Assistant Professor

Department of Neurological Surgery and
Center for Molecular Neurobiology

Ph.D.: University of Buenos Aires, Argentina
Post-doctoral Training:
University of Sao Paulo, Brazil
Yale University School of Medicine

Center for Molecular Neurobiology
The Ohio State University
226B Rightmire Hall
1060 Carmack Road
Columbus, OH 43210

Phone: 614-292-4362
Fax: 614-292-5379
E-mail:viapiano.1@osu.edu / mariano.viapiano@osumc.edu

Link to NLM & NIH PubMed publications list for Mariano Viapiano (last 10 years)

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Research Area:

• Organization and functions of the extracellular matrix in central nervous system development and disease.

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Research Description:

The extracellular matrix (ECM) of the central nervous system plays multiple roles in cell migration, neurite extension, synaptogenesis and the regulation of synaptic plasticity. The research in my lab focuses on 1) the mechanisms by which the neural ECM regulates cell movement and communication during neural development and 2) the disruption of these processes in neuropathologies.

The neural ECM has a unique molecular composition based on a scaffold of hyaluronic acid with associated glycoproteins and proteoglycans. Currently, our research is centered on a family of chondroitin sulfate proteoglycans (CSPGs) that organize the ECM scaffold around neurons and glia. The members of this family, known as lecticans, include two CSPGs found in several tissues (aggrecan and versican) and two CNS-specific CSPGs (neurocan and brevican).

A major focus of our work stems from the uncommon effect that some of these CSPGs exhibit in malignant brain tumors of glial origin (gliomas): Although these molecules are predominantly inhibitors of cell and neurite motility, lecticans such as versican and brevican can markedly increase the migration of glioma cells in the brain. Accordingly, we are dedicated to understanding the molecular mechanisms by which the neural CSPGs and other matrix components affect the motility of normal glial and glioma cells. Our goal is to develop novel targeting strategies against these molecules to prevent brain tumor dispersion.

To further understand the roles of the neural ECM in the normal and diseased nervous system, our research is currently developing along three major directions:

1. The induction and molecular interactions of ECM components: These studies are focused on the brain- and tumor-derived extracellular factors that induce CSPG expression, and the downstream signaling initiated by CSPG association to cell-surface receptors in glial and glioma cells.
   
   
2. The reorganization of the ECM by protein cleavage: Here, we are analyzing the proteolytic processing of the neural CSPGs and how this processing is affected in neuropathologies such as brain tumors and acute CNS injury. The focus of this research is a family of CSPG-processing metalloproteases, the ADAMTS, and their endogenous inhibitors known as TIMPs.
   
   
3. The role of differential glycosylation of ECM molecules: Our research here is aimed at understanding the composition, molecular interactions and functions of the different carbohydrates bound to the CSPGs in the normal and diseased CNS.

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Techniques and Methods:

• Cellular biology: cell cultures (primary cells, cell lines), cell transfection, viral transduction, adhesion assays, random movement ("scratch") assays, chemo- and hapto-taxis, matrix invasion, time-lapse microscopy, in vivo tumor growth.
• Recombinant DNA/RNA: cloning, PCR techniques, mutagenesis, siRNA knockdown, epitope-tagging, recombinant protein engineering.
• Biochemisty: cell and tissue processing, subcellular fractionation, protein/protein and protein/carbohydrate association assays, glycochemistry, protease assays.
• Morphology: immunocytochemistry, immunohistochemistry, lectin-histochemistry.