Literature DB >> 2072867

Mechanisms of inflammatory cell attachment in chronic relapsing experimental allergic encephalomyelitis: a scanning and high-voltage electron microscopic study of the injured mouse blood-brain barrier.

A S Lossinsky1, R Pluta, M J Song, V Badmajew, R C Moretz, H M Wisniewski.   

Abstract

Brain and spinal cord blood vessels from mice subjected to chronic relapsing experimental allergic encephalomyelitis were examined by scanning (SEM) and high-voltage electron microscopy (HVEM). SEM analysis of veins and venules from affected tissue regions demonstrated inflammatory cells (ICs), primarily lymphocytes or monocytes, attached to the luminal endothelial cell (EC) surface adjacent to the junctional complexes. In transverse section these cells were shown by HVEM to extend and to insert filopodia (lymphocytes) or flap-like lamellapodia (monocytes) into the luminal EC surfaces. Affected ECs often expressed increased microvillar projection as well as parajunctional crater-like structures on their luminal surfaces. Based on scanning and high-voltage electron microscopy, we present morphological evidence that some populations of sensitized ICs do not penetrate the EC junctions initially during EC attachment but instead insert pseudopodial projections into specialized openings in the ECs that are formed in response to chronic inflammation.

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Year:  1991        PMID: 2072867     DOI: 10.1016/0026-2862(91)90030-f

Source DB:  PubMed          Journal:  Microvasc Res        ISSN: 0026-2862            Impact factor:   3.514


  11 in total

Review 1.  In vitro methods in the study of viral and prion permeability across the blood-brain barrier.

Authors:  Ryota Nakaoke; William A Banks
Journal:  Cell Mol Neurobiol       Date:  2005-02       Impact factor: 5.046

Review 2.  Mouse models of neurological disorders: a view from the blood-brain barrier.

Authors:  William A Banks
Journal:  Biochim Biophys Acta       Date:  2009-10-29

Review 3.  Endothelial junction regulation: a prerequisite for leukocytes crossing the vessel wall.

Authors:  Anna E Daniel; Jaap D van Buul
Journal:  J Innate Immun       Date:  2013-04-03       Impact factor: 7.349

4.  Variable restriction of albumin diffusion across inflamed cerebral microvessels of the anaesthetized rat.

Authors:  A S Easton; P A Fraser
Journal:  J Physiol       Date:  1994-02-15       Impact factor: 5.182

5.  Transcellular gaps in microvascular walls of frog and rat when permeability is increased by perfusion with the ionophore A23187.

Authors:  C R Neal; C C Michel
Journal:  J Physiol       Date:  1995-10-15       Impact factor: 5.182

6.  Permeability of disrupted cerebral microvessels in the frog.

Authors:  P A Fraser; A D Dallas
Journal:  J Physiol       Date:  1993-02       Impact factor: 5.182

7.  A chemokine self-presentation mechanism involving formation of endothelial surface microstructures.

Authors:  Catherine Whittall; Oksana Kehoe; Sophie King; Antal Rot; Angela Patterson; Jim Middleton
Journal:  J Immunol       Date:  2013-01-16       Impact factor: 5.422

8.  Reassessment of a new model of complete cerebral ischemia in rats. Method of induction of clinical death, pathophysiology and cerebrovascular pathology.

Authors:  R Pluta; A S Lossinsky; M J Mossakowski; L Faso; H M Wisniewski
Journal:  Acta Neuropathol       Date:  1991       Impact factor: 17.088

9.  Ultrastructural studies of cerebral vascular spasm after cardiac arrest-related global cerebral ischemia in rats.

Authors:  H M Wisniewski; R Pluta; A S Lossinsky; M J Mossakowski
Journal:  Acta Neuropathol       Date:  1995       Impact factor: 17.088

Review 10.  Settings and mechanisms for trans-cellular diapedesis.

Authors:  Peter T Sage; Christopher V Carman
Journal:  Front Biosci (Landmark Ed)       Date:  2009-06-01
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