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Genesis (New York, N.Y. : 2000) May 2019The meninges are membranous layers surrounding the central nervous system. In the head, the meninges lie between the brain and the skull, and interact closely with both... (Review)
Review
The meninges are membranous layers surrounding the central nervous system. In the head, the meninges lie between the brain and the skull, and interact closely with both during development. The cranial meninges originate from a mesenchymal sheath on the surface of the developing brain, called primary meninx, and undergo differentiation into three layers with distinct histological characteristics: the dura mater, the arachnoid mater, and the pia mater. While genetic regulation of meningeal development is still poorly understood, mouse mutants and other models with meningeal defects have demonstrated the importance of the meninges to normal development of the calvaria and the brain. For the calvaria, the interactions with the meninges are necessary for the progression of calvarial osteogenesis during early development. In later stages, the meninges control the patterning of the skull and the fate of the sutures. For the brain, the meninges regulate diverse processes including cell survival, cell migration, generation of neurons from progenitors, and vascularization. Also, the meninges serve as a stem cell niche for the brain in the postnatal life. Given these important roles of the meninges, further investigation into the molecular mechanisms underlying meningeal development can provide novel insights into the coordinated development of the head.
Topics: Animals; Arachnoid; Brain; Cell Differentiation; Developmental Biology; Dura Mater; Humans; Meninges; Pia Mater; Skull
PubMed: 30801905
DOI: 10.1002/dvg.23288 -
Cell Feb 2021Despite the established dogma of central nervous system (CNS) immune privilege, neuroimmune interactions play an active role in diverse neurological disorders. However,...
Despite the established dogma of central nervous system (CNS) immune privilege, neuroimmune interactions play an active role in diverse neurological disorders. However, the precise mechanisms underlying CNS immune surveillance remain elusive; particularly, the anatomical sites where peripheral adaptive immunity can sample CNS-derived antigens and the cellular and molecular mediators orchestrating this surveillance. Here, we demonstrate that CNS-derived antigens in the cerebrospinal fluid (CSF) accumulate around the dural sinuses, are captured by local antigen-presenting cells, and are presented to patrolling T cells. This surveillance is enabled by endothelial and mural cells forming the sinus stromal niche. T cell recognition of CSF-derived antigens at this site promoted tissue resident phenotypes and effector functions within the dural meninges. These findings highlight the critical role of dural sinuses as a neuroimmune interface, where brain antigens are surveyed under steady-state conditions, and shed light on age-related dysfunction and neuroinflammatory attack in animal models of multiple sclerosis.
Topics: Animals; Antigen Presentation; Antigen-Presenting Cells; Antigens; Cellular Senescence; Chemokine CXCL12; Cranial Sinuses; Dura Mater; Female; Homeostasis; Humans; Immunity; Male; Mice, Inbred C57BL; Phenotype; Stromal Cells; T-Lymphocytes; Mice
PubMed: 33508229
DOI: 10.1016/j.cell.2020.12.040 -
Arquivos de Neuro-psiquiatria Dec 2020Hypertrophic pachymeningitis (HP) is a non-usual manifestation of rheumatologic, infectious, and neoplastic diseases. Etiological diagnosis is a challenge, but when made...
IMPORTANCE
Hypertrophic pachymeningitis (HP) is a non-usual manifestation of rheumatologic, infectious, and neoplastic diseases. Etiological diagnosis is a challenge, but when made promptly it creates a window of opportunity for treatment, with the possibility of a total reversal of symptoms.
OBSERVATIONS
HP is an inflammatory process of the dura mater that can occur as a manifestation of sarcoidosis, granulomatosis with polyangiitis, and IgG4-related disease. The HP case evaluation is extensive and includes central nervous system imaging, cerebrospinal fluid analysis, serology, rheumatologic tests, and systemic survey for other manifestations sites. After systemic investigation, meningeal biopsy might be necessary. Etiology guides HP treatment, and autoimmune disorders are treated with corticosteroids alone or associated with an immunosuppressor.
CONCLUSION
HP is a manifestation of several diseases, and a precise etiological diagnosis is crucial because of the difference among treatments. An extensive investigation of patients with HP helps early diagnosis and correct treatment.
Topics: Adrenal Cortex Hormones; Dura Mater; Humans; Hypertrophy; Magnetic Resonance Imaging; Meningitis
PubMed: 33295420
DOI: 10.1590/0004-282X20200073 -
Clinical Interventions in Aging 2019Lumbar disc herniation into the dural space is a very rare phenomenon of degenerative lumbar lesions in the elderly population, and its potential pathogenesis and... (Review)
Review
BACKGROUND
Lumbar disc herniation into the dural space is a very rare phenomenon of degenerative lumbar lesions in the elderly population, and its potential pathogenesis and natural course remain unclear.
CASE DESCRIPTION
We describe a rare case of intradural lumbar disc herniation. A 68-year-old man presented with progressive lower back pain and radiating pain and numbness in both legs for 3 years. Magnetic resonance imaging revealed a large herniated disc at L4-L5. Posterior discectomy and fusion of the L4-L5 was performed after conservative treatment failed. Intraoperatively, only minimal disc fragments in the epidural space were found after meticulous probing following laminectomy of the L4-L5 vertebrae. The dorsal dura mater was saturated, tense, and bulged at the L4-L5 levels; additionally, an intradural mass was palpable and confirmed by intraoperative ultrasonography. Subsequently, dorsal middle durotomy was performed. Upon opening the dural sac, a large cauliflower-like mass similar to nucleus pulposus tissue was found near the arachnoid membrane. The mass was dissociative and could be completely resected. The dorsal dural incisions were closed after careful exploration, followed by fixation and fusion of the L4-L5 levels. Pathological examination revealed disc tissue with central balloon-type cystic degenerative changes. The patient's lower back pain and radiating pain and numbness of both legs improved remarkably postoperatively, and he became asymptomatic at 3 months postoperatively.
CONCLUSION
Intradural lumbar disc herniation should be highly suspected when intraoperative findings are incompatible with findings from the preoperative imaging examination, and it could be further confirmed via intraoperative ultrasonography and pathological examination of the resected tissue from the dural space. Prompt surgery is recommended, and surgical results are usually favorable. We also reviewed the literature and discussed the potential pathogenesis, natural course, diagnosis, and treatment of intradural lumbar disc herniation.
Topics: Aged; Dura Mater; Humans; Intervertebral Disc Displacement; Low Back Pain; Lumbar Vertebrae; Magnetic Resonance Imaging; Male; Radiculopathy
PubMed: 31920293
DOI: 10.2147/CIA.S228717 -
Arquivos de Neuro-psiquiatria Dec 2022RNA extraction is a step that precedes several molecular techniques. The fibrous tissue, more specifically the dura mater, has several limitations in routine protocols,...
BACKGROUND
RNA extraction is a step that precedes several molecular techniques. The fibrous tissue, more specifically the dura mater, has several limitations in routine protocols, and lacks optimization protocols to overcome these problems.
OBJECTIVE
To test stock reagents and purification kits, optimizing commercial kit protocols for RNA extraction from the dura mater.
METHODS
Dura mater samples were obtained from eight Wistar rats and maintained in two different stabilizers. The samples were purified using four different protocols, and the RNA was evaluated for the yield and purity in NanoDrop 2000 (Thermo Scientific, Wilmington, DE, United States). Beta-actin gene was used for analyzing gene expression, since is one of the most used reference genes.
RESULTS
The RNA preservation was similar in both stabilizers. The addition of an incubation step prior the purification protocols allowed better tissue digestion and RNA recovery. The RNA purified using the protocols membrane-based showed higher quality than liquid-liquid purification. This impact was observed in the 3-week evaluation using RT-qPCR.
CONCLUSION
Stabilizers are efficient for RNA preservation and membrane-based purification protocols are more suitable for RNA recovery from dura mater tissue, allowing the evaluation of gene expression in this type of tissue. Adaptations in the dura mater RNA extraction protocol differ from the pre-established protocols because it takes into account the peculiarity of fibrous tissue and low cellularity. In addition to providing a low-cost mechanism, based on techniques that are part of the laboratory routine, it is possible to improve the quality of the extracted material, ensuring greater efficiency in the use of subsequent techniques.
Topics: Animals; Rats; Rats, Wistar; RNA; Dura Mater
PubMed: 36580958
DOI: 10.1055/s-0042-1758865 -
Stem Cell Reviews and Reports Dec 2022Patient-derived cells hold great promise for precision medicine approaches in human health. Human dermal fibroblasts have been a major source of cells for reprogramming...
Patient-derived cells hold great promise for precision medicine approaches in human health. Human dermal fibroblasts have been a major source of cells for reprogramming and differentiating into specific cell types for disease modeling. Postmortem human dura mater has been suggested as a primary source of fibroblasts for in vitro modeling of neurodegenerative diseases. Although fibroblast-like cells from human and mouse dura mater have been previously described, their utility for reprogramming and direct differentiation protocols has not been fully established. In this study, cells derived from postmortem dura mater are directly compared to those from dermal biopsies of living subjects. In two instances, we have isolated and compared dermal and dural cell lines from the same subject. Notably, striking differences were observed between cells of dermal and dural origin. Compared to dermal fibroblasts, postmortem dura mater-derived cells demonstrated different morphology, slower growth rates, and a higher rate of karyotype abnormality. Dura mater-derived cells also failed to express fibroblast protein markers. When dermal fibroblasts and dura mater-derived cells from the same subject were compared, they exhibited highly divergent gene expression profiles that suggest dura mater cells originated from a mixed mural lineage. Given their postmortem origin, somatic mutation signatures of dura mater-derived cells were assessed and suggest defective DNA damage repair. This study argues for rigorous karyotyping of postmortem derived cell lines and highlights limitations of postmortem human dura mater-derived cells for modeling normal biology or disease-associated pathobiology.
Topics: Humans; Animals; Mice; Transcriptome; Dura Mater; Cell Differentiation; Fibroblasts; Cells, Cultured
PubMed: 35809166
DOI: 10.1007/s12015-022-10416-x -
AJNR. American Journal of Neuroradiology Feb 2022Intracranial dural AVFs are abnormal communications between arteries that supply the dura mater and draining cortical veins or venous sinuses. They are believed to form... (Review)
Review
Intracranial dural AVFs are abnormal communications between arteries that supply the dura mater and draining cortical veins or venous sinuses. They are believed to form as a response to venous insults such as thrombosis, trauma, or infection. Classification and management are dependent on the presence of drainage/reflux into cortical veins because such drainage markedly elevates the risk of hemorrhage or venous congestion, resulting in neurologic deficits. AVFs with tolerable symptoms and benign drainage patterns can be managed conservatively. Intolerable symptoms, presentation with hemorrhage/neurologic deficits, or aggressive drainage patterns are indications for intervention. Treatment options include microsurgical disconnection, endovascular transarterial embolization, transvenous embolization, or a combination. This is the first in a series of 3 articles on endovascular management of intracranial dural AVFs, in which we outline the principles and outcomes of endovascular treatment.
Topics: Central Nervous System Vascular Malformations; Cerebral Angiography; Drainage; Dura Mater; Embolization, Therapeutic; Endovascular Procedures; Humans; Veins
PubMed: 34674996
DOI: 10.3174/ajnr.A7304 -
PloS One 2023The cornea and cranial dura mater share sensory innervation. This link raises the possibility that pathological impulses mediated by corneal injury may be transmitted to...
The cornea and cranial dura mater share sensory innervation. This link raises the possibility that pathological impulses mediated by corneal injury may be transmitted to the cranial dura, trigger dural perivascular/connective tissue nociceptor responses, and induce vascular and stromal alterations affecting dura mater blood and lymphatic vessel functionality. In this study, using a mouse model, we demonstrate for the first time that two weeks after the initial insult, alkaline injury to the cornea leads to remote pathological changes within the coronal suture area of the dura mater. Specifically, we detected significant pro-fibrotic changes in the dural stroma, as well as vascular remodeling characterized by alterations in vascular smooth muscle cell (VSMC) morphology, reduced blood vessel VSMC coverage, endothelial cell expression of the fibroblast specific protein 1, and significant increase in the number of podoplanin-positive lymphatic sprouts. Intriguingly, the deficiency of a major extracellular matrix component, small leucine-rich proteoglycan decorin, modifies both the direction and the extent of these changes. As the dura mater is the most important route for the brain metabolic clearance, these results are of clinical relevance and provide a much-needed link explaining the association between ophthalmic conditions and the development of neurodegenerative diseases.
Topics: Humans; Cranial Sutures; Skull; Connective Tissue; Dura Mater; Corneal Injuries
PubMed: 37079653
DOI: 10.1371/journal.pone.0284082 -
Distinct origins of dura mater graft-associated Creutzfeldt-Jakob disease: past and future problems.Acta Neuropathologica Communications Mar 2014Dura mater graft-associated Creutzfeldt-Jakob disease (dCJD) can be divided into two subgroups that exhibit distinct clinical and neuropathological features, with the... (Review)
Review
Dura mater graft-associated Creutzfeldt-Jakob disease (dCJD) can be divided into two subgroups that exhibit distinct clinical and neuropathological features, with the majority represented by a non-plaque-type of dCJD (np-dCJD) and the minority by a plaque-type of dCJD (p-dCJD). The two distinct phenotypes of dCJD had been considered to be unrelated to the genotype (methionine, M or valine, V) at polymorphic codon 129 of the PRNP gene or type (type 1 or type 2) of abnormal isoform of prion protein (PrPSc) in the brain, while these are major determinants of clinicopathological phenotypes of sporadic CJD (sCJD). The reason for the existence of two distinct subgroups in dCJD had remained elusive. Recent progress in research of the pathogenesis of dCJD has revealed that two distinct subgroups of dCJD are caused by infection with different PrPSc strains from sCJD, i.e., np-dCJD caused by infection with sCJD-MM1/MV1, and p-dCJD caused by infection with sCJD-VV2 or -MV2. These studies have also revealed previously unrecognized problems as follows: (i) the numbers of p-dCJD patients may increase in the future, (ii) the potential risks of secondary infection from dCJD, particularly from p-dCJD, may be considerable, and (iii) the effectiveness of the current PrPSc decontamination procedures against the PrPSc from p-dCJD is uncertain. To prevent secondary infection from p-dCJD, the establishment of effective decontamination procedures is an urgent issue. In this review, we summarize the past and future problems surrounding dCJD.
Topics: Animals; Brain Tissue Transplantation; Creutzfeldt-Jakob Syndrome; Dura Mater; Humans
PubMed: 24685293
DOI: 10.1186/2051-5960-2-32 -
Scientific Reports Mar 2022Galanin (GAL) is a nociceptive transmitter or modulator in the trigeminal sensory system. In this study, GAL expression was investigated in the rat dura mater to...
Galanin (GAL) is a nociceptive transmitter or modulator in the trigeminal sensory system. In this study, GAL expression was investigated in the rat dura mater to demonstrate its possible function in headache using immunohistochemical techniques. The cerebral falx and cerebellar dura mater received abundant blood and nerve supply, and were significantly thicker compared to other portions in the cerebral dura mater. GAL-immunoreactivity was expressed by cell and nerve fiber profiles. Presumed macrophages and dendritic cells contained GAL-immunoreactivity, and co-expressed with CD11b-immunoreactivity. Many isolated and perivascular nerve fibers also showed GAL-immunoreactivity. In addition, GAL-immunoreactive nerve fibers were present in the vicinity of macrophages and dendritic cells with either GAL- or ED1-immunoreactivity. GAL-immunoreactive cells and nerve fibers were common in the cerebral falx and cerebellar dura mater and infrequent in other portions. And, GAL-immunoreactive nerve fibers usually co-expressed calcitonin gene-related peptide (CGRP)-immunoreactivity. In the trigeminal ganglion, a substantial proportion of sensory neurons innervating the dura mater contained GAL-immunoreactivity (mean ± SD, 3.4 ± 2.2%), and co-expressed CGRP-immunoreactivity (2.7 ± 2.1%). The present study may suggest that GAL is associated with nociceptive transduction or modulation in the dura mater. GAL also possibly plays a role in the immune mechanism of the dura mater.
Topics: Animals; Calcitonin Gene-Related Peptide; Dura Mater; Galanin; Headache; Immune System; Rats; Sensory Receptor Cells
PubMed: 35338230
DOI: 10.1038/s41598-022-09325-3