S100B protein is released from rat neonatal neurons, astrocytes, and microglia by in vitro trauma and anti-S100 increases trauma-induced delayed neuronal injury and negates the protective effect of exogenous S100B on neurons

• Published in: Journal of neurochemistry Vol. 101; no. 6; pp. 1463 - 1470
• Main Authors: Ellis, Earl F, Willoughby, Karen A, Sparks, Sallie A, Chen, Tao
• Format: Journal Article
• Language: English
• Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.06.2007; Blackwell Publishing Ltd; Blackwell
• Subjects: Adult and adolescent clinical studies; Animals; Animals, Newborn; Antibodies - pharmacology; Astrocytes - secretion; Biochemistry; Biological and medical sciences; Brain damage; Brain Injuries - physiopathology; Cells, Cultured; Cellular biology; Injuries of the nervous system and the skull. Diseases due to physical agents; Medical sciences; Microglia - secretion; Nerve Growth Factors - immunology; Nerve Growth Factors - pharmacology; Nerve Growth Factors - secretion; Neurology; Neurons - drug effects; Neurons - secretion; neuroprotection; Organic mental disorders. Neuropsychology; Proteins; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Rats; Rodents; S100 Calcium Binding Protein beta Subunit; S100 Proteins - immunology; S100 Proteins - pharmacology; S100 Proteins - secretion; S100B; Stress, Mechanical; Traumas. Diseases due to physical agents; traumatic brain injury; Nervous system diseases; Neonatal; Rat; Neuroglia; Rodentia; Central nervous system; traumatic brain injury; Astrocyte; S100B; In vitro; Protein; Encephalon; Microglia; Strain; Vertebrata; Mammalia; Neuron; neuroprotection; Models; Head trauma; Release
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1111/j.1471-4159.2007.04515.x

S100B protein is found in brain, has been used as a marker for brain injury and is neurotrophic. Using a well-characterized in vitro model of brain cell trauma, we have previously shown that strain injury causes S100B release from neonatal rat neuronal plus glial cultures and that exogenous S100B reduces delayed post-traumatic neuronal damage even when given at 6 or 24 h post-trauma. The purpose of the current studies was to measure post-traumatic S100B release by specific brain cell types and to examine the effect of an antibody to S100 on post-traumatic delayed (48 h) neuronal injury and the protective effect of exogenous S100B. Neonatal rat cortical cells grown on a deformable elastic membrane were subjected to a strain (stretch) injury produced by a 50 ms displacement of the membrane. S100B was measured with an ELISA kit. Trauma released S100B from pure cultures of astrocytes, microglia, and neurons. Anti-S100 reduced released S100B to below detectable levels, increased delayed neuronal injury in traumatized cells and negated the protective effect of exogenous S100B on injured cells. Heat denatured anti-S100 did not exacerbate injury. These studies provide further evidence for a protective role for S100B following neuronal trauma.