Thesis
Exploring the Role of Endoplasmic Reticulum Stress in Macrophage Polarization Regulation
Exposure to harmful stimuli could induce tissue damage. Failure to remove the harmful stimuli and to
repair its resulting damages is associated with increased level of ER stress, which is also closely
associated with development of age-related diseases including cancer and metabolic diseases.
Additionally, chronic inflammation, characterized by the imbalance of M1/M2 macrophage ratio, is
also associated with these diseases. The objective of this study is to determine the role of ER stress in
altering M1/M2 ratio through modulation of macrophage polarization. This study was conducted by
co-treating BMDMs with an ER stress inducer, Tunicamycin, during stimulation into M1 or M2,
followed by analyzing the expression of M1 or M2 marker, respectively. Results show that tunicamycin
treatment induces ER stress in stimulated BMDMs, showed from the increased transcriptional
expression level of CHOP and ATF6α, and increased spliced XBP1 mRNA level. Tunicamycin treatment
also show to decreases M2 population and unexpectedly decreases M1 population, as indicated from
decreased expression level of both M1 and M2 markers. This study provides insights on the effect of
ER stress in altering M1/M2 ratio.
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