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Title: | The effect of differentiation, polarization and MOX-LDL treatment on RPS3 and RPL17 expression in THP-1 monocytes and macrophages | Authors: | Hamoui, Nouha | Advisors: | Nasr, Zeina Daher, Jalil |
Keywords: | Atherosclerosis, cardiovascular diseases, ribosomal proteins, RPS3, RPL17, M1 macrophages, M2 macrophages, THP-1 monocytes | Subjects: | University of Balamand--Dissertations Dissertations, Academic |
Issue Date: | 2024 | Publisher: | [Kalhat, Lebanon] : [University of Balamand], 2024 | Abstract: | Atherosclerosis is an inflammatory disorder marked by the lipid buildup that forms plaques within artery walls. It is a major worldwide cause of death and a root cause of significant cardiovascular events like heart attacks and strokes. Macrophages are the main immune cells that significantly contribute to atherosclerosis onset, progression, and complication. This involves the ingestion of modified low-density lipoprotein (LDL), like myeloperoxidase oxidized LDL (Mox-LDL) to form foam cells. Previous studies have implicated various ribosomal proteins (RPs), such as RPS3 and RPL17, in cell signaling, DNA damage repair, and apoptosis that are relevant to cardiovascular diseases (CVDs). This study investigates the impact of differentiation, polarization and Mox-LDL treatment on the expression of RPS3 and RPL17 in differentiated and polarized macrophages in vitro using the THP-1 cell line model. This would help expand the body of knowledge concerning the pathophysiology of atherosclerosis and pave the way for future research into the therapeutic implications of targeting RPs in CVDs. First, THP-1 monocytes were cultured and differentiated into M0 macrophages followed by in vitro polarization into M1 and M2 macrophages. Then the monocytes and macrophages were treated with Mox-LDL, after which the protein expression levels of RPS3 and RPL17 were evaluated through Western blot analysis. Our results showed that RPS3 portrayed a significant decrease of 5.1-fold in expression between monocytes and M1 macrophages indicating that polarization had caused the downregulation. However, RPL17 showed no significant results across all groups, thus differentiation and polarization did not affect its expression. Finally, Mox-LDL did not significantly affect the expression of RPS3 and RPL17 in THP-1 monocytes and derived macrophages. This work might implicate the involvement of RPS3 in macrophage polarization and provide insights into its potential role in the inflammatory process underlying atherosclerosis. |
Description: | Includes bibliographical references (p. 42-57) |
URI: | https://scholarhub.balamand.edu.lb/handle/uob/7761 | Rights: | This object is protected by copyright, and is made available here for research and educational purposes. Permission to reuse, publish, or reproduce the object beyond the personal and educational use exceptions must be obtained from the copyright holder | Type: | Thesis |
Appears in Collections: | UOB Theses and Projects |
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