After traumatic spinal cord injury (SCI), disruption and plasticity of the microvasculature within injured spinal tissue contribute to the pathological cascades associated with the evolution of both primary and secondary injury. Conversely, preserved vascular function most likely results in tissue sparing and subsequent functional recovery. It has been difficult to identify subclasses of damaged or regenerating blood vessels at the cellular level. Here, adult mice received a single intravenous injection of the Griffonia simplicifolia isolectin B4 (IB4) at 1-28 days following a moderate thoracic (T9) contusion. Vascular binding of IB4 was maximally observed 7 days following injury, a time associated with multiple pathologic aspects of the intrinsic adaptive angiogenesis, with numbers of IB4 vascular profiles decreasing by 21 days postinjury. Quantitative assessment of IB4 binding shows that it occurs within the evolving lesion epicenter, with affected vessels expressing a temporally specific dysfunctional tight junctional phenotype as assessed by occludin, claudin-5, and ZO-1 immunoreactivities. Taken together, these results demonstrate that intravascular lectin delivery following SCI is a useful approach not only for observing the functional status of neovascular formation but also for definitively identifying specific subpopulations of reactive spinal microvascular elements.

Griffonia simplicifolia isolectin B4 identifies a specific subpopulation of angiogenic blood vessels following contusive spinal cord injury in the adult mouse.

Dysfunction of the blood-brain barrier (BBB) is a hallmark of inflammatory diseases of the central nervous system (CNS) such as multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). The molecular mechanisms leading to BBB breakdown are not well understood. In order to find molecules involved in this process, we used oligonucleotide microarrays and proteomics to analyze gene and protein expression of the microvascular compartment isolated from brains of C57BI/6 and SJL/N mice afflicted with EAE and the microvascular compartment isolated from healthy controls. Out of the 6500 known genes and expressed sequence tags (ESTs) studied, expression of 288 genes was found to be changed. Of these genes 128 were altered in the microvascular compartment in both EAE models. Six proteins were identified to be present at altered levels. In addition to the expected increased expression of genes coding for molecules involved in leukocyte recruitment, genes not yet ascribed to EAE pathogenesis were identified. Thus, proteomics and gene array screens of the microvascular compartment are valid approaches, that can be used to define novel candidate molecules involved in EAE pathogenesis at the level of the BBB.

Gene and Protein Expression Profiling of the Microvascular Compartment in Experimental Autoimmune Encephalomyelitis in C57BI/6 and SJL Mice

Experimental studies to test the latest cytokine (or antibodies to it) in models of glomerular injury appear on an almost industrial scale. Most show modest benefits without providing serious mechanistic insights or the confidence that they will ever become clinical therapies. The article by

Interferon-beta: a novel way to treat nephrotic syndrome?

The neurovascular unit (NVU) is a relatively recent concept in neuroscience that broadly describes the relationship between brain cells and their blood vessels. The NVU incorporates cellular and extracellular components involved in regulating cerebral blood flow and blood-brain barrier function. The NVU within the adult brain has attracted strong research interest and its structure and function is well described, however, the NVU in the developing brain over the fetal and neonatal period remains much less well known. One area of particular interest in perinatal brain development is the impact of known neuropathological insults on the NVU. The aim of this review is to synthesize existing literature to describe structure and function of the NVU in the developing brain, with a particular emphasis on exploring the effects of perinatal insults. Accordingly, a brief overview of NVU components and function is provided, before discussion of NVU development and how this may be affected by perinatal pathologies. We have focused this discussion around three common perinatal insults: prematurity, acute hypoxia, and chronic hypoxia. A greater understanding of processes affecting the NVU in the perinatal period may enable application of targeted therapies, as well as providing a useful basis for research as it expands further into this area.

/pdf/the-neurovascular-unit-effects-of-brain-insults-during-the-3d5c3in4gk.pdf

The Neurovascular Unit: Effects of Brain Insults During the Perinatal Period.

To elucidate mechanisms of endothelial cell (EC) dysfunction in CNS inflammatory responses and beneficial effects of interferon-beta (IFN-gamma) in multiple sclerosis (MS), we analyzed effects of individual and combinations of soluble inflammatory mediators on the intracellular localization of the EC tight junction-associated molecules zonula occludens-1 and -2 (ZO-1 and ZO-2) in human brain ECs. The cytoplasm in the majority of cells in control EC cultures was clear; ZO-1 and ZO-2 were localized peripherally near sites of cell contact and associated with submembranous cytoplasmic filaments. H2O2 induced reversible time- and concentration-dependent translocation of ZO-1 and ZO-2 to a random distribution within EC cytoplasm and retraction of EC borders. For low concentrations, these effects were accompanied by less prominent submembranous filaments but not by evidence of cytotoxicity, increased cell death or altered amounts of ZO-1. Tumor necrosis factor-beta induced similar alterations but interferon-y did not. Co-treatment with either cytokine increased H2O2 effects whereas IFN-beta reversed H2O2-induced effects. In control white matter samples, EC cytoplasm was clear and ZO-1 was located on cell borders. In inflammatory/demyelinating lesions, EC ZO-1 was diffuse, indicating that the alterations induced in vitro mimic those in active MS lesions. These findings suggest that in MS patients, IFN-beta treatment may counteract inflammatory mediator effects on CNS EC tight junction molecules, thereby preserving EC barrier function.

Interferon-β counteracts inflammatory mediator-induced effects on brain endothelial cell tight junction molecules: Implications for multiple sclerosis

Interferon β-1a prevents the effects of lipopolysaccharide on embryonic brain microvessels

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Interferon β-1a prevents the effects of lipopolysaccharide on embryonic brain microvessels