Histological investigations on the dura mater vascular system of mice

Mecheri, Badreddine; Paris, Frank; Lübbert, Hermann

doi:10.1016/j.acthis.2018.09.009

Cited by 17 publications

(26 citation statements)

References 39 publications

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Section: Discussionmentioning

confidence: 99%

“…Our study demonstrates the critical role dura mater BVs play in the functional regeneration of the dura mater tissue, with respect to its immunological function and stromal integrity. Although the dura mater vascular bed is separate from the pia mater and brain interconnected beds 8 , 9 and therefore does not inflict direct vascular damage to the latter if injured, how the functional recovery of the dura mater potentially affects brain function also requires further investigation. While the debate on employing anti-VEGF therapy to manage cerebral edema in stroke and HI patients continues 12 , 43 – 46 , our results suggest that targeting this angiogenic pathway in HI patients may impede dura mater recovery and compromise its primary functions.…”

Section: Discussionmentioning

confidence: 99%

“…The meninges are composed of the dura mater, arachnoid membrane, subarachnoid space, and pia mater, all of which protect the brain 6,7 . The dura mater is highly vascularized with precapillary arterioles, capillary beds, and postcapillary venules 8,9 , of which the latter two vessel types support immune cell trafficking and surveillance for the protection of the central nervous system 10 .…”

mentioning

confidence: 99%

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VEGFR2 signaling drives meningeal vascular regeneration upon head injury

et al. 2020

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Upon severe head injury (HI), blood vessels of the meninges and brain parenchyma are inevitably damaged. While limited vascular regeneration of the injured brain has been studied extensively, our understanding of meningeal vascular regeneration following head injury is quite limited. Here, we identify key pathways governing meningeal vascular regeneration following HI. Rapid and complete vascular regeneration in the meninges is predominantly driven by VEGFR2 signaling. Substantial increase of VEGFR2 is observed in both human patients and mouse models of HI, and endothelial cell-specific deletion of Vegfr2 in the latter inhibits meningeal vascular regeneration. We further identify the facilitating, stabilizing and arresting roles of Tie2, PDGFRβ and Dll4 signaling, respectively, in meningeal vascular regeneration. Prolonged inhibition of this angiogenic process following HI compromises immunological and stromal integrity of the injured meninges. These findings establish a molecular framework for meningeal vascular regeneration after HI, and may guide development of wound healing therapeutics.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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VEGFR2 signaling drives meningeal vascular regeneration upon head injury

et al. 2020

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“…While the possible transit of immune cells from the dura to the CNS parenchyma remains unclear, different interchanges between dura and SAS can occur and remain an active area of study (97). Recent investigations have highlighted direct venous connections allowing neutrophils and potentially other myeloid cells to transit between the brain dural vasculature and the skull bone marrow (117,118). Dural resident macrophages are characterized as a dense Lyve1 low MHCII high population, with few Lyve1 high MHCII + cells present (15) in a different relative proportion compared to the SAS (119).…”

Section: Resident Dural Macrophagesmentioning

confidence: 99%

Section: Barrier-associated Dwellers: Location and Homeostatic Functimentioning

confidence: 99%

Dwellers and Trespassers: Mononuclear Phagocytes at the Borders of the Central Nervous System

et al. 2021

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The central nervous system (CNS) parenchyma is enclosed and protected by a multilayered system of cellular and acellular barriers, functionally separating glia and neurons from peripheral circulation and blood-borne immune cells. Populating these borders as dynamic observers, CNS-resident macrophages contribute to organ homeostasis. Upon autoimmune, traumatic or neurodegenerative inflammation, these phagocytes start playing additional roles as immune regulators contributing to disease evolution. At the same time, pathological CNS conditions drive the migration and recruitment of blood-borne monocyte-derived cells across distinct local gateways. This invasion process drastically increases border complexity and can lead to parenchymal infiltration of blood-borne phagocytes playing a direct role both in damage and in tissue repair. While recent studies and technical advancements have highlighted the extreme heterogeneity of these resident and CNS-invading cells, both the compartment-specific mechanism of invasion and the functional specification of intruding and resident cells remain unclear. This review illustrates the complexity of mononuclear phagocytes at CNS interfaces, indicating how further studies of CNS border dynamics are crucially needed to shed light on local and systemic regulation of CNS functions and dysfunctions.

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Immune compartments at the brain’s borders in health and neurovascular diseases

et al. 2023

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Recent evidence implicates cranial border immune compartments in the meninges, choroid plexus, circumventricular organs, and skull bone marrow in several neuroinflammatory and neoplastic diseases. Their pathogenic importance has also been described for cardiovascular diseases such as hypertension and stroke. In this review, we will examine the cellular composition of these cranial border immune niches, the potential pathways through which they might interact, and the evidence linking them to cardiovascular disease.

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Histological investigations on the dura mater vascular system of mice

Cited by 17 publications

References 39 publications

VEGFR2 signaling drives meningeal vascular regeneration upon head injury

VEGFR2 signaling drives meningeal vascular regeneration upon head injury

Dwellers and Trespassers: Mononuclear Phagocytes at the Borders of the Central Nervous System

Immune compartments at the brain’s borders in health and neurovascular diseases

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