Master of Science
Dr. Claudio Martin
The disruption of myocardial extracellular matrix (ECM) has been implicated in myocardial dysfunction during sepsis. However, the underlying mechanism(s) are not clear. Interleukin-33 (IL-33) is a cytokine which regulates collagen synthesis in various cardiac pathologies. The purpose of the present study is to test whether IL-33 contributes to sepsis-induced myocardial dysfunction through regulation of matrix metalloproteinase-9 (MMP-9). The in vivo, feces-induced peritonitis (FIP) in mice and in vitro lipopolysaccharide (LPS) treatments to isolated cardiomyocytes were used. In FIP mice, myocardial IL-33 and MMP-9 expression were increased and myocardial contractility was decreased. Myocardial function in FIP mice was improved when treated with soluble ST2 (sST2), a decoy receptor of IL-33. The in vitro expression of IL-33 and MMP-9 in LPS-treated cardiomyocytes was increased. Addition of sST2 prevented the increase of MMP-9 expression in LPS-treated cardiomyocytes. Our results support that IL-33 plays an important role in mediating sepsis-induced myocardial dysfunction.
Choe, Yoonmi, "Involvement of Interleukin-33/ST2 in Myocardial Dysfunction in Murine Model of Sepsis" (2012). Electronic Thesis and Dissertation Repository. 1038.