Research Interests:

Oligodendroglial biology (development, pathophysiology, and remyelination), Regeneration of the nervous system, and live cell imaging.

Current Research:

Oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system produce the lipid rich cellular structure, called myelin, which ensheathes neuronal axons. Myelin is essential for fast saltatory conduction of nerve impulses along myelinated axons. However, selective loss of myelin and oligodendrocytes occurs under several pathological conditions such as hypoxia/ischemia, inflammation and genetic abnormalities, which is primarily responsible for neurological deficits of white matter diseases including multiple sclerosis, genetic leukodystrophies, and periventricular leukomalacia.

One of my current projects deals with a group of proteins called 'Bcl-2-related proteins', which play pivotal roles in determining cell survival or death in response to activation of various intracellular signaling pathways. My hypothesis is that Bcl-2-related proteins are major contributors to differential susceptibility to apoptosis of oligodendrocytes depending on their developmental stage. My comprehensive study of expression of Bcl-2-related proteins in the oligodendroglial lineage revealed distinctive alterations in expression levels of several Bcl-2-related members during oligodendroglial development. I have also recently found that oligodendrocytes from mice doubly deficient of Bax and Bak, two principal members of proapoptotic Bcl-2-related proteins, are highly resistant to apoptosis, yet retains ability to differentiate into myelin-forming oligodendrocytes.

Another research project I am currently pursuing is mitogen activated protein kinase (MAPK) pathways which are known to modulate Bcl-2-related proteins. Our recent study demonstrated that activation of ERK signaling, one of the MAPK pathways, contributes to death of oligodendroglial progenitor cells induced by interferon-gamma, a proinflammatory cytokin produced in inflammatory lesions. This mechanism might be attributable to persistent demyelination after white matter inflammation.

Noteworthy Publications: