A manual of pathological histology : to serve as an introduction to the study of morbid anatomy / by Eduard Rindfleisch ; translated by E. Buchanan Baxter.

Baxter, Emily; Rindfleisch, Georg Eduard von

doi:10.5962/bhl.title.30945

Cited by 6 publications

(3 citation statements)

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“…In his histological studies, Rindfleisch observed that MS lesions were commonly associated with abnormal-looking blood vessels (Rindfleisch 1872). More recently, within the last ten years, MRI studies have described enhanced cerebral blood flow within relapsing-remitting and secondary-progressive MS lesions (Rashid et al 2004), and one of these studies documented increased blood flow three weeks prior to gadolinium enhancement of the vessels, suggesting a potential role for vascular changes early in lesion evolution (Wuerfel et al 2004).…”

Section: Discussionmentioning

confidence: 99%

Extensive vascular remodeling in the spinal cord of pre-symptomatic experimental autoimmune encephalomyelitis mice; increased vessel expression of fibronectin and the α5β1 integrin

Boroujerdi

Welser-Alves

Milner

2013

Experimental Neurology

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Alterations in vascular structure and function are a central component of demyelinating disease. In addition to blood-brain barrier (BBB) breakdown, which occurs early in the course of disease, recent studies have described angiogenic remodeling, both in multiple sclerosis tissue and in the mouse demyelinating model, experimental autoimmune encephalomyelitis (EAE). As the precise timing of vascular remodeling in demyelinating disease has yet to be fully defined, the purpose of the current study was to define the time-course of these events in the MOG35-55 EAE model. Quantification of endothelial cell proliferation and vessel density revealed that a large part of angiogenic remodeling in cervical spinal cord white matter occurs during the pre-symptomatic phase of EAE. At the height of vascular remodeling, blood vessels in the cervical spinal cord showed strong transient upregulation of fibronectin and the α5β1 integrin. In vitro experiments revealed that α5 integrin inhibition reduced brain endothelial cell proliferation under inflammatory conditions. Interestingly, loss of vascular integrity was evident in all vessels during the first 4–7 days post-immunization, but after 14 days, was localized predominantly to venules. Taken together, our data demonstrate that extensive vascular remodeling occurs during the pre-symptomatic phase of EAE and point to a potential role for the fibronectin-α5β1 integrin interaction in promoting vascular remodeling during demyelinating disease.

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Section: Discussionmentioning

confidence: 99%

Extensive vascular remodeling in the spinal cord of pre-symptomatic experimental autoimmune encephalomyelitis mice; increased vessel expression of fibronectin and the α5β1 integrin

Boroujerdi

Welser-Alves

Milner

2013

Experimental Neurology

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“…Statements about mechanical stresses and atherosclerosis appear in the 19th century ( Rindfleisch, 1872 ) but the experimental study of localising factors began in the early 20th century with the work of Anitschkow (alt.—Anichkov, Russian—Ани́чков) and his colleagues. A retrospective review of that work ( Anitschkow, 1933 ) remains of interest today for its scientific content, as well as for its historical significance.…”

Section: Historical Backgroundmentioning

confidence: 99%

Haemodynamic Wall Shear Stress, Endothelial Permeability and Atherosclerosis—A Triad of Controversy

Weinberg

2022

Front. Bioeng. Biotechnol.

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A striking feature of atherosclerosis is its patchy distribution within the vascular system; certain arteries and certain locations within each artery are preferentially affected. Identifying the local risk factors underlying this phenomenon may lead to new therapeutic strategies. The large variation in lesion prevalence in areas of curvature and branching has motivated a search for haemodynamic triggers, particular those related to wall shear stress (WSS). The fact that lesions are rich in blood-derived lipids has motivated studies of local endothelial permeability. However, the location of lesions, the underlying haemodynamic triggers, the role of permeability, the routes by which lipids cross the endothelium, and the mechanisms by which WSS affects permeability have all been areas of controversy. This review presents evidence for and against the current consensus that lesions are triggered by low and/or oscillatory WSS and that this type of shear profile leads to elevated entry of low density lipoprotein (LDL) into the wall via widened intercellular junctions; it also evaluates more recent evidence that lesion location changes with age, that multidirectional shear stress plays a key role, that LDL dominantly crosses the endothelium by transcytosis, and that the link between flow and permeability results from hitherto unrecognised shear-sensitive mediators.

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“…Blood vessel abnormalities such as impaired barrier function have long been associated with MS lesions [ 16 ]; however only recently has there been evidence confirming both the presence of angiogenesis in MS patients as well as establishing its onset in relation to disease progression. Angiogenesis, as measured by an increase in vessel number and size, was first described to be present not only within and at the edge of acute MS lesions but also in the area surrounding the plaque, where it is often associated with areas of inflammation [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

The role of angiogenesis in the pathology of multiple sclerosis

2014

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Angiogenesis, or the growth of new blood vessels from existing vasculature, is critical for the proper development of many organs. This process is inhibited and tightly regulated in adults, once endothelial cells have acquired organ-specific properties. Within the central nervous system (CNS), angiogenesis and acquisition of blood–brain barrier (BBB) properties by endothelial cells is essential for CNS function. However, the role of angiogenesis in CNS pathologies associated with impaired barrier function remains unclear. Although vessel abnormalities characterized by abnormal barrier function are well documented in multiple sclerosis (MS), a demyelinating disease of the CNS resulting from an immune cell attack on oligodendrocytes, histological analysis of human MS samples has shown that angiogenesis is prevalent in and around the demyelinating plaques. Experiments using an animal model that mimics several features of human MS, Experimental Autoimmune Encephalomyelitis (EAE), have confirmed these human pathological findings and shed new light on the contribution of pre-symptomatic angiogenesis to disease progression. The CNS-infiltrating inflammatory cells that are a hallmark of both MS and EAE secrete several factors that not only contribute to exacerbating the inflammatory process but also promote and stimulate angiogenesis. Moreover, chemical or biological inhibitors that directly or indirectly block angiogenesis provide clinical benefits for disease progression. While the precise mechanism of action for these inhibitors is unknown, preventing pathological angiogenesis during EAE progression holds great promise for developing effective treatment strategies for human MS.

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A manual of pathological histology : to serve as an introduction to the study of morbid anatomy / by Eduard Rindfleisch ; translated by E. Buchanan Baxter.

Cited by 6 publications

References 0 publications

Extensive vascular remodeling in the spinal cord of pre-symptomatic experimental autoimmune encephalomyelitis mice; increased vessel expression of fibronectin and the α5β1 integrin

Extensive vascular remodeling in the spinal cord of pre-symptomatic experimental autoimmune encephalomyelitis mice; increased vessel expression of fibronectin and the α5β1 integrin

Haemodynamic Wall Shear Stress, Endothelial Permeability and Atherosclerosis—A Triad of Controversy

The role of angiogenesis in the pathology of multiple sclerosis

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