HSU CIRM Scholars Program
 
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Current HSU-CIRM Scholars

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

To see a list of past HSU-CIRM scholars, click here.

The 2013-2014 HSU-CIRM Scholars List

William Oakley
"Investigating the function of repulsive guidance molecule B in intestinal stem cell biology"

Host lab: Calvin Kuo
Stanford University
Read more about William's research >

Janell Rivera
"The Impact of Obesity Induced Inflammation on the Cancer Stem Cell Phenotype"

Host lab: William J. Murphy
University of California, Davis
Read more about Janell's research >

Veronica Spandler
"Measuring chemotactic factors secreted from mesenchymal stromal cells on an extracellular matrix for myocardial infarction"

Host lab: Claus Svane Sondergaard
University of California, Davis
Read more about Veronica's research >

Jessica Torkelson
"Regulation by Long Non-Coding RNAs in Epidermal Differentiation"

Host lab: Anthony Oro
Stanford University School of Medicine
Read more about Jessica's research >

Taylor Wearda
"Finding the Human Skeletal Stem Cel"

Host lab: Michael Longaker
Stanford University
Read more about Taylor's research >

 

HSU-CIRM Host Labs

Jennifer Burkett - "The Role of Planar Cell Polarity Proteins in Granule Neuron Differentiation"
Matt Scott Laboratory, Stanford University

Planar Cell Polarity (PCP) is required for proper orientation of a cell within a tissue and organ during development and regeneration. PCP has been described in adult neurons but its role during neuronal differentiation remains enigmatic. During postnatal cerebellum development granule neural precursors (GNPs) proliferate on the surface in the external granule layer, then start to migrate inward in a directed way to later form granule neurons (GN), the most abundant cell type in the brain. The differentiation process of GNPs is characterized by the highly conserved formation of three axons, the first two extending on opposite sides of the cell. Clusters of such axons are called parallel fibers, which thread through the Purkinje Neuron (PN) dendrites, forming synapses that each PN receives from more than 105 granule neurons. Defects in parallel fiber formation lead to reduced synaptic plasticity in the cerebellum, resulting in cognitive and behavior defects. Our study focuses on the role and effect of PCP in correct axon formation and orientation during early GNP differentiation. Through this study we aim to understand which mechanisms may contribute to proper neuronal development and orientation, leading to a more detailed insight of neuronal diseases and towards better treatments of these patients on a more global scale.

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Morgaine Green - "Smooth Muscle Cell Derivation for Treatment of Stress Incontinence"
Renee Reijo Pera Laboratory, Stanford University

The Reijo Pera Laboratory investigates a range of areas including germ cell and embryo development, sex-linked developmental disorders, degenerative diseases like Parkinson’s and urinary incontinence. The project I work on focuses on the differentiation of human Embryonic Stem Cells (hESCs) to smooth muscle cells for the treatment of Stress Urinary Incontinence. This condition is predominantly caused by loss of function in the urethral sphincter, which is often a result of pregnancy, childbirth, and aging. This sphincter is composed primarily of smooth muscle cells (SMCs) under involuntary control of the autonomic nervous system. It is believed that regeneration of these cells would result in a renewal of function in the sphincter. Previous studies in the lab have shown that vascular progenitors (CD31+ & CD34+) can differentiate into functional smooth muscle cells as well as endothelial cells. Currently I am using hESCs to optimize this differentiation by using xeno-free and defined culture conditions, in order to make GMP/clinical grade SMCs. These SMCs would then be injected into an incontinent rat model to demonstrate their functional efficiency in vivo and their ability to repair the damaged sphincter. Concurrently their safety and long term survival in vivo will also be assessed. Additionally, I am also deriving clinical grade iPSCs using episomal vectors which would be an excellent source of autologous cells. I will assess the potential of these iPSCs to generate functional SMCs, which would more closely tailor the cell treatment to each patient’s unique biological makeup and could potentially reduce immune rejection.

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Kyle Hendrix - "Generation of an immune deficient mouse model of Huntington’s disease for efficacy testing of human cell based therapies"
Jan A. Nolta Laboratory, University of California, Davis

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder afflicting nearly one in 10,000 people in the United States. Linked to expanded trinucleotide repeats in exon 1 of the huntingtin gene, HD causes death in 100% of those afflicted through an accumulation of protein aggregates and aberrant gene regulation. The disease is characterized by neuronal atrophy of the striatum which results in uncontrollable bodily movements, aggression, cognitive decline, and psychosis. Currently available treatments target only symptoms of the disease and there is no available therapy or cure. At the UC Davis Institute for Regenerative Cures we are developing a cell therapy designed to slow onset and progression through intracranial injections of Mesenchymal Stem Cells engineered to deliver brain derived neurotrophic factor, crucial to neuron maintenance and highly down regulated in HD, to injured neurons. Before any cell treatment can be introduced into the clinic, efficacy must first be shown in animal models. Efficacy testing of human stem cell therapies in animal models is challenged by a xenogeneic response by the animal resulting in rejection of the human cells. My project is to develop an immune deficient and xeno-tolerant animal model of Huntington’s disease to allow efficacy testing of these human cell based therapies without the need for highly toxic immune suppressants through the introduction of the Nod.Scid.Il2rg-/- background onto the full length human HD protein expressing Yac128 mouse model. Once completed, further manipulation through humanization of the mouse immune system through engraftment of umbilical cord derived hematopoietic stem cells may provide a more “allogeneic-like” system for efficacy testing of current and future human cell based therapies for HD.

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Akela Kuwahara - "VEGF signaling in adult neural progenitor cells"
Tony Weiss-Coray Laboratory, Stanford University

Adult neurogenesis is a highly regulated process through which the adult mammalian brain produces new neurons. Understanding the factors that regulate this process is important to our general knowledge of the adult brain, as well as neurodegenerative or neurological disease. Previous studies show that vascular endothelial growth factor (VEGF) enhances neural progenitor cell proliferation, both in vitro and in vivo. The Wyss-Coray lab recently demonstrated that neural progenitor cells (NPCs) express significant levels of VEGF themselves, leading to the hypothesis that NPCs may contribute significantly to the neurogenic niche through VEGF signaling. In this study, we examine VEGF signaling in NPCs in vitro through the exogenous addition and removal of VEGF, and the inhibition of VEGF signaling. This study will complement other studies in the lab using an in vivo knockout model of NPC secreted VEGF by exploring the mechanisms of VEGF signaling in NPCs at a cellular level.

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William Oakley - "Extracellular Matrix Bioscaffold Augmented with Human Mesenchymal Stem Cells for Cardiovascular Repair"
Calvin Kuo Laboratory, Stanford University

My work as a CIRM bridges scholar focuses on the intestinal stem cell (ISC) niche. The surfaces of the intestine and colon are covered in a highly regenerative epithelial layer, which rapidly renews itself in response to mechanical and chemical damage. This renewal is affected by a stem cell population that resides in small invaginations of the intestine known as crypts. Crypt base cells presenting the g-protein couple receptor Lgr5 are thought to represent the actively cycling stem cells and have been shown to repopulate the intestinal epithelium in a clonal manner. The proliferation of these cells is tightly regulated by growth factors released by adjacent paneth cells and the sub-epithelial compartment, such as WNT and bone morphogenetic protein ligands. Previous transcriptome analysis of FACS sorted Lgr5+ cells has revealed a number of transcripts present at higher levels compared to the surrounding tissue. I focus on the protein product of one of these upregulated genes; Repulsive Guidance Molecule B (RGMb). RGMb is a GPI-linked cell surface protein that is known to act as a BMP co-receptor in conjunction with BMP type 1 receptors and another receptor known as Neogenin. Thus far I have generated adenoviruses that can infect mice and express the extracellular domains of these receptors in their blood plasma, allowing me to investigate the role of this molecule by observing changes in intestinal stem cell dynamics through histology and antibody staining. I’m generating siRNA reagents that will allow me to knockdown RGMb transcripts in organotypic culture in-vitro­ and also plan to purify the ectodomains of RGMb and Neogenin for use in-vitro. Ultimately I would like to know if RGMb is playing a role as a BMP co-receptor in Lgr5+ ISCs and whether or not it’s essential for maintenance of a functional ISC niche.

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Janell Rivera - "The Impact of Obesity Induced Inflammation on the Cancer Stem Cell Phenotype"
William J. Murphy Laboratory, University of California, Davis

Cancer stem cells (CSC) are a subpopulation of cells residing within a tumor that are hypothesized to be responsible for tumor initiation, metastasis, and recurrence. These cells have stem-cell-like characteristics including the capability to self-renew, be in a quiescent state, and be capable of long-term clonal repopulation. Increased stress, hypoxia and inflammation have been demonstrated to induce a plastic phenotype for CSCs, allowing for either tumor growth or tumor escape. Increasing data has suggested that inflammation induces a pluripotent and aggressive CSC population, yet the mechanism of how inflammation can direct plasticity is not fully understood. In addition, obesity within the United States has reached epidemic proportions and is associated with more than nine types of cancers. The obese environment is characterized as participating in a chronic, low-level, pro-inflammatory state that is self-perpetuating, yet how the obese microenvironment affects CSC plasticity and tumor progression is unknown. Therefore, the purpose of this study is to investigate the mechanism of how obesity induced inflammation can impact the CSC population, and the association between increased adiposity and aggressive cancer phenotypes. This study will allow for an enhanced mechanistic understanding of the CSC phenotype within obesity and may lead towards the development of novel anti-cancer immunotherapies.

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Veronica Spandler - "Measuring chemotactic factors secreted from mesenchymal stromal cells on an extracellular matrix for myocardial infarction"
Claus Svane Sondergaard, University of California, Davis

Coronary heart disease is a leading cause of death in the United States.  Current therapies only slow disease progression with heart transplantation being the only curative option.  This project proposes to use an extracellular matrix (ECM) device to deliver mesenchymal stromal cells (MSC) to damaged cardiac tissue after myocardial infarction in order to regenerate and restore its function.  My project aims to prove that seeding MSCs on matrix alters chemotactic cytokine secretion in a manner that is beneficial for the MSCs and surrounding target tissue.  The specific cytokines being tested are chemotactic factors: hepatocyte growth factor (HGF) and stromal cell derived factor one (SDF1α).  Thus far, results show clear indication that secretion of both HGF and SDF1α are altered when cells are seeded on ECM with resulting improvement in vitro on endothelial cells function.   

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Jessica Torkelson - "Regulation by Long Non-coding RNAs in Epidermal Differentiation"
Anthony Oro Laboratory, Stanford University School of Medicine

Stem cell based therapies are a promising treatment option for patients who suffer from extensive burns or genetic skin diseases such as Dystrophic Epidermolysis Bullosa. Differentiating epidermal cells requires understanding of molecular signals, gene expression patterns and transcriptional regulatory networks involved in skin development. Developmental regulation is influenced by both coding and non-coding genes. Long non-coding RNAs (lncRNAs) resemble mRNA transcripts yet are not translated to proteins. It is expected that lncRNA transcripts coordinated with a network of transcription factors play an essential role in developmental regulation and lineage commitment from the stem cell state to stratified skin. The underlying mechanism of non-coding RNA regulation in skin commitment and development is unknown. Here we investigate differentially expressed lncRNAs and novel transcription factors and their role in differentiation and self-renewal in human keratinocytes, representing the latest stage of skin development. Transcriptome analysis revealed expression patterns from over 100 differentially expressed lncRNA targets in 4 stages of epidermal development. Loss of function studies indicate lncRNAs are necessary for proper keratinocyte viability, proliferation and self-renewal. In addition the lncRNA targets are essential for stratification determined by lift-up assays in organotypic cultures.  Based on the current results it is anticipated that functional assays will define the molecular mechanisms of the lncRNA targets in epidermal stratification. Impending work will identify essential lncRNAs in early ectoderm and late epidermal differentiation that may improve stem cell based therapies for patient use.

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Taylor Wearda - "Finding the Human Skeletal Stem Cell"
Anthony Oro Laboratory, Stanford University School of Medicine

The clinical problems relating to the skeleton (bone, cartilage and bone marrow stromal niche) could be ultimately addressed by a thorough understanding of how the skeleton develops and is maintained from a stem cell point of view. By identifying and characterizing the human skeletal stem cell (hSSC) and its downstream progenitors, novel cell-based therapies can be developed for treating conditions affecting the bone marrow stromal niche. We seek to define the cellular origins of skeletal tissues to study how the human skeleton is formed and maintained throughout life. We want to understand how bone and cartilage tissue are generated and organized into skeletal structures at the cellular level, and how skeletal progenitors respond to regenerative demands in response to injury and stress. We also hope to understand the underlying molecular mechanisms involved in these processes, and how they are genetically programmed. Our experimental strategy is designed to address these questions by identifying and analyzing the distinct progenitors of skeletal tissue, beginning with the human skeletal stem cell (hSSC), and its progression through intermediate multipotent progenitor phases into the committed progenitors of mature osteoblasts, chondrocytes and stroma. We will accompany functional assays with transcriptome analyses to identify defining genetic changes occurring at each progenitor stage. We have identified several distinct populations of skeletal progenitor cells from human fetal bones including a unipotent cartilage progenitor population, a bone and stroma forming population, and what we believe to be the human bone, cartilage and stromal niche progenitor (BCSP). 

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