Mariano Viapiano, Ph.D.

Assistant Professor
Department of Neurological Surgery and Center for Molecular Neurobiology

Degree: University of Buenos Aires
Postdoctoral Training: University of Sao Paulo, Brazil and Yale University School of Medicine

Contact Information
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 PubMed publications list for Mariano Viapinao (last 10 years)

Research Area:

Extracellular matrix in the central nervous system: Organization and functions in neural development and disease.

Current Research:

The extracellular matrix (ECM) of the central nervous system plays multiple roles in cell migration, neurite extension, synaptogenesis and regulation of synaptic plasticity. Research in my laboratory is focused 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. Our research is currently dedicated to understanding the functions of 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 specifically expressed in the central nervous system (neurocan and brevican).

A major focus of our work stems from an uncommon effect of these CSPGs in malignant brain tumors of glial origin, known as gliomas: Although most CSPGs predominantly inhibit cell and neurite motility, two lecticans (versican and brevican) are highly overexpressed by gliomas and enhance the invasion of these tumors 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 in gliomas, to prevent the spread of the disease in the brain and render these tumors therapeutically accessible.

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

Expression and interactions of the 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.
The reorganization of the ECM by protein cleavage: We are also 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.
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.

Techniques:
We employ several in vitro and in vivo models to study the formation, changes and functions of the neural matrix. The variety of techniques used in our lab includes:

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.