Karen Chase Karen Chase
Undergraduate: University of Michigan
Research Lab: Dr. Elaine Raines
Monja Dishman Monja Dishmon
Undergraduate: Arizona State University
Research Lab: Dr. Dan Bowen-Pope Although apoptosis is classically considered a silent event, it has been shown that macrophages colocalize with areas of apoptosis in atherosclerotic lesions and after arterial injury. We find that regulated induction of vascular smooth muscle cell (SMC) apoptosis through overexpression of Fas-associated death domain (FADD) in the rat carotid artery results in an accumulation of macrophages within the neointima and the transcriptional upregulation of the monocyte-chemoattractant protein 1 (MCP-1). Cultured human vascular SMCs also upregulate pro-inflammatory genes, including MCP-1 and IL-1, in response to FADD overexpression or exposure to FasL/cycloheximide. In contrast to leukocytes, SMCs are relatively resistant to apoptosis, which may be a precondition for Fas/FADD-induced pro-inflammatory gene upregulation. The mechanism of this resistance is not known. My project focuses on elucidating the role of cFLIP, an endogenous caspase-8 inhibitor, in vascular SMC resistance to apoptosis and pro-inflammatory gene upregulation. Joshua Kachner Joshua Kachner
Undergraduate: University of Pennsylvania
Research Lab: Dr. Steve Schwartz
I am interested in vascular biology and the causes of vascular disease. Specifically, I study the gene RGS5 in vascular smooth muscle cells and its relationship to vessel function. RGS5 is a member of the RGS (regulator of G-protein signalling) family and is a GTPase for G-proteins. It has been shown in vitro to inhibit angiotensin receptor signalling and is the most highly differentially expressed gene in arterial smooth muscle cells compared to venous smooth muscle cells. It is my goal to understand why RGS5 is highly expressed in arteries and what effect this has on arterial function. Jiang Li Jiang Li
Undergraduate: China Medical University
Research Lab: Dr. Bumgarner The overall goal of the project is to elucidate the regulation of EC apoptosis and its signaling pathway focusing on PI3 kinase and NF-kB. Di Nguyen Di Kim Nguyen
Undergraduate: School of Medicine, Saigon; Evergreen State College
Research Lab: Dr. Christine Disteche Monosomy of the X chromosome due to divergence between the sex chromosomes has lead to dosage compensation mechanisms that restore balanced genome expression. In Drosophila, up-regulation of the male X achieves dosage compensation. S. Ohno predicted that mammals would likewise up-regulate their active X chromosome. Together with X inactivation, this mechanism would maintain balanced expression between the X and autosomes and between the sexes. Here, I showed that doubling of the global expression level of the X chromosome achieves dosage compensation in adult somatic tissues from several mammalian species. Furthermore, X-linked genes were highly expressed in brain tissues, consistent with a role in brain function. The X chromosome was expressed but not up-regulated in spermatids and secondary oocytes, preserving balanced expression of the genome in these haploid cells. Upon fertilization or at X inactivation onset up-regulation of the active X must happen to achieve the observed dosage compensation in early embryos. Weiliang Tang Weiliang Tang
Undergraduate: Fudan University, China
Research Lab: Dr. Nelson Fausto
Roland Walter Roland Walter
Undergraduate: University of Zurich Medical School, Switzerland
Research Lab: Dr. Steven Collins We are studying internalization and trafficking of gemtuzumab ozogamicin (Mylotarg), a CD33 targeting immunoconjugate used for treatment of acute myeloid leukemia (AML); we aim to expand our understanding of CD33 biology and to define novel approaches for enhanced clinical efficacy of immunoconjugate therapy of AML.