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Glial expression of small heat shock proteins following an excitotoxic lesion in the immature rat brain
Author(s) -
Acarin Laia,
Paris Jaume,
González Berta,
Castellano Bernardo
Publication year - 2002
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.10040
Subject(s) - biology , lesion , neuroscience , heat shock protein , shock (circulatory) , neuroglia , microbiology and biotechnology , central nervous system , pathology , medicine , biochemistry , gene
Heat shock proteins (HSPs) are chaperones induced under pathological conditions and involved in protein stabilization and cellular protection. In this study, we have evaluated the expression pattern of the glial cell–related HSP27, HSP32, and HSP47 following an excitotoxic lesion in the immature rat brain. Postnatal day 9 rats received an intracortical injection of N‐methyl‐D‐aspartate and tissue was processed immunohistochemically for HSPs and double labeling using astroglial and microglial markers. HSP expression was quantified by image analysis. Excitotoxic damage caused primary cortical degeneration and secondary damage in the corresponding thalamus. In the injured cortex, reactive microglia/macrophages expressed HSP32 from 10 h until 14 days postlesion (PL), showing maximal levels at days 3–5. In parallel, most cortical reactive astrocytes showed expression of HSP47 from 10 h until 14 days PL and a population of them also displayed HSP27 labeling from 1 day PL. In addition, some cortical reactive astrocytes showed a temporary expression of HSP32 at day 1. In general, astroglial HSP expression in the cortex achieved maximal levels at days 3–5 PL. In the damaged thalamus, HSP32 was not significantly induced, but reactive astrocytes expressed HSP47 and some of them also HSP27. Thalamic astroglial HSP induction was transient, peaked at 5 days PL and reached basal levels by day 14. The injury‐induced expression of HSP32, HSP27, and HSP47 in glial cells may contribute to glial cell protection and adaptation to damage, therefore playing an important role in the evolution of the glial response and the excitotoxic lesion outcome. HSP32 may provide antioxidant protective mechanisms to microglia/macrophages, whereas HSP47 could contribute to extracellular matrix remodeling and HSP27 may stabilize the astroglial cytoskeleton and participate in astroglial antioxidant mechanisms. GLIA 38:1–14, 2002. © 2002 Wiley‐Liss, Inc.