Junctions between pericytes and the endothelium in rat myocardial capillaries: A morphometric and immunogold study

Schulze, C.; Firth, J. A.

doi:10.1007/bf00297552

Cited by 17 publications

(13 citation statements)

References 22 publications

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“…AJs are formed by homodimerization of cadherins, with VE-cadherin being the endothelial-specific cadherin. In endothelial cells, it is difficult to distinguish between TJs and AJs, because the two types of structures occur intermingled (25,26). Here we show that p80 and p130 angiomotin are membrane proteins involved in control of permeability in cell-cell junctions but that the effect of angiostatin is limited to inhibiting migration of angiomotin-expressing cells.…”

mentioning

confidence: 69%

Angiomotin Regulates Endothelial Cell-Cell Junctions and Cell Motility

Bratt

Birot²,

Sinha

et al. 2005

Journal of Biological Chemistry

162

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We have previously identified angiomotin by its ability to bind to and mediate the anti-angiogenic properties of angiostatin. In vivo and in vitro data indicate an essential role of angiomotin in endothelial cell motility. Here we show that angiostatin binds angiomotin on the cell surface and provide evidence for a transmembrane model for the topology of both p80 and p130 angiomotin isoforms. Immunofluorescence analysis shows that angiomotin co-localized with ZO-1 in cell-cell contacts in endothelial cells in vitro and in angiogenic blood vessels of the postnatal mouse retina in vivo. Transfection of p80 as well as p130 angiomotin in Chinese hamster ovary cells resulted in junctional localization of both isoforms. Furthermore, p130 angiomotin could recruit ZO-1 to actin stress fibers. The p130 but not p80 isoform could be coprecipitated with MAGI-1b, a component of endothelial tight junctions. Paracellular permeability, as measured by diffusion of fluorescein isothiocyanate-dextran, was reduced by p80 and p130 angiomotin expression with 70 and 88%, respectively, compared with control. Angiostatin did not have any effect on cell permeability but inhibited the migration of angiomotin-expressing cells in the Boyden chamber assay. We conclude that angiomotin, in addition to controlling cell motility, may play a role in the assembly of endothelial cell-cell junctions.

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confidence: 69%

Angiomotin Regulates Endothelial Cell-Cell Junctions and Cell Motility

Bratt

Birot²,

Sinha

et al. 2005

Journal of Biological Chemistry

162

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“…The subendothelial arterial intimal thickness at P L ϭ 150 mmHg is only 20% that at 0 mm Hg. Region TM is not only able to sustain compression due to the porous nature of its fiber matrix, but also to resist stretching due to focal adhesion plaques of integrin origin (7,8) to extracellular matrix fibers between the ECs and the surrounding PCs. EMs shown in ref.…”

Section: Discussionmentioning

confidence: 99%

“…Subsequent researchers demonstrated that PCs are highly ramified and in close association with microvessels, including arterioles, capillaries and venules, in virtually every organ and tissue over a wide range of species. Electron microscopy (EM) has demonstrated that PCs have single prominent nuclei and long processes extending circumferentially as well as longitudinally around microvessels and are anchored to the neighboring ECs by adhesion plaques (7,8). PC coverage varies among the types of tissues and microvessels, with overall coverage ranging between 11% in cardiac muscle capillaries to Ϸ50% in the retinal capillaries in rat with more extensive coverage on VMs than capillaries (9).…”

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confidence: 99%

Transient regulation of transport by pericytes in venular microvessels via trapped microdomains

Zhang

Adamson

Curry

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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A phenomenon that has defied explanation for two decades is the time scale for transient reabsorption in the classic experiments of Michel and Phillips on individually perfused frog mesentery microvessels. One finds that transient reabsorption lasts <2 min before a new steady state of low filtration is established when the lumen pressure is abruptly dropped from a high to a low value. Our experiments in frog and rat venular microvessels under a variety of conditions revealed the same time trend for new steady states to be established as in Michel and Phillips' experiments. In contrast, one theoretically predicts herein that the time required for the tissue albumin concentration to increase to values for a new steady state to be achieved through reabsorption is in the order of several hours. In this paper we propose a new hypothesis and theoretical model for this rapid regulation, namely that pericytes covering the interendothelial cleft exits create small trapped microdomains outside the cleft exits which regulate this transient behavior. Our electron microscopy studies on rat mesenteric venular microvessels reveal an average pericyte coverage of Ϸ85%. The theoretical model based on this ultrastructural study predicts an equilibration time on the order of 1 min when the lumen pressure is abruptly lowered. The basic concept of a trapped microdomain can also be extended to microdomains in the interstitial space surrounding skeletal muscle capillaries. microvascular exchange ͉ pericyte regulation ͉ revised Starling hypothesis ͉ trapped microdomains ͉ venous reabsorption I n the pioneering study of transvascular fluid exchange on individually perfused frog mesentery microvessels, Michel and Phillips (1) concluded that, at steady state, no reabsorption (fluid flows from tissue to lumen) was possible at low pressure under the conditions of their experiments. They observed that transient reabsorption lasts Ͻ2 min before a new steady state of low filtration (fluid flows from lumen to tissue) is reestablished when the lumen pressure (P L ) is abruptly dropped from a high to a low value. These observations form the starting point for the model of dynamic fluid exchange in venular microvessels (VMs) described in this paper. Theoretically, one predicts herein using the model in ref. 2 that the time required for the albumin concentration in the tissue (large continuous interstitial space outside microvessels containing the lymphatic system) to increase to values necessary to establish the new low filtration steady state is in the order of several hours if the tissue concentration (C T ) is to rise to its filtration steady state value through reabsorption. We propose that pericytes (PCs) surrounding the endothelial cells (ECs) in these VMs create a previously overlooked trapped microdomain (TM) at the cleft exit which regulates the temporal response of these VMs to changes in P L . This regulation can explain the huge discrepancy between the experimentally observed and the theoretically predicted equilibration times when P L ...

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“…Three types of junctions are found: Adherens junctions [106], tight junctions [41,107,108], and possibly gap junctions [80,[109][110][111].…”

Section: Junctional Complexes At the Bbbmentioning

confidence: 99%

The Blood–Brain Barrier: An Introduction to Its Structure and Function

Mahringer¹,

Ott²,

Fricker³

2013

Topics in Medicinal Chemistry

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The blood-brain barrier (BBB) formed by the brains microvascular system is impermeable for most therapeutically used compounds and overcoming this barrier remains to be one of the big challenges in modern medicine. It is composed of highly specialized endothelial cells, which are surrounded by pericytes and a basal membrane. Together with nearby astrocytes and neurons they constitute the so-called neurovascular unit, which restricts substance transfer from blood to brain and vice versa and maintains the cerebral ion homeostasis. Chapters of this book describe the discovery of the BBB, its evolutionary development as well as the cellular and molecular mechanisms, which underlay its structure and function in health and disease. The organization of tight junctional complexes or specific transport processes at the BBB will be addressed as well as methods to investigate BBB function in vitro and in vivo. Changes in the barrier function under several diseases conditions such as stroke or inflammation will be discussed as well as approaches to overcome the barrier by colloidal carriers or ultrasound.

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Junctions between pericytes and the endothelium in rat myocardial capillaries: A morphometric and immunogold study

Cited by 17 publications

References 22 publications

Angiomotin Regulates Endothelial Cell-Cell Junctions and Cell Motility

Angiomotin Regulates Endothelial Cell-Cell Junctions and Cell Motility

Transient regulation of transport by pericytes in venular microvessels via trapped microdomains

The Blood–Brain Barrier: An Introduction to Its Structure and Function

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