Browse
Submit Data
Databases
API
Help

Dataset Information

30 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

S100A4 in the Physiology and Pathology of the Central and Peripheral Nervous System.

ABSTRACT: S100A4 is a member of the large family of S100 proteins, exerting a broad range of intracellular and extracellular functions that vary upon different cellular contexts. While S100A4 has long been implicated mainly in tumorigenesis and metastatization, mounting evidence shows that S100A4 is a key player in promoting pro-inflammatory phenotypes and organ pro-fibrotic pathways in the liver, kidney, lung, heart, tendons, and synovial tissues. Regarding the nervous system, there is still limited information concerning S100A4 presence and function. It was observed that S100A4 exerts physiological roles contributing to neurogenesis, cellular motility and chemotaxis, cell differentiation, and cell-to cell communication. Furthermore, S100A4 is likely to participate to numerous pathological processes of the nervous system by affecting the functions of astrocytes, microglia, infiltrating cells and neurons and thereby modulating inflammation and immune reactions, fibrosis as well as neuronal plasticity and survival. This review summarizes the current state of knowledge concerning the localization, deregulation, and possible functions of S100A4 in the physiology of the central and peripheral nervous system. Furthermore, we highlight S100A4 as a gene involved in the pathogenesis of neurological disorders such as brain tumors, neurodegenerative diseases, and acute injuries.

SUBMITTER: D'Ambrosi N

PROVIDER: S-EPMC8066633 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Autophagy in the physiology and pathology of the central nervous system.

Project description:Neurons are highly specialized postmitotic cells that depend on dynamic cellular processes for their proper function.These include among others, neuronal growth and maturation, axonal migration, synapse formation and elimination, all requiring continuous protein synthesis and degradation. Therefore quality-control processes in neurons are directly linked to their physiology. Autophagy is a tightly regulated cellular degradation pathway by which defective or superfluouscytosolic proteins, organelles and other cellular constituents are sequestered in autophagosomes and delivered to lysosomes for degradation. Here we present emerging evidence indicating that constitutive autophagic fluxin neurons has essential roles in key neuronal processes under physiological conditions.Moreover, we discuss how perturbations of the autophagic pathway may underlie diverse pathological phenotypes in neurons associated with neurodevelopmental and neurodegenerative diseases.

| S-EPMC4326580 | biostudies-other

Olfactory Pathology in Central Nervous System Demyelinating Diseases.

Project description:Olfactory dysfunction is common in multiple sclerosis (MS). Olfactory bulb and tract pathology in MS and other demyelinating diseases remain unexplored. A human autopsy cohort of pathologically confirmed cases encompassing the spectrum of demyelinating disease (MS; n = 17), neuromyelitis optica [(NMO); n = 3] and acute disseminated encephalomyelitis [(ADEM); n = 7] was compared to neuroinflammatory [herpes simplex virus encephalitis (HSE); n = 3], neurodegenerative [Alzheimer's disease (AD); n = 4] and non-neurologic (n = 8) controls. For each case, olfactory bulbs and/or tracts were stained for myelin, axons and inflammation. Inferior frontal cortex and hippocampus were stained for myelin in a subset of MS and ADEM cases. Olfactory bulb/tract demyelination was frequent in all demyelinating diseases [MS 12/17 (70.6%); ADEM 3/7 (42.9%); NMO 2/3 (66.7%)] but was absent in HSE, AD and non-neurologic controls. Inflammation was greater in the demyelinating diseases compared to non-neurologic controls. Olfactory bulb/tract axonal loss was most severe in MS where it correlated significantly with the extent of demyelination (r = 0.610, P = 0.009) and parenchymal inflammation (r = 0.681, P = 0.003). The extent of olfactory bulb/tract demyelination correlated with that found in the adjacent inferior frontal cortex but not hippocampus. We provide unequivocal evidence that olfactory bulb/tract demyelination is frequent, can occur early and is highly inflammatory, and is specific to demyelinating disease.

| S-EPMC8029356 | biostudies-literature

Sox10 Binding Analysis in the Central and Peripheral Nervous System

Project description:ChIP-seq of Sox10 in spinal cord and sciatic nerve 2 independent Sox10 ChIP samples each for spinal cord (CNS) and sciatic nerve (PNS), with respective inputs

2015-04-01 | E-GEOD-64703 | biostudies-arrayexpress

Sox10 Binding Analysis in the Central and Peripheral Nervous System

Project description:ChIP-seq of Sox10 in spinal cord and sciatic nerve was performed to determine shared and unique binding sites for Sox10 in oligodendrocytes and Schwann cells, respectively. Sox10 is required for both Schwann cell and oligodendrocyte development. In addition, differentiation of myelinating glia is dependent upon axonal signaling, so these studies were performed in vivo.

2015-04-01 | GSE64703 | GEO

Role of the Peripheral Nervous System in PD Pathology, Diagnosis, and Treatment.

Project description:Studies on Parkinson disease (PD) have mostly focused on the central nervous system-specifically, on the loss of mesencephalic dopaminergic neurons and associated motor dysfunction. However, the peripheral nervous system (PNS) is gaining prominence in PD research, with increasing clinical attention being paid to non-motor symptoms. Researchers found abnormal deposition of α-synuclein and neuroinflammation in the PNS. Attempts have been made to use these pathological changes during the clinical diagnosis of PD. Animal studies demonstrated that combined transplantation of autologous peripheral nerves and cells with tyrosine hydroxylase activity can reduce dopaminergic neuronal damage, and similar effects were observed in some clinical trials. In this review, we will systematically explain PNS performance in PD pathology and its clinical diagnostic research, describe PNS experimental results [especially Schwann cell (SC) transplantation in the treatment of PD animal models] and the results of clinical trials, and discuss future directions. The mechanism by which SCs produce such a therapeutic effect and the safety of transplantation therapy are briefly described.

| S-EPMC8119739 | biostudies-literature

DNA methylation temporal profiling following peripheral versus central nervous system axotomy.

Project description:The regulatory mechanisms responsible for the gene expression pattern associated with axotomy-dependent signaling affecting the neuronal phenotype, including the axonal regenerative program, remain unclear. To further this understanding, we recently performed DNA methylation temporal profiling in lumbar dorsal root ganglia (DRG) after axotomy of the central spinal (non-regenerating) and of the peripheral sciatic nerve (regenerating) axonal branches. DNA methylation microarrays for mouse gene promoters and CpG islands (Roche/NimbleGen) were employed after immunoprecipitation of 5-methylcytosine-DNA. Here we provide a detailed data descriptor of this DNA methylation dataset, which allows in depth evaluation of the experimental design, assessment of data reproducibility and a full interactive operator-based systematic data analysis. In fact, we offer a methylation 'hit' scoring map of the whole microarray data in a workable spreadsheet that allows data sorting by genes, conditions or hits of interests that is ready for functional gene annotation and classification. This dataset allows investigators bioinformatic comparison to other epigenetic and gene expression datasets and further experimental characterization of the role of DNA methylation in axotomy-dependent pathways.

| S-EPMC4411011 | biostudies-literature

<i>BRAF</i> Alteration in Central and Peripheral Nervous System Tumors.

Project description:BRAF (alternately referred to as v-raf murine sarcoma viral oncogene homolog B1) is a proto-oncogene involved in the mitogen-activated protein kinase (MAPK) pathway. BRAF alterations are most commonly missense mutations or aberrant fusions. These mutations are observed in numerous primary central nervous system tumors as well as metastases. This review discusses the prevalence of BRAF alteration within select notable CNS tumors, and their prognostic associations. Included are some novel entities such as diffuse leptomeningeal glioneuronal tumor (DLGNT), polymorphous low grade neuroepithelial tumor of the young (PLNTY), and multinodular and vacuolating neuronal tumor (MVNT). Knowledge of this gene's integrity in CNS and PNS tumors can have profound diagnostic and therapeutic implications. Also reviewed are the current state of targeted therapy against aberrant BRAF as it pertains mostly to the CNS and to a lesser extent in PNS, and certain diagnostic aspects.

| S-EPMC7523461 | biostudies-literature

Molecular Pathology and Targeted Therapies for Personalized Management of Central Nervous System Germinoma.

Project description:Intracranial germinomas are rare tumours, usually affecting male paediatric patients. They frequently develop in the pineal and suprasellar regions, causing endocrinological disturbances, visual deficits, and increased intracranial pressure. The diagnosis is established on magnetic resonance imaging (MRI), serum and cerebrospinal fluid (CSF) markers, and tumour stereotactic biopsy. Imaging techniques, such as susceptibility-weighted imaging (SWI), T2* (T2-star) gradient echo (GRE) or arterial spin labelling based perfusion-weighted MRI (ASL-PWI) facilitate the diagnosis. Germinomas are highly radiosensitive tumours, with survival rates >90% in the context of chemoradiotherapy. However, patients with resistant disease have limited therapeutic options and poor survival. The aim of this review is to highlight the genetic, epigenetic, and immunologic features, which could provide the basis for targeted therapy. Intracranial germinomas present genetic and epigenetic alterations (chromosomal aberrations, KIT, MAPK and PI3K pathways mutations, DNA hypomethylation, miRNA dysregulation) that may represent targets for therapy. Tyrosine kinase and mTOR inhibitors warrant further investigation in these cases. Immune markers, PD-1 (programmed cell death protein 1) and PD-L1 (programmed death-ligand 1), are expressed in germinomas, representing potential targets for immune checkpoint inhibitors. Resistant cases should benefit from a personalized management: genetic and immunological testing and enrolment in trials evaluating targeted therapies in intracranial germinomas.

| S-EPMC8306901 | biostudies-literature

Boundary cap cells are peripheral nervous system stem cells that can be redirected into central nervous system lineages.

Project description:Boundary cap cells (BC), which express the transcription factor Krox20, participate in the formation of the boundary between the central nervous system and the peripheral nervous system. To study BC stemness, we developed a method to purify and amplify BC in vitro from Krox20(Cre/+), R26R(YFP/+) mouse embryos. We show that BC progeny are EGF/FGF2-responsive, form spheres, and express neural crest markers. Upon growth factor withdrawal, BC progeny gave rise to multiple neural crest and CNS lineages. Transplanted into the developing murine forebrain, they successfully survived, migrated, and integrated within the host environment. Surprisingly, BC progeny generated exclusively CNS cells, including neurons, astrocytes, and myelin-forming oligodendrocytes. In vitro experiments indicated that a sequential combination of ventralizing morphogens and glial growth factors was necessary to reprogram BC into oligodendrocytes. Thus, BC progeny are endowed with differentiation plasticity beyond the peripheral nervous system. The demonstration that CNS developmental cues can reprogram neural crest-derived stem cells into CNS derivatives suggests that BC could serve as a source of cell type-specific lineages, including oligodendrocytes, for cell-based therapies to treat CNS disorders.

| S-EPMC3127889 | biostudies-other

Drug Targets in Neurotrophin Signaling in the Central and Peripheral Nervous System.

Project description:Neurotrophins are a family of proteins that play an important role in the regulation of the growth, survival, and differentiation of neurons in the central and peripheral nervous system. Neurotrophins were earlier characterized by their role in early development, growth, maintenance, and the plasticity of the nervous system during development, but recent findings also indicate their complex role during normal physiology in both neuronal and non-neuronal tissues. Therefore, it is important to recognize a deficiency in the expression of neurotrophins, a major factor driving the debilitating features of several neurologic and psychiatric diseases/disorders. On the other hand, overexpression of neurotrophins is well known to play a critical role in pathogenesis of chronic pain and afferent sensitization, underlying conditions such as lower urinary tract symptoms (LUTS)/disorders and osteoarthritis. The existence of a redundant receptor system of high-and low-affinity receptors accounts for the diverse, often antagonistic, effects of neurotrophins in neurons and non-neuronal tissues in a spatial and temporal manner. In addition, studies looking at bladder dysfunction because of conditions such as spinal cord injury and diabetes mellitus have found alterations in the levels of these neurotrophins in the bladder, as well as in sensory afferent neurons, which further opens a new avenue for therapeutic targets. In this review, we will discuss the characteristics and roles of key neurotrophins and their involvement in the central and periphery nervous system in both normal and diseased conditions.

| S-EPMC7444275 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data