• Skip to main content
  • Skip to after header navigation
  • Skip to site footer
ERN: Emerging Researchers National Conference in STEM

ERN: Emerging Researchers National Conference in STEM

  • About
    • About AAAS
    • About NSF
    • About the Conference
    • Project Team
    • Advisory Board
  • Conference
  • Abstracts
    • Abstract Submission Process
    • Abstract Submission Guidelines
    • Presentation Guidelines
  • Travel Awards
  • Resources
    • Award Winners
    • Code of Conduct-AAAS Meetings
    • Code of Conduct-ERN Conference
    • Conference Agenda
    • Conference Materials
    • Conference Program Books
    • ERN Photo Galleries
    • Events | Opportunities
    • Exhibitor Info
    • HBCU-UP PI/PD Meeting
    • In the News
    • NSF Harassment Policy
    • Plenary Session Videos
    • Professional Development
    • Science Careers Handbook
    • Additional Resources
    • Archives
  • Engage
    • Webinars
    • 2023 ERN Recap Video
    • ERN 10-Year Anniversary Videos
    • Plenary Session Videos
  • Contact Us
  • Login

Neuroprotective Role of Galectin-1 on the Neuropathogenesis of HIV-1

Undergraduate #110
Discipline: Biological Sciences
Subcategory: Microbiology/Immunology/Virology

Courtney S. Mangum - Tougaloo College
Co-Author(s): Jessica L. Reynolds, Stanley A. Schwartz, and Supriya D. Mahajan, State University of New York at Buffalo, Clinical Translational Research Center, Buffalo, NY



Human immunodeficiency virus (HIV) enters the central nervous system (CNS) early in HIV infection and impacts neuronal cells such as astrocytes, microglia, and neurons, causing mild to moderate neurological deficits. This leads to a disease known as HIV associated neurocognitive disorder (HAND). Nitric oxide (NO) is a cellular signaling molecule that plays an important role in neuroinflammation. iNOS is involved in immune response and produces NO, which is proinflammatory. L-arginine is used as a substrate by both nitric oxide synthase (NOS) and arginase to produce nitric oxide (NO) and urea. NO production may be reduced by arginase via depleting the common substrate Larginine in microglia. Therefore, an increase in arginase activity reduces the available arginine substrate for NO production. Galectin-1, found within astrocytes, is neuroprotective and decreases NO via the increased arginase I expression. This protein will reduce neuroinflammation in the human microglia cell line CHME5 and CHME5-HIV. Treatment of Microglia with proinflammatory cytokines TNF-a/INF-g or LPS treatment, which stimulates proinflammatory cytokines results in increase in oxidative stress as measured by oxygen species (ROS) production. ROS include superoxide (O2), hydrogen peroxide (H2O2) and hydroxyl radical (OH), which under physiological conditions are generated at low levels and play important roles in signaling and metabolic pathways. Increased oxidative stress causes the generation of ROS, which are potentially toxic for cells further contributing to neuroinflammation. Treatment of microglia with pro-inflammatory cytokines TNF-a/INF-g or LPS resulted in 60 % increase (p<0.01) in oxidative stress in CHME-5 and a 26% increase (p<0.05) in CHME5/HIV respectively compared to the untreated control. Treatment of microglia with Galectin-1 (1mM) reduced oxidative stress by ~ 25% (p<0.05) in CHME5 and by ~60% in CHME-5/HIV. With the addition of Galectin-1, NO production was reduced while the arginase activity increase. Galectin-1 shows to reduce neuroinflammation via the modulation of the nitric oxide network and may potentially play a neuroprotective role in HAND.

Funder Acknowledgement(s): Department of Medicine, State University of New York at Buffalo, Clinical Translational Research Center

Faculty Advisor: Supriya Mahajan,

Sidebar

Abstract Locators

  • Undergraduate Abstract Locator
  • Graduate Abstract Locator

This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

AAAS

1200 New York Ave, NW
Washington,DC 20005
202-326-6400
Contact Us
About Us

  • LinkedIn
  • Facebook
  • Instagram
  • Twitter
  • YouTube

The World’s Largest General Scientific Society

Useful Links

  • Membership
  • Careers at AAAS
  • Privacy Policy
  • Terms of Use

Focus Areas

  • Science Education
  • Science Diplomacy
  • Public Engagement
  • Careers in STEM

Focus Areas

  • Shaping Science Policy
  • Advocacy for Evidence
  • R&D Budget Analysis
  • Human Rights, Ethics & Law

© 2023 American Association for the Advancement of Science