Cardiovascular Psychiatry and Neurology

S100B Protein in the Nervous System and Cardiovascular Apparatus in Normal and Pathological Conditions


Publishing date
01 Oct 2010
Status
Published
Submission deadline
01 Apr 2010

1Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia, Italy


S100B Protein in the Nervous System and Cardiovascular Apparatus in Normal and Pathological Conditions

Description

Accumulating evidence suggests that S100B, a Ca2+-binding protein of the EF-hand type, functions as a regulator of intracellular activities and as an extracellular signal. Within cells, S100B interacts with a relatively large number of protein targets (e.g., enzymes, enzyme substrates, cytoskeletal proteins, transcription factors) thereby regulating their function. S100B is also secreted by certain cell types and released by damaged/necrotic cells. Secreted/released S100B can affect cellular functions with varying effects depending on its local concentration mostly via interaction with the receptor for advanced glycation end products (RAGE). S100B is not an ubiquitous protein, its expression being restricted to astrocytes, Schwann cells, ependymocytes, certain neuronal populations, adipocytes, chondrocytes, melanocytes, dendritic cells, skeletal muscles, and arterial smooth muscle cells, in normal physiological conditions. However, the S100B cell expression pattern during prenatal and postnatal development might be different (there is limited information about this issue); S100B expression levels in certain cell types vary in response to extracellular factors; levels of S100B are high in several cancer cells; and S100B expression is induced in cardiomyocytes and arterial endothelium in response to norepinephrine. Serum levels of S100B in normal postpubescent human subjects are low, and increases in S100B serum levels are found in a number of pathological conditions (mostly, brain diseases, certain psychiatric disorders, melanoma, and heart infarction and insufficiency).

This special issue focuses on innovative proposals for the brain-heart role of S100B.

The authors are invited to present original review articles on hypotheses or research articles on mechanisms of action of S100B in nervous cells, cardiomyocytes, endothelial cells, and arterial smooth muscle cells and on mechanisms of autocrine, paracrine, and endocrine effects of S100B, in normal and pathological conditions. We also welcome submitting review/research articles on cell expression pattern of S100B during prenatal and postnatal development of the nervous tissue and the cardiovascular apparatus. The presentation of the original hypothesis in a review article does not require any new data. The hypothesis should be explicitly stated, the testing of the hypothesis should be detailed including the existing data in support and against the hypothesis (extensive review of the literature should be avoided), and the implications of the hypothesis should be clearly identified. Submission of supporting figures and tables is encouraged.

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/cpn/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable:

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