Heat Shock Protein‐27 Is Upregulated in the Temporal Cortex of Patients with Epilepsy

• Published in: Epilepsia (Copenhagen) Vol. 45; no. 12; pp. 1549 - 1559
• Main Authors: Bidmon, Hans‐J, Görg, Boris, Palomero‐Gallagher, Nicola, Behne, Friedrich, Lahl, Rainer, Pannek, Hans W., Speckmann, Erwin‐J, Zilles, Karl
• Format: Journal Article
• Language: English
• Published: 350 Main Street , Malden , MA 02148 , USA and 9600 Garsington Road , Oxford , OX4 2XG , England Blackwell Science Inc 01.12.2004; Blackwell
• Subjects: Adolescent; Adult; Aged; Anticonvulsants. Antiepileptics. Antiparkinson agents; Astrocytes - chemistry; Astrocytes - metabolism; Biological and medical sciences; Biomarkers; Blood; Blood-Brain Barrier - metabolism; Blotting, Western; brain barrier; Child, Preschool; Epilepsy; Epilepsy - diagnosis; Epilepsy - metabolism; Epilepsy - surgery; Female; Glia; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Heat shock protein; Heat-Shock Proteins - analysis; Heat-Shock Proteins - metabolism; HSP27 Heat-Shock Proteins; Human; Humans; Immunohistochemistry; Investigative techniques, diagnostic techniques (general aspects); Male; Medical sciences; Middle Aged; Neocortex - chemistry; Neocortex - metabolism; Neoplasm Proteins - analysis; Neoplasm Proteins - metabolism; Nervous system; Nervous system (semeiology, syndromes); Neurology; Neuropharmacology; Pharmacology. Drug treatments; Radiodiagnosis. Nmr imagery. Nmr spectrometry; Temporal lobe; Temporal Lobe - chemistry; Temporal Lobe - metabolism; Temporal Lobe - surgery; Up-Regulation; Human; Temporal lobe; Nervous system diseases; Epilepsy; Heat shock protein-Glia-Temporal lobe-Blood-brain barrier-Human-Epilepsy; Central nervous system disease; Central nervous system; Heat shock protein; Temporal cortex; Blood brain barrier; Cerebral disorder
• ISSN: 0013-9580; 1528-1167
• DOI: 10.1111/j.0013-9580.2004.14904.x

Purpose: Heat shock protein‐27 (HSP‐27) belongs to the group of small heat shock proteins that become induced in response to various pathologic conditions. HSP‐27 has been shown to protect cells and subcellular structures, particularly mitochondria, and serves as a carrier for estradiol. It is a reliable marker for tissues affected by oxidative stress. Oxidative stress and related cellular defence mechanisms are currently thought to play a major role during experimentally induced epileptic neuropathology. We addressed the question whether HSP‐27 becomes induced in the neocortex resected from patients with pharmacoresistant epilepsy. Methods: Human epileptic temporal neocortex was obtained during neurosurgery, and control tissue was obtained at autopsy from subjects without known neurologic diseases. The tissues were either frozen for Western blot analysis or fixed in Zamboni's fixative for the topographic detection of HSP‐27 at the cellular level by means of immunohistochemistry. Results: HSP‐27 was highly expressed in all epilepsy specimens and in the cortex of a patient who died in the final stage of multiple sclerosis (positive control), whereas only low amounts of HSP‐27 were detectable in control brains. In epilepsy patients, HSP‐27 was present in astrocytes and in the walls of blood vessels. The intracortical distribution patterns varied strongly among the epilepsy specimens. Conclusions: These results demonstrate that HSP‐27 becomes induced in response to epileptic pathology. Although the functional aspects of HSP‐27 induction during human epilepsy have yet to be elucidated, it can be concluded that HSP‐27 is a marker for cortical regions in which a stress response has been caused by seizures.