S100B Protein, A Damage-Associated Molecular Pattern Protein in the Brain and Heart, and Beyond. (25th July 2010)

• Record Type: Journal Article
• Authors: Sorci, Guglielmo; Bianchi, Roberta; Riuzzi, Francesca; Tubaro, Claudia; Arcuri, Cataldo; Giambanco, Ileana; Donato, Rosario
• Other Names: Heizmann Claus W. Academic Editor.
• Is Part Of: Cardiovascular psychiatry and neurology. Volume 2010(2010)
• Publication Date: 2010-07-25
• Subjects: Cardiovascular system -- Diseases -- Periodicals; Cardiovascular system -- Diseases -- Psychological aspects -- Periodicals; Psychiatry -- Periodicals; Cardiology -- Periodicals; Neurology -- Periodicals; Nervous system -- Diseases -- Periodicals; Cardiology; Cardiovascular system -- Diseases; Cardiovascular system -- Diseases -- Psychological aspects; Nervous system -- Diseases; Neurology; Psychiatry; Cardiovascular Diseases -- complications; Nervous System Diseases -- complications; Mental Disorders -- complications; Cardiology; Neurology; Psychiatry; Cardiovascular Diseases -- complications -- Periodicals; Nervous System Diseases -- complications -- Periodicals; Mental Disorders -- complications -- Periodicals; Cardiology -- Periodicals; Neurology -- Periodicals; Psychiatry -- Periodicals; Periodicals; Electronic journals; 616.81
• DOI: 10.1155/2010/656481
• Languages: English
• ISSNs: 2090-0163

Abstract

Abstract : S100B belongs to a multigenic family ofCa 2+ -binding proteins of the EF-hand type and is expressed in high abundance in the brain. S100B interacts with target proteins within cells thereby altering their functions once secreted/released with the multiligand receptor RAGE. As an intracellular regulator, S100B affects protein phosphorylation, energy metabolism, the dynamics of cytoskeleton constituents (and hence, of cell shape and migration), Ca 2+ homeostasis, and cell proliferation and differentiation. As an extracellular signal, at low, physiological concentrations, S100B protects neurons against apoptosis, stimulates neurite outgrowth and astrocyte proliferation, and negatively regulates astrocytic and microglial responses to neurotoxic agents, while at high doses S100B causes neuronal death and exhibits properties of a damage-associated molecular pattern protein. S100B also exerts effects outside the brain; as an intracellular regulator, S100B inhibits the postinfarction hypertrophic response in cardiomyocytes, while as an extracellular signal, (high) S100B causes cardiomyocyte death, activates endothelial cells, and stimulates vascular smooth muscle cell proliferation.