HSU CIRM Scholars Program
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HSU-CIRM Scholars participate in a 12-month, research-intensive internship at either the Stanford University Center for Human Embryonic Stem Cell Research and Education or at the University of California, San Francisco (UCSF) Institute for Regenerative Medicine. Scholars receive a monthly stipend of $2,500 in addition to a $5,000 scholarship to be put towards their Humboldt State enrollment fees.

The 2009-2010 HSU-CIRM Scholars List
Andrew Chin
Peter Din
Julia Freewoman
Jennifer Hampton
Dan Hunter
Kate Steeper

HSU-CIRM Host Labs

Andrew Chin's Research with Dr. Valerie Weaver, UCSF

The Weaver lab is multi-disciplinary lab dedicated toward understanding the role of mechanical force on breast cancer progression and human embryonic stem cell (hESC) differentiation. Forces exerted upon and by the cell are mediated by the extracellular matrix (ECM), which varies in structure and stiffness throughout the body. Most cell culture work is done on tissue culture plastic which is several orders of magnitude
stiffer than physiological ECM stiffness. Culturing cells on substrates closer to their physiological stiffness may improve survival and differentiation efficiency by more closely mimicking their physiological niche. My work focuses on characterizing and differentiating hESCs grown on stiffness-tuned polyacrylamide gels.

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Peter Din's Research with Dr. Theo Palmer, Stanford

The Palmer lab examines neural stem cells in development and in the adult brain. The lab has been able to reconstruct the conditions of neurogenesis in the Petri dish. Their studies of stem cells in the adult
focus on the hippocampus, an area of the brain where neurogenesis naturally continues throughout life. The generation of new neurons within the hippocampus is mediated by proliferating neural stem
or progenitor cells (NPCs). NPCs in the mammalian central nervous system have the ability to self-renew as well as differentiate into mature neurons. This inherent neurogenic potential suggests that tissue-
derived or embryonic stem (ES) cell-derived NPCs may be used to replace the damaged neurons in individuals suffering from traumatic brain injuries, Alzheimer’s or Parkinson’s Disease. Understanding
the mechanisms regulating NPC survival and integration in the brain is critical to improve the outcome of future clinical transplantations. My current work is focused on how the immune system influences
NPC transplant integration, maturation, and survival in a murine model.

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Julia Freewoman's Research with Dr. Theo Palmer, Stanford

Theo Palmer’s lab focused on the ability of adult neuronal precursors to develop into mature neurons and many focuses particularly on the dentate gyrus (DG) of the hippocampus which among other things has been associated with learning. My work has focused on understanding the interaction between learning and forgetting in particular Rac1 a Rho GTPase protein that has been associated with in neuronal morphogenesis, survival, neural transmitter release, neurogenesis, and neuronal migration and forgetting. We are studying how Rac1 deficit in neuronal cells resulting in the reduced performance in the working memory (ability to remember what is happening here and now compared to previously) tasks effects the survival and proliferation of new born neurons, and how the learning ability of these mice can be improved and how this effects the survival and proliferation of new born neurons. We also aim to understand the biochemical pathways involved in Rac1’s interactions with memory and to this aim we also investigated how β-catenin (part of the Wnt conical pathway) which has recently been shown to stabilize or signal Rac1. We are therefore also investigation how β-catenin effects the survival and proliferation of new born neurons during working memory trails.

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Jennifer Hampton's Research with Dr. Didier Stainier, UCSF

The Stainier lab uses the zebrafish as a model to investigate vertebrate organ development. The lab is interested in understanding molecular events that drive processes such as cellular differentiation and morphogenesis. The zebrafish is an ideal model organism to study early embryological development. It grows quickly and provides clear resolution of single cells in any tissue during all developmental stages. Diabetes is a detrimental disease that affects more and more people each year. Because an understanding of pancreatic development is essential for developing a therapy for this disease, we are currently investigating the pathways that influence the regeneration of insulin secreting -cells. Previous research has implicated anti-histamines with an increased rate of -cell regeneration. My project deals with determining the effects of various anti-histamines on the known pathways of cell regeneration in the zebrafish.

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Dan Hunter's Research with Dr. Jill Helms, Stanford

In humans, injuries to the retina can cause irreversible damage that results in vision impairment and blindness. The potential of stem cell-based treatments for these devastating conditions depends upon a detailed understanding of the growth factors and cytokines that maintain retinal homeostasis, and the roles they may play in activating retinal progenitor cells in the mammalian retina. Here, we demonstrate that potentiated Wnt signaling in the mammalian retina results in the increased production of retinal progenitor cells. Because the Wnt signal is transient, Axin2LacZ/LacZ retinal progenitor cells differentiate into Müller glia, interneurons, and photoreceptors. This leads to two distinct phenotypes: first, the intact Axin2LacZ/LacZ retina is hyper-cellular and contains more Müller glial cells and second, these Axin2LacZ/LacZ Müller glia give rise to more retinal progenitor cells after injury. The consequence of amplified Wnt signaling in the retina is a more robust
reparative response. Given the highly conserved nature of the Wnt pathway in non-mammalian retinal regeneration, therapeutic strategies that exploit this unique property of the Wnt pathway may have therapeutic applications for neural injuries.

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Kate Steeper's Research with Dr. Thomas A. Rando, Stanford

Quiescent satellite cells (SCs) display heterogeneous expression of Pax3 which has been shown to play a role in proliferation and myogenic determination. p53 is known to be involved in the regulation of quiescence, self-renewal, cell fate, and cellular senescence. SCs from the
diaphragm lose their myogenic fate at a much higher rate than SCs from the hindlimb. Early results show that p53 displays differential activity in the diaphragm versus the limb SCs. Indeed, when Pax3 is overexpressed in C2C12 cells p53 is destabilized. In addition, overexpression of
Pax3 in C2C12 cells treated with an inhibitor of the proteasome, MG132, show an increase of p53 polyubiquitination, suggesting that overexpression of Pax3 induces proteasomal degradation of p53. Furthermore, p53 knock-down in hindlimb SCs increased fibrogenic conversion while Pax3 knock-down in diaphragm SCs increased the myogenic cell fate choice.

Our findings suggest that Pax3 and p53 degradation pathway mayinterfere with each other and may explain the differential fibrogenic conversion observed in the diaphragm versus the limb of patients with Duchenne muscular dystrophy (DMD) and in old mdx mice, the mouse model used for DMD.

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