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Titolo:
Choroid plexus recovery after transient forebrain ischemia: Role of growthfactors and other repair mechanisms
Autore:
Johanson, CE; Palm, DE; Primiano, MJ; McMillan, PN; Chan, P; Knuckey, NW; Stopa, EG;
Indirizzi:
Brown Univ, Rhode Isl Hosp, Dept Clin Neurosci, Providence, RI 02903 USA Brown Univ Providence RI USA 02903 lin Neurosci, Providence, RI 02903 USA Florida A&M Univ, Coll Pharm & Pharmaceut Sci, Tallahassee, FL 32307 USA Florida A&M Univ Tallahassee FL USA 32307 Sci, Tallahassee, FL 32307 USA Brown Univ, Rhode Isl Hosp, Dept Pathol, Providence, RI 02903 USA Brown Univ Providence RI USA 02903 Dept Pathol, Providence, RI 02903 USA Univ Western Australia, Queen Elizabeth II Med Ctr, Dept Neurosurg, Nedlands, WA 6009, Australia Univ Western Australia Nedlands WA Australia 6009 nds, WA 6009, Australia
Titolo Testata:
CELLULAR AND MOLECULAR NEUROBIOLOGY
fascicolo: 2, volume: 20, anno: 2000,
pagine: 197 - 216
SICI:
0272-4340(200004)20:2<197:CPRATF>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBROSPINAL-FLUID FORMATION; RAT-BRAIN; MESSENGER-RNA; FACTOR-BETA; IMMUNOHISTOCHEMICAL LOCALIZATION; RECEPTOR IMMUNOREACTIVITY; INSITU HYBRIDIZATION; CEREBRAL-ISCHEMIA; CHLORIDE EFFLUX; ANGIOTENSIN-II;
Keywords:
choroidal epithelium; lateral ventricle; cerebrospinal fluid (CSF); blood-CSF barrier; choroid plexus reperfusion injury; necrosis; epithelial restitution; growth factors and brain repair; autocrine; paracrine; CSF bulk flow; hippocampus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
69
Recensione:
Indirizzi per estratti:
Indirizzo: Johanson, CE Brown Univ, Rhode Isl Hosp, Dept Clin Neurosci, 593 Eddy St, Providence, RI 02903 USA Brown Univ 593 Eddy St Providence RI USA 02903 , RI 02903 USA
Citazione:
C.E. Johanson et al., "Choroid plexus recovery after transient forebrain ischemia: Role of growthfactors and other repair mechanisms", CELL MOL N, 20(2), 2000, pp. 197-216

Abstract

1. Transient forebrain ischemia in adult rats, induced by 10 min of bilateral carotid occlusion and an arterial hypotension of 40 mmHg, caused substantial damage not only to CA-1 neurons in hippocampus but also to epithelialcells in lateral ventricle choroid plexus.2 When transient forebrain ischemia was followed by reperfusion (recovery)intervals of 0 to 12 hr, there was moderate to severe damage to many frondregions of the choroidal epithelium. In some areas, epithelial debris was sloughed into cerebrospinal fluid (CSF). Although some epithelial cells were disrupted and necrotic, their neighbors exhibited normal morphology. Thispatchy response to ischemia was probably due to regional differences in reperfusion or cellular metabolism.3. Between 12 and 24 hr postischemia, there was marked restoration of the Na+, K+, water content, and ultrastructure of the choroid plexus epithelium. Since there was no microscopical evidence for mitosis, we postulate that healthy epithelial cells either were compressed together on the villus or migrated from the choroid plexus stalk to more distal regions, in order to "fill in gaps" along the basal lamina caused by necrotic epithelial cell disintegration.4. Epithelial cells of mammalian choroid plexus synthesize and secrete many growth factors and other peptides that are of trophic benefit following injury to regions of the cerebroventricular system. For example, several growth factors are upregulated in choroid plexus after ischemic and traumatic insults to the central nervous system.5. The presence of numerous types of growth factor receptors in choroid plexus allows growth factor mediation of recovery processes by autocrine and paracrine mechanisms.6. The capability of choroid plexus after acute ischemia to recover its barrier and CSF formation functions is an important factor in stabilizing brain fluid balance.7. Moreover, growth factors secreted by choroid plexus into CSF are distributed by diffusion and convection into brain tissue near the ventricular system, e.g., hippocampus. By this endocrine-like mechanism, growth factors are conveyed throughout the choroid plexus-CSF-brain nexus and can consequently promote repair of ischemia-damaged tissue in the ventricular wall and underlying brain.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/01/20 alle ore 18:39:38