OBJECTIVE: Our purpose was to study the neuronal responses of heat shock protein-72 (a stress-inducible protein) and microtubule-associated protein-2 (a constitutive protein of the neuronal cytoskeleton) after hypoxia-ischemia and their relationship with permanent damage in the newborn rat brain. STUDY DESIGN: Seven-day-old rats were exposed to unilateral carotid artery ligation followed by 2 hours of hypoxia (8% oxygen/92% nitrogen) and then killed at time points ranging from 1 to 72 hours after injury. Brains were removed for immunohistochemical and routine staining. RESULTS: Heat shock protein-72 appearance and microtubule-associated protein-2 disappearance occurred from 1 hour after injury, mainly in the dentate gyrus of the hippocampal formation and the cerebral cortex. Such alterations reached maximal levels at 24 hours for both proteins. Microtubule-associated protein-2 staining recovered in almost all parts of the brain. However, the hippocampal CA3 showed a delay in the responses for both proteins, and microtubule-associated protein-2 did not recover the response to immunostaining. Histologic evaluation at 72 hours after hypoxia by routine methods showed predominant damage in the hippocampal CA3. CONCLUSION: Our results show that delayed responses of heat shock protein-72 and microtubule-associated protein-2 are related to a high incidence of neuronal cell loss in the hippocampal CA3 region.
OBJECTIVE: Our purpose was to study the neuronal responses of heat shock protein-72 (a stress-inducible protein) and microtubule-associated protein-2 (a constitutive protein of the neuronal cytoskeleton) after hypoxia-ischemia and their relationship with permanent damage in the newborn rat brain. STUDY DESIGN: Seven-day-old rats were exposed to unilateral carotid artery ligation followed by 2 hours of hypoxia (8% oxygen/92% nitrogen) and then killed at time points ranging from 1 to 72 hours after injury. Brains were removed for immunohistochemical and routine staining. RESULTS: Heat shock protein-72 appearance and microtubule-associated protein-2 disappearance occurred from 1 hour after injury, mainly in the dentate gyrus of the hippocampal formation and the cerebral cortex. Such alterations reached maximal levels at 24 hours for both proteins. Microtubule-associated protein-2 staining recovered in almost all parts of the brain. However, the hippocampal CA3 showed a delay in the responses for both proteins, and microtubule-associated protein-2 did not recover the response to immunostaining. Histologic evaluation at 72 hours after hypoxia by routine methods showed predominant damage in the hippocampal CA3. CONCLUSION: Our results show that delayed responses of heat shock protein-72 and microtubule-associated protein-2 are related to a high incidence of neuronal cell loss in the hippocampal CA3 region.
Authors: M Schwab; I Antonow-Schlorke; B Kühn; T Müller; H Schubert; B Walter; U Sliwka; P W Nathanielsz Journal: J Physiol Date: 2001-02-01 Impact factor: 5.182
Authors: L E Durán-Carabali; E F Sanches; F K Odorcyk; F Nicola; R G Mestriner; L Reichert; D Aristimunha; A S Pagnussat; C A Netto Journal: Neurochem Res Date: 2019-09-28 Impact factor: 3.996
Authors: M Schwab; M Roedel; M A Anwar; T Müller; H Schubert; L F Buchwalder; B Walter; W Nathalielsz Journal: J Physiol Date: 2000-11-01 Impact factor: 5.182