and the spinal cord. When stimulated by disease or injury, astrocytes become activated and undergo a series of changes, including alterations in gene expression, hypertrophy, the loss of inherent functions, and the acquisition of new ones. Studies have shown that astrocytes are highly heterogeneous with respect to their gene expression profiles, and this heterogeneity accounts for their observed context-dependent phenotypic diversity. In the inured CNS, activated astrocytes play a dual role both as regulators of neuroinflammation and in scar formation. Identifying the subpopulations of reactive astrocytes that exert beneficial or harmful effects will aid in deciphering the pathological mechanisms underlying CNS injuries and ultimately provide a theoretical basis for the development of effective strategies for the treatment of associated conditions. Following CNS injury, as the disease progresses, astrocyte phenotypes undergo continuous changes. Although current research methods do not allow a comprehensive and accurate classification of astrocyte subpopulations in complex pathological contexts, they can nonetheless aid in understanding the roles of astrocytes in disease. In this review, after a brief introduction to the pathology of CNS injury, we summarize current knowledge regarding astrocyte activation following CNS injury, including: (a) the regulatory factors involved in this process; (b) the functions of different astrocyte subgroups based on the existing classification of astrocytes; and (c) attempts at astrocyte-targeted therapy.

scholarly journals Progression of myocardial ischemia leads to unique changes in immediate-early gene expression in the spinal cord dorsal horn

2018 ◽  
Vol 315 (6) ◽  
pp. H1592-H1601 ◽  
Author(s):  
Louis A. Saddic ◽  
Kimberly Howard-Quijano ◽  
Jasmine Kipke ◽  
Yukiko Kubo ◽  
Erica A. Dale ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Spinal Cord ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Dorsal Horn ◽  
Myocardial Injury ◽  
Spinal Cord Dorsal Horn ◽  
Spinal Cord Dorsal ◽  
Over Time

The pathological consequences of ischemic heart disease involve signaling through the autonomic nervous system. Although early activation may serve to maintain hemodynamic stability, persistent aberrant sympathoexcitation contributes to the development of lethal arrhythmias and heart failure. We hypothesized that as the myocardium reacts and remodels to ischemic injury over time, there is an analogous sequence of gene expression changes in the thoracic spinal cord dorsal horn, the processing center for incoming afferent fibers from the heart to the central nervous system. Acute and chronic myocardial ischemia (MI) was induced in a large animal model of Yorkshire pigs, and the thoracic dorsal horn of treated pigs, along with control nonischemic pigs, was harvested for transcriptome analysis. We identified 32 differentially expressed genes between healthy and acute ischemia cohorts and 46 differentially expressed genes between healthy and chronic ischemia cohorts. The canonical immediate-early gene c-fos was upregulated after acute MI, along with fosB, dual specificity phosphatase 1 and 2 ( dusp1 and dusp2), and early growth response 2 (egr2). After chronic MI, there was a persistent yet unique activation of immediate-early genes, including fosB, nuclear receptor subfamily 4 group A members 1−3 ( nr4a1, nr4a2, and nr4a3), egr3, and TNF-α-induced protein 3 ( tnfaip3). In addition, differentially expressed genes from the chronic MI signature were enriched in pathways linked to apoptosis, immune regulation, and the stress response. These findings support a dynamic progression of gene expression changes in the dorsal horn with maturation of myocardial injury, and they may explain how early adaptive autonomic nervous system responses can maintain hemodynamic stability, whereas prolonged maladaptive signals can predispose patients to arrhythmias and heart failure. NEW & NOTEWORTHY Activation of the autonomic nervous system after myocardial injury can provide early cardiovascular support or prolonged aberrant sympathoexcitation. The later response can lead to lethal arrhythmias and heart failure. This study provides evidence of ongoing changes in the gene expression signature of the spinal cord dorsal horn as myocardial injury progresses over time. These changes could help explain how an adaptive nervous system response can become maladaptive over time.

scholarly journals Identification and Characterization of a Rat Novel Gene RSEP4 Expressed Specifically in Central Nervous System

2004 ◽  
Vol 36 (7) ◽  
pp. 501-507
Author(s):  
Xi-Dao Wang ◽  
Ling-Wei Kong ◽  
Zhi-Qin Xie ◽  
Yu-Qiu Zhang ◽  
Zhi-Xin Lin ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Motor Neurons ◽  
Ventral Horn ◽  
Normal Brain ◽  
Reading Frame ◽  
Brain Functions ◽  
Egfp Fusion Protein ◽  
Large Motor

Abstract The low-abundantly expressed genes composed the majorities of the mRNAs expressed in the central nervous system (CNS), and were thought to be important for the normal brain functions. Through differential screening a low-abundance cDNA sublibrary with mRNA from neuropathic pain of chronic constriction injury (CCI) model, we have identified a novel rat gene, rat spinal-cord expression protein 4 gene (RSEP4). The total length of RSEP4 cDNA is 2006 bp, with a 501 nucleotide open reading frame (ORF) that encodes a 167 amino acid polypeptide. Northern blot revealed that RSEP4 was expressed specifically in the CNS. In situ hybridization showed that the mRNA of RSEP4 was strongly expressed in the CA1, CA2, CA3 and DG regions of hippocampus, the Purkinje cells of cerebellum, and the small sensory neurons of dorsal horn and large motor neurons of ventral horn of spinal cord. Over-expression of RSEP4-EGFP fusion protein in the human embryonic kidney 293T cells showed that RSEP4 protein was mainly localized in the cell cytoplasm. These results suggest that RSEP4 may play some roles in the CNS.

scholarly journals c-fos proto-oncogene expression in the nervous system during mouse development.

1989 ◽  
Vol 9 (5) ◽  
pp. 2269-2272 ◽  
Author(s):  
J F Caubet
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
In Situ Hybridization ◽  
Dorsal Root ◽  
Olfactory Lobe ◽  
Mouse Development ◽  
Fos Protein ◽  
Spinal Cord Dorsal ◽  
Late Stages

I show, by in situ hybridization, that c-fos is expressed in the nervous system during mouse development. This expression was found to be restricted to specific regions at late stages of development (day 16 postcoitum), particularly to the spinal cord, dorsal root ganglia, and olfactory lobe. The c-fos protein may play a role in the maturation of these structures by activating specific genes.

β-Mannosidosis: Myelin and oligodendrocyte lesions in brain and spinal cord

1984 ◽  
Vol 42 ◽  
pp. 694-695
Author(s):  
Kathryn L. Lovell ◽  
Margaret Z. Jones
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Genetic Disorder ◽  
Neurological Deficits ◽  
Axonal Spheroids ◽  
South Wales ◽  
Pendular Nystagmus ◽  
Myelin Deficits ◽  
Recessive Defect ◽  
Brain And Spinal Cord

Caprine β-mannosidosis, an autosomal recessive defect of glycoprotein catabolism, is associated with a deficiency of tissue and plasma -mannosidase and with tissue accumulation and urinary excretion of oligosaccharides, including the trisaccharide Man(β1-4)GlcNAc(βl-4)GlcNAc and the disaccharide Man(β1-4)GlcNAc. This genetic disorder is evident at birth, with severe neurological deficits including a marked intention tremor, pendular nystagmus, ataxia and inability to stand. Major pathological characteristics described in Nubian goats in Michigan and in Anglo-Nubian goats in New South Wales include widespread cytoplasmic vacuolation in the nervous system and viscera, axonal spheroids, and severe myelin paucity in the brain but not spinal cord or peripheral nerves. Light microscopic examination revealed marked regional variation in the severity of central nervous system myelin deficits, with some brain areas showing nearly complete absence of myelin and other regions characterized by the presence of 25-50% of the control number of myelin sheaths.

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