scholarly journals The Roles of GABA in Ischemia-Reperfusion Injury in the Central Nervous System and Peripheral Organs

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Chaoran Chen ◽  
Xiang Zhou ◽  
Jialiang He ◽  
Zhenxing Xie ◽  
Shufang Xia ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Vital Role ◽  
Pathological Process ◽  
Peripheral Organs ◽  
Multiple Organs ◽  
Long Time ◽  
The Central Nervous System

Ischemia-reperfusion (I/R) injury is a common pathological process, which may lead to dysfunctions and failures of multiple organs. A flawless medical way of endogenous therapeutic target can illuminate accurate clinical applications. γ-Aminobutyric acid (GABA) has been known as a marker in I/R injury of the central nervous system (mainly in the brain) for a long time, and it may play a vital role in the occurrence of I/R injury. It has been observed that throughout cerebral I/R, levels, syntheses, releases, metabolisms, receptors, and transmissions of GABA undergo complex pathological variations. Scientists have investigated the GABAergic enhancers for attenuating cerebral I/R injury; however, discussions on existing problems and mechanisms of available drugs were seldom carried out so far. Therefore, this review would summarize the process of pathological variations in the GABA system under cerebral I/R injury and will cover corresponding probable issues and mechanisms in using GABA-related drugs to illuminate the concern about clinical illness for accurately preventing cerebral I/R injury. In addition, the study will summarize the increasing GABA signals that can prevent I/R injuries occurring in peripheral organs, and the roles of GABA were also discussed correspondingly.

scholarly journals A review of the relationship between long noncoding RNA and post-stroke injury repair

2019 ◽  
Vol 47 (10) ◽  
pp. 4619-4624
Author(s):  
Yao Wang ◽  
Wei-Yi Pan ◽  
Jun-Sheng Ge ◽  
Xiao-Dong Wang ◽  
Wei Chen ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Noncoding Rna ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Regulatory Sequences ◽  
Post Injury ◽  
Injury Repair ◽  
Post Stroke ◽  
The Central Nervous System

Stroke is a cerebrovascular circulation disorder with sudden onset, which causes disorder of ion balance, inflammation, and acidosis, and that in turn induces ischemia-reperfusion injury, influencing the prognosis of stroke patients. Long noncoding RNAs (lncRNAs) are regulatory sequences involved at the transcriptional, post-transcriptional, and epigenetic levels, have high specific expression in the central nervous system, and effectively regulate the development of the central nervous system and progression of diseases. Stroke induces changes in the expression of many lncRNAs. Therefore, lncRNAs play an important role in the complex pathological process of stroke. Exploring lncRNA could facilitate a comprehensive understanding of the pathological mechanism of stroke and the post-injury molecular regulatory network. However, there are few reports on the role of lncRNA in the pathological development of stroke. In the present review, we discuss the association of lncRNA with post-stroke injury repair.

CXCL12/CXCR4/CXCR7 Chemokine Axis in the Central Nervous System: Therapeutic Targets for Remyelination in Demyelinating Diseases

2017 ◽  
Vol 23 (6) ◽  
pp. 627-648 ◽  
Author(s):  
Tianci Chu ◽  
Lisa B. E. Shields ◽  
Yi Ping Zhang ◽  
Shi-Qing Feng ◽  
Christopher B. Shields ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vital Role ◽  
Pathological Process ◽  
Demyelinating Diseases ◽  
Myelin Repair ◽  
Chemokine Cxcl12 ◽  
The Central Nervous System ◽  
Oligodendrocyte Precursor ◽  
Oligodendrocyte Development

The chemokine CXCL12 plays a vital role in regulating the development of the central nervous system (CNS) by binding to its receptors CXCR4 and CXCR7. Recent studies reported that the CXCL12/CXCR4/CXCR7 axis regulates both embryonic and adult oligodendrocyte precursor cells (OPCs) in their proliferation, migration, and differentiation. The changes in the expression and distribution of CXCL12 and its receptors are tightly associated with the pathological process of demyelination in multiple sclerosis (MS), suggesting that modulating the CXCL12/CXCR4/CXCR7 axis may benefit myelin repair by enhancing OPC recruitment and differentiation. This review aims to integrate the current findings of the CXCL12/CXCR4/CXCR7 signaling pathway in the CNS and to highlight its role in oligodendrocyte development and demyelinating diseases. Furthermore, this review provides potential therapeutic strategies for myelin repair by analyzing the relevance between the pathological changes and the regulatory roles of CXCL12/CXCR4/CXCR7 during MS.

The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis

2019 ◽  
Vol 20 (7) ◽  
pp. 750-758 ◽  
Author(s):  
Yi Wu ◽  
Hengxun He ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropeptide Y ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
Vital Role ◽  
Gut Peptides ◽  
Nonalcoholic Fatty Liver ◽  
The Central Nervous System

Obesity is one of the main challenges of public health in the 21st century. Obesity can induce a series of chronic metabolic diseases, such as diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver, which seriously affect human health. Gut-brain axis, the two-direction pathway formed between enteric nervous system and central nervous system, plays a vital role in the occurrence and development of obesity. Gastrointestinal signals are projected through the gut-brain axis to nervous system, and respond to various gastrointestinal stimulation. The central nervous system regulates visceral activity through the gut-brain axis. Brain-gut peptides have important regulatory roles in the gut-brain axis. The brain-gut peptides of the gastrointestinal system and the nervous system regulate the gastrointestinal movement, feeling, secretion, absorption and other complex functions through endocrine, neurosecretion and paracrine to secrete peptides. Both neuropeptide Y and peptide YY belong to the pancreatic polypeptide family and are important brain-gut peptides. Neuropeptide Y and peptide YY have functions that are closely related to appetite regulation and obesity formation. This review describes the role of the gutbrain axis in regulating appetite and maintaining energy balance, and the functions of brain-gut peptides neuropeptide Y and peptide YY in obesity. The relationship between NPY and PYY and the interaction between the NPY-PYY signaling with the gut microbiota are also described in this review.

scholarly journals Risdiplam distributes and increases SMN protein in both the central nervous system and peripheral organs

2018 ◽  
Vol 6 (6) ◽  
pp. e00447 ◽  
Author(s):  
Agnès Poirier ◽  
Marla Weetall ◽  
Katja Heinig ◽  
Franz Bucheli ◽  
Kerstin Schoenlein ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Peripheral Organs ◽  
The Central Nervous System ◽  
Smn Protein

scholarly journals Yolk sac-derived Pdcd11-positive cells modulate zebrafish microglia differentiation through the NF-κB-Tgfβ1 pathway

2020 ◽  
Vol 28 (1) ◽  
pp. 170-183
Author(s):  
Ruimeng Yang ◽  
Ming Zhan ◽  
Miaomiao Guo ◽  
Hao Yuan ◽  
Yiqin Wang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Susceptibility Gene ◽  
Physiological Role ◽  
Vital Role ◽  
Yolk Sac ◽  
Cerebral White Matter ◽  
Neuron Development ◽  
Mature Brain ◽  
The Central Nervous System

AbstractMicroglia are the primary immune cells in the central nervous system, which plays a vital role in neuron development and neurodegenerative diseases. Microglial precursors in peripheral hematopoietic tissues colonize the central nervous system during early embryogenesis. However, how intrinsic and extrinsic signals integrate to regulate microglia’s differentiation remains undefined. In this study, we identified the cerebral white matter hyperintensities susceptibility gene, programmed cell death protein 11 (PDCD11), as an essential factor regulating microglia differentiation. In zebrafish, pdcd11 deficiency prevents the differentiation of the precursors to mature brain microglia. Although, the inflammatory featured macrophage brain colonization is augmented. At 22 h post fertilization, the Pdcd11-positive cells on the yolk sac are distinct from macrophages and neutrophils. Mechanistically, PDCD11 exerts its physiological role by differentially regulating the functions of nuclear factor-kappa B family members, P65 and c-Rel, suppressing P65-mediated expression of inflammatory cytokines, such as tnfα, and enhancing the c-Rel-dependent appearance of tgfβ1. The present study provides novel insights in understanding microglia differentiation during zebrafish development.

scholarly journals CX3CL1/CX3CR1 in Alzheimer’s Disease: A Target for Neuroprotection

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Peiqing Chen ◽  
Wenjuan Zhao ◽  
Yanjie Guo ◽  
Juan Xu ◽  
Ming Yin
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Early Diagnosis ◽  
Vital Role ◽  
Therapeutic Interventions ◽  
Chemokine Ligand ◽  
The Central Nervous System ◽  
Receptor Cx3cr1

CX3C chemokine ligand 1 (CX3CL1) is an intriguing chemokine belonging to the CX3C family. CX3CL1 is secreted by neurons and plays an important role in modulating glial activation in the central nervous system after binding to its sole receptor CX3CR1 which mainly is expressed on microglia. Emerging data highlights the beneficial potential of CX3CL1-CX3CR1 in the pathogenesis of Alzheimer’s disease (AD), a common progressive neurodegenerative disease, and in the progression of which neuroinflammation plays a vital role. Even so, the importance of CX3CL1/CX3CR1 in AD is still controversial and needs further clarification. In this review, we make an attempt to present a concise map of CX3CL1-CX3CR1 associated with AD to find biomarkers for early diagnosis or therapeutic interventions.

scholarly journals Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin

2016 ◽  
Vol 2 ◽  
pp. 205521731663099 ◽  
Author(s):  
Bert A ’t Hart ◽  
Robert Weissert
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Physiological Function ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Primary Target ◽  
Autoimmune Attack ◽  
Long Time ◽  
The Central Nervous System ◽  
Antigen Presenting ◽  
Draining Lymph Nodes

Background Myelin oligodendrocyte glycoprotein (MOG) is a candidate primary target of the autoimmune attack on the central nervous system (CNS) in multiple sclerosis (MS). However, the physiological function of MOG has been unclear for a long time. Objective We propose that MOG has a central role in the regulation of tolerance and autoimmunity. Conclusion The interaction of MOG with DC-SIGN, an innate antigen receptor of myeloid antigen-presenting cells (m-APCs), present inside the CNS (microglia) or in draining lymph nodes (dendritic cells; DCs), keeps these cells in an immature/tolerogenic state. We postulate that this tolerogenic mechanism may be disturbed in MS by unknown factors.

scholarly journals Neuroinvasion in Prion Diseases: The Roles of Ascending Neural Infection and Blood Dissemination

2010 ◽  
Vol 2010 ◽  
pp. 1-16 ◽  
Author(s):  
Sílvia Sisó ◽  
Lorenzo González ◽  
Martin Jeffrey
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Prion Protein ◽  
Prion Diseases ◽  
Autonomic Nerves ◽  
Peripheral Organs ◽  
Prion Strains ◽  
New Variant ◽  
Jakob Disease ◽  
The Central Nervous System

Prion disorders are infectious, neurodegenerative diseases that affect humans and animals. Susceptibility to some prion diseases such as kuru or the new variant of Creutzfeldt-Jakob disease in humans and scrapie in sheep and goats is influenced by polymorphisms of the coding region of the prion protein gene, while other prion disorders such as fatal familial insomnia, familial Creutzfeldt-Jakob disease, or Gerstmann-Straussler-Scheinker disease in humans have an underlying inherited genetic basis. Several prion strains have been demonstrated experimentally in rodents and sheep. The progression and pathogenesis of disease is influenced by both genetic differences in the prion protein and prion strain. Some prion diseases only affect the central nervous system whereas others involve the peripheral organs prior to neuroinvasion. Many experiments undertaken in different species and using different prion strains have postulated common pathways of neuroinvasion. It is suggested that prions access the autonomic nerves innervating peripheral organs and tissues to finally reach the central nervous system. We review here published data supporting this view and additional data suggesting that neuroinvasion may concurrently or independently involve the blood vascular system.

EFFECT OF SEROTONIN AND NEUROPEPTIDES ON ADENYLATE CYCLASE OF THE CENTRAL NERVOUS SYSTEM AND PERIPHERAL ORGANS OF THE FRESHWATER SNAIL PLANORBARIUS CORNEUS

1996 ◽  
Vol 28 (4) ◽  
pp. 417-424 ◽  
Author(s):  
MARIA ENRICA FERRETTI ◽  
DARIO SONETTI ◽  
MARIA CRISTINA PARESCHI ◽  
MARCO BUZZI ◽  
MARIA LUISA COLAMUSSI ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adenylate Cyclase ◽  
Freshwater Snail ◽  
Planorbarius Corneus ◽  
Peripheral Organs ◽  
The Central Nervous System
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