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Hypoxia Dramatically Increases the Nonspecific Transport of Blood‐Borne Proteins to the Brain
Author(s) -
Plateel Monique,
Teissier Elisabeth,
Cecchelli Roméo
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.68020874.x
Subject(s) - transcellular , paracellular transport , blood–brain barrier , hypoxia (environmental) , albumin , microbiology and biotechnology , vascular permeability , tight junction , cytoplasm , in vivo , permeability (electromagnetism) , chemistry , serum albumin , in vitro , biology , biophysics , biochemistry , neuroscience , endocrinology , central nervous system , oxygen , organic chemistry , membrane
Increased cerebrovascular permeability is an important factor for the development of cerebral edema. To investigate the effect of hypoxia on the transport of blood‐borne proteins to the brain, we used a cell culture model of the blood‐brain barrier (BBB) consisting of a coculture of brain capillary endothelial cells and astrocytes that closely mimics the in vivo situation. The permeability of albumin, a marker of the nonspecific transcellular route, is extremely low in this in vitro model of the BBB. After hypoxia, a huge increase in the permeability of albumin is detected. Despite the opening of the tight junctions already demonstrated after hypoxia, the increase in the permeability of albumin is mainly attributed to an increase of the nonspecific vesicular transport in the cell, attested by the temperature dependence of the phenomenon and the visualization of labeled apotransferrin in the cytoplasm. The increase of this pathway could participate in the development of brain edema during hypoxia.