Resume

• 2006

  Doctor of Philosophy (Ph.D.)

  Molecular & Systems Pharmacology

  Emory University

• 2000

  Bachelor of Science

  Biology

  Clark Atlanta University

• Fellowships in Research and Science Teaching

  IRACDA ) is supported by theDivision of Training

  Workforce Development

  and Diversity at NIGMS

  one of the National Institutes of Health

  and provides interdisciplinary biomedical research training by a faculty with the expertise to nurture the foundation critical for outstanding postdoctoral research training.

  Fellowships in Research and Science Teaching

  Gathered information from various sources and subject matter experts for factual content. Composed science and medicine articles under deadline pressure for publication in the Emory In Scripto Newsletter. \n

  Science Writers Association of Emory

  Writer/Contributor

  Prepared an article covering the 2014 Georgia Bio Innovation Summit for publication in the Emerging Leaders Network (ELN) Newsletter.

  Emerging Leaders Network (ELN)

  Writer/Contributor

  Collaborated with colleagues to write

  edit and produce articles covering the Emory University Office of Postdoctoral Education (OPE) Careers Symposium for publication in the OPE Newsletter.

  Emory University Postdoctoral Association

  Technical Writing

  Fluorescence Microscopy

  real-time PCR

  Western Blotting

  Laboratory

  Scientific Writing

  PCR

  Animal Models

  Cellular Assays

  Molecular Biology

  Confocal Microscopy

  Medical Writing

  Immunohistochemistry

  Experimental Design

  Science

  Higher Education

  Cell Culture

  Tissue Culture

  ELISA

  qPCR

  Cathepsin Protease Inhibition Reduces Endometrial Lesion Establishment

  N Sidell

  FA Wieser

  Endometriosis is a gynecologic disease characterized by the ectopic presence of endometrial tissue on organs within the peritoneal cavity

  causing debilitating abdominal pain and infertility. Current treatments alleviate moderate pain symptoms associated with the disorder but exhibit limited ability to prevent new or recurring lesion establishment and growth. Retrograde menstruation has been implicated for introducing endometrial tissue into the peritoneal cavity

  but molecular mechanisms underlying attachment and invasion are not fully understood. We hypothesize that cysteine cathepsins

  a group of powerful extracellular matrix proteases

  facilitate endometrial tissue invasion and endometriosis lesion establishment in the peritoneal wall and inhibiting this activity would decrease endometriosis lesion implantation. To test this

  we used an immunocompetent endometriosis mouse model and found that endometriotic lesions exhibited a greater than 5-fold increase in active cathepsins compared to tissue from peritoneal wall or eutopic endometrium

  with cathepsins L and K specifically implicated. Human endometriosis lesions also exhibited greater cathepsin activity than adjacent peritoneum tissue

  supporting the mouse results. Finally

  we tested the hypothesis that inhibiting cathepsin activity could block endometriosis lesion attachment and implantation in vivo. Intraperitoneal injection of the broad cysteine cathepsin inhibitor

  E-64

  significantly reduced the number of attached endometriosis lesions in our murine model compared to vehicle-treated controls demonstrating that cathepsin proteases contribute to endometriosis lesion establishment

  and their inhibition may provide a novel

  nonhormonal therapy for endometriosis.

  Cathepsin Protease Inhibition Reduces Endometrial Lesion Establishment

  Pulmonary Hypertension (PH) is a progressive disorder characterized by endothelial dysfunction and proliferation. Hypoxia induces PH by increasing vascular remodeling. A potential mediator in hypoxia-induced PH development is arachidonate 5-Lipoxygenase (ALOX5). While ALOX5 metabolites have been shown to promote pulmonary vasoconstriction and endothelial cell proliferation

  the contribution of ALOX5 to hypoxia-induced proliferation remains unknown. We hypothesize that hypoxia exposure stimulates HPAEC proliferation by increasing ALOX5 expression and activity. To test this

  human pulmonary artery endothelial cells (HPAEC) were cultured under normoxic (21% O2) or hypoxic (1% O2) conditions for 24-

  48-

  or 72 hours. In a subset of cells

  the ALOX5 inhibitor

  zileuton

  or the 5-lipoxygenase activating protein inhibitor

  MK-886 was administered during hypoxia exposure. ALOX5 expression was measured by qRT-PCR and western blot and HPAEC proliferation was assessed. Our results demonstrate that 24- and 48 hours of hypoxia exposure have no effect on HPAEC proliferation or ALOX5 expression. Seventy two hours of hypoxia significantly increases HPAEC ALOX5 expression

  hydrogen peroxide (H2O2) release

  and HPAEC proliferation. We also demonstrate that targeted ALOX5 gene silencing or inhibition of the ALOX5 pathway by pharmacological blockade attenuates hypoxia-induced HPAEC proliferation. Furthermore

  our findings indicate that hypoxia-induced increases in cell proliferation and ALOX5 expression are dependent on H2O2 production

  as administration of the antioxidant

  PEG-catalase blocks these effects and addition of H2O2 to HPAEC promotes proliferation. Overall

  these studies indicate that hypoxia exposure induces HPAEC proliferation by activating the ALOX5 pathway via the generation of H2O2.

  Chronic Hypoxia Promotes Pulmonary Artery Endothelial Cell Proliferation through H2O2-induced 5-Lipoxygenase

  BA Jocob

  Elms SC

  Cheng PY

  Jones DP

  Sutlff RL

  HIV-1-induced Pulmonary Oxidative and Nitrosative Stress: Exacerbated Response to Endotoxin Administration in HIV-1 Transgenic Mouse Model

  Roy Sutliff

  David Guidot

  Patrick Mitchell

  Robert Raynor

  Pulmonary arterial hypertension (PAH) is a progressive disease characterized by increased pulmonary arterial resistance and vessel remodeling. Patients living with human immunodeficiency virus-1 (HIV-1) have an increased susceptibility to develop severe pulmonary hypertension (PH) irrespective of their CD4+ lymphocyte counts. While the underlying cause of HIV-PAH remains unknown

  the interaction of HIV-1 proteins with the vascular endothelium may play a critical role in HIV-PAH development. Hypoxia promotes PH in experimental models and in humans

  but the impact of HIV-1 proteins on hypoxia-induced pulmonary vascular dysfunction and PAH has not been examined. Therefore

  we hypothesize that the presence of HIV-1 proteins and hypoxia synergistically augment the development of pulmonary vascular dysfunction and PH. We examined the effect of HIV-1 proteins on pulmonary vascular resistance by measuring pressure-volume relationships in isolated lungs from wild-type (WT) and HIV-1 Transgenic (Tg) rats. WT and HIV-1 Tg rats were exposed to 10% O2 for four weeks to induce experimental pulmonary hypertension to assess whether HIV-1 protein expression would impact the development of hypoxia-induced PH. Our results demonstrate that HIV-1 protein expression significantly increased pulmonary vascular resistance (PVR). HIV-1 Tg mice demonstrated exaggerated pulmonary vascular responses to hypoxia as evidenced by greater increases in right ventricular systolic pressures

  right ventricular hypertrophy and vessel muscularization when compared to wild-type controls. This enhanced PH was associated with enhanced expression of HIF-1α and PCNA. In addition

  in vitro studies reveal that medium from HIV-infected monocyte derived macrophages (MDM) potentiates hypoxia-induced pulmonary artery endothelial proliferation. These results indicate that the presence of HIV-1 proteins likely impact pulmonary vascular resistance and exacerbate hypoxia-induced PH.

  Human immunodeficiency virus-1 transgene expression increases pulmonary vascular resistance and exacerbates hypoxia-induced pulmonary hypertension development.

  Roy L. Sutliff

  Over 1 million people in the United States and 33 million individuals worldwide suffer from HIV/AIDS. Since its discovery

  HIV/AIDS has been associated with an increased susceptibility to opportunistic infection due to immune dysfunction. Highly active antiretroviral therapies restore immune function and

  as a result

  people infected with HIV-1 are living longer. This improved survival of HIV-1 patients has revealed a previously unrecognized risk of developing vascular complications

  such as atherosclerosis and pulmonary hypertension. The mechanisms underlying these HIV-associated vascular disorders are poorly understood. However

  HIV-induced elevations in reactive oxygen species (ROS)

  including superoxide and hydrogen peroxide

  may contribute to vascular disease development and progression by altering cell function and redox-sensitive signaling pathways. In this review

  we summarize the clinical and experimental evidence demonstrating HIV- and HIV antiretroviral therapy-induced alterations in reactive oxygen species and how these effects are likely to contribute to vascular dysfunction and disease.

  HIV-1

  Reactive Oxygen Species

  and Vascular Complications

  Kristi M.

  Porter

  Ph.D.

  Atlanta Metropolitan College

  Emory University

  The National Institutes of Health

  Georgia Institute of Technology

  MedThink SciCom

  prIME Oncology

  While an intern with prIME Oncology

  I acquired medical writing and editing experience by developing the agenda and clinical content for a mock seminar series reviewing breast cancer therapies and treatment strategies for oncologists and hematologists. I also determined the learning objectives

  identified experts in field of oncology and hematology

  as well as researched

  organized

  wrote

  and revised written materials under deadline pressure. I also gathered information about metastatic

  HER2-positive

  and triple-negative breast cancers from various sources and organizations

  such as Pubmed

  WebMD

  and the Centers of Disease Control (CDC) as well as analyzed and interpreted gap analyses regarding breast cancer treatment strategies.

  prIME Oncology

  Atlanta Metropolitan College

  As an Adjunct Professor

  I taught one General Biology class (lecture) and a General Biology laboratory section for science

  math

  and pre-health profession students. In this capacity

  I developed the class syllabus

  maintained class attendance and grade rosters

  as well as managed exams

  homework assignments

  quizzes

  and online exercises. I also facilitated class instruction

  ensuring science information was accurate and understandable to students. Moreover

  I used PowerPoint presentations

  class discussions

  group exercises

  and online assignments via the Desire2Learn web portal to ensure comprehension of class learning objectives.

  Adjunct Professor

  Greater Atlanta Area

  Greater Atlanta Area

  I worked as part of a multi-disciplinary team of clinicians

  engineers

  and researchers to investigate the contribution of cathepsin proteases to lesion establishment in endometriosis. My studies focused on small molecule cathepsin inhibitors to reduce endometriotic lesion formation. I also performed pre-clinical research and trouble shooting for the examination of HIV antiretroviral therapies and macrophage-derived cathepsin proteases in atherosclerosis development. In this capacity

  I analyzed and interpreted scientific findings for the production of abstracts

  presentations

  and manuscripts for dissemination to key opinion leaders and subject matter experts. My results were included in 3 presentations at international conferences and 4 external grant application. During this time

  I also trained and supervised one undergraduate and 2 high school students in science research methods and analysis.

  FIRST Postdoctoral Fellow

  Georgia Institute of Technology

  Project: The Role and Regulation of 5-Lipoxygenase in HIV-related Pulmonary Hypertension\n\nMy project objective was to determine how HIV-induced 5-Lipoxygenase contributes to the pathogenesis and progression of HIV-related Pulmonary Hypertension by using real-time PCR

  western blot

  immunohistochemistry

  and ELISA in cell culture and HIV-1 transgenic animal models. \n\nMy in vitro studies demonstrated that ALOX5 expression and activity are increased in response to hypoxia- and HIV-1 Tat protein exposure. My findings also showed that enhanced reactive oxygen species (ROS) generation and reduced antioxidant availability mediate these hypoxia- and Tat-induced alterations. Moreover

  my studies revealed that increased ALOX5 expression promotes pulmonary vascular remodeling

  a key pathogenic feature of PH

  by inducing endothelial dysfunction and proliferation

  and that ALOX5 inhibitors and leukotriene receptor antagonists reduce vascular cell proliferation. Overall

  we concluded that HIV-induced ALOX5 promotes HIV-PH development and progression by altering pulmonary endothelial function.

  NIH Predoctoral Fellow

  Greater Atlanta Area

  Emory University

  As a medical writer

  I collaborated with key opinion leaders and internal team members to develop and edit congress abstracts and poster presentations

  create comprehensive slide decks for presentation to lay and expert audiences

  and author manuscripts in the therapeutic areas of HIV/AIDS and rheumatoid arthritis. My job responsibilities also included preparing weekly publication alerts for multiple clients and therapeutic areas and identifying congress venues and journals for strategic data dissemination.\n

  Medical Writer

  Raleigh-Durham

  North Carolina Area

  MedThink SciCom

  Bethesda

  MD

  Scientific Program Specialist

  The National Institutes of Health

  The Black Graduate Student Association is dedicated to the enhancement of the graduate experience of African American Students and students of African descent at Emory University. These efforts extend across the entire spectrum of the graduate experience. This experience includes facilitating the transition from undergraduate to graduate school

  providing academic support

  recruiting

  and providing opportunity for fellowship

  service

  and activism. In addition to these efforts

  this organization will also seek to expose the Emory University community to African American culture.

  President

  Vice-President

  Event Chair

  Secretary

  Emory University Black Graduate Student Association (BGSA)

  Emory University Postdoctoral Association

  SWAE is dedicated to providing an open venue for young scientists to improve their communication skills through writing

  editing

  and publishing and will achieve this through the production of the student-operated

  periodic science publication

  In Scripto. This publication will feature high quality science writing and news reporting by graduate students across diverse disciplines at Emory. \n\nThe SWAE Magazine

  in scripto will provide timely and pertinent information about recent scientific accomplishments at Emory. In particular

  it will draw on current issues and trends affecting the national scientific community to highlight how cutting edge research at Emory fits into the larger picture. The magazine will serve to aid in learning about the process of publishing and editing and the dissemination of scientific information in a newsworthy format.\n\n

  Science Writers Association of Emory (SWAE)