Toe Ein Kyawt
You know when you're making an epic Sunday breakfast and the fat in your bacon gets cooked? That's kind of what's happening in your brain all the time.
Hi! My name is Ein - rhymes with Brain - and I'm a senior in the Department of Pharmacology & Toxicology. I've been working with Dr. Fraser Sim for the past three years, and this is the project I've been working on for the past year! I assisted a PhD candidate during my first two years, and we made an observation about cell density in a culture of cells that had one of their genes removed.
So those cells are precursors to cells called oligodendrocytes that cover your neurons with a fatty layer - the myelin sheath, and it is what helps the electric signals in the brain travel faster, like frying bacon. In multiple sclerosis, the myelin sheath is destroyed and that causes the breakdown of the neuron itself. When this happens, the oligodendrocyte precursor cells - OPCs - come in and remyelinate. Obviously, we want more of these. My project is about a specific gene that might help control this process of remyelination.
Demyelination is a process found in neurodegenerative diseases including Multiple Sclerosis (MS) where the neuronal axon is stripped of its protective layer despite available neural stem cells. In such lesions, Heparan Sulfate Proteoglycans (HSPGs), modulators of cellular response, are found. Their span of modulation includes proliferation, a process controlled by Platelet-Derived Growth Factor (PDGF-AA). HSPG modulation depends on their pattern of sulfation, modified by extracellular sulfatases, including Sulfatase 2 (SULF2). It was hypothesised that knocking down the SULF2 gene would decrease proliferation drastically, as it was thought to be necessary for hOPC proliferation. In order to investigate the effect of SULF2 and HSPG sulfation on PDGF-AA signaling on human oligodendrocyte progenitor cells (hOPCs), the SULF2 gene was knocked down in fetal hOPCs using a lentivirus, and PDGF content in the cultures were modulated. The resulting cultures were stained with EdU and proliferation cells were quantified using fluorescent microscopy. Results show similar levels of proliferation at low and high levels of PDGF-AA (26% proliferation at 0.2 ng/mL, 33% at 200 ng/mL; n = 3) for SULF2 knockdown culture. Proliferation is decreased for the negative control culture (17% at 0.2 ng/mL and 33% at 200 ng/mL; n = 3). While further investigation is necessary to elucidate the mechanism of inhibition, it is evident from the data that SULF2 potentiates the proliferation of hOPCs via the PDGF-AA pathway.
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