RCMI Center for Collaborative Research in Health Disparities
Research Capacity Core -Translational Proteomics Facility

Research Areas

  • Viral innate immunity-macrophages against HIV, Zika, SARS-CoV2
  • Use of quantitative proteomics to uncover targets for therapy
  • Understanding the role of HIV in neurocognitive disorders
  • Role of the placenta in protection against viral infections
  • Quantitative proteomics in neuroscience, cancer, infectious diseases

Scientific Achievements

  • Understanding of the role of macrophages cell receptors and function in innate immunity against HIV-1
  • HIV maternal to fetal transmission and biology of placental macrophages using proteomics.
  • Role of monocyte biomarkers in HIV dementia using proteomics.
  • Role of macrophage secreted cathepsin B in HIV- neurotoxicity using proteomics.
  • A method of reducing HIV-Replication on human body tissue by downregulating the expression of the protein Cystatin B. Patent No. 8,143,231

Funding

RCMI Funding:

  • NIH/NIMHD U54MD007600

Other funding obtained with RCMI support:

  • U54MD007600-29, NIH/NIMHD, RCMI Translational Proteomics Center – Research Capacity Core (2022–2027)
  • NCRR-P20 RR016470, NIH/NCRR, Centralized Instrumentation Proteomics Leader (2021–2026)
  • SC1GM113691, NIH/NIGMS, Targeting Monocyte/macrophage cathepsin B interactome in HIV-1 neurocognitive disorders (2015–2021)

Scientific Advance

Upregulation of MMP3 Promotes Cisplatin Resistance in Ovarian Cancer
Published in International Journal of Molecular Sciences, Volume 26, 2025, PMCID: PMC12071843.
This study investigates why some ovarian cancer cells stop responding to cisplatin, a commonly used chemotherapy drug, by focusing on the role of a protein called MMP3. They found that cisplatin-resistant ovarian cancer cells have much higher levels of MMP3 than cisplatin-sensitive ones. When they reduce MMP3 levels using molecular tools, the resistant cells become less able to survive, grow, or invade, especially when combined with cisplatin treatment. They also looked at the changes in many genes and proteins when MMP3 is reduced, showing that many pathways related to cell cycle control, death (apoptosis), metabolism, stress responses, and the structure around cells are affected. In mouse models, targeting MMP3 together with cisplatin led to slower tumor growth compared to treatments alone. The research suggests that MMP3 contributes to multiple processes that allow cancer cells to resist treatment, and that targeting MMP3 may improve response to cisplatin in ovarian cancer.
U54-MD007600/NIMHD NIH HHS/United States, 5R16GM145558/NIGMS NIH HHS/United States, 5R25GM061151-20/NIGMS NIH HHS/United States, R25-GM061838/NIGMS NIH HHS/United States, P20GM103475/NIMHD NIH HHS/United States, U54NS043011/NIMHD NIH HHS/United States
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