Dissertation/Thesis Abstract

Complement protein C1q modulates macrophage molecular signaling and inflammatory responses during ingestion of atherogenic lipoproteins
by Ho, Minh-Minh, M.S., California State University, Long Beach, 2016, 58; 10131681
Abstract (Summary)

Foam cell formation from arterial intima macrophages and defective clearance of apoptotic foam cells drive the progression of the inflammatory disease atherosclerosis. The role of innate immune protein C1q in autoimmune disease and pathogen defense is well characterized, however its role in atherosclerosis remains largely uninvestigated. Prior studies have characterized the complement independent role of C1q in polarizing macrophages towards an anti-inflammatory phenotype during uptake of apoptotic cells and modified lipoproteins. To further understand the role of C1q in programming human monocyte-derived macrophages during foam cell formation, we used RNA-sequencing to elucidate pathways that are modulated by C1q during clearance of atherogenic lipoproteins. Expression of genes in JAK-STAT, PPAR, apoptotic, and TLR signaling pathways were modulated by C1q in this study. In addition, C1q suppressed STAT1 and PPAR transcriptional activity. This study identifies potential molecular mechanisms that support a beneficial role for C1q in early atherosclerosis.

Indexing (document details)
Advisor: Fraser, Deborah A.
Commitee: Brusslan, Judy, Sinchak, Kevin
School: California State University, Long Beach
Department: Biological Sciences
School Location: United States -- California
Source: MAI 55/06M(E), Masters Abstracts International
Subjects: Molecular biology, Immunology
Keywords: Atherosclerosis, C1q, Inflammation, Innate immunity, JAK-STAT, PPAR
Publication Number: 10131681
ISBN: 978-1-339-89452-2
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