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The Role of Mindin, a Member of the Mindin-F-spondin Family, in Immune Responses and Cardiac Remodeling Post Myocardial Infarction

Mindin (Spondin 2) is a highly conserved extracellular matrix protein of the Mindin-F-spondin family and a regulator of host innate immunity. Despite its expression in the heart, its role in cardiac stress response is unknown. The objective of this study was to determine the role of mindin following myocardial infarction (MI). C57/BL6 wild-type (mindin+/+) or mindin knockout (mindin-/-) mice were randomized to permanent left anterior descending (LAD) coronary artery ligation or sham operation. Mindin expression level increased maximally on day 7 post MI, but returned to baseline by day 28. Mindin-/- mice showed reduced mortality, rupture rate, cardiac MMP-9/-2 activities, NF-kB activation, cytokines and macrophage recruitment. We concluded that mindin is a significant contributor to mortality and acute adverse remodeling post MI, partly through its unique attributes of innate immune regulator and inhibitor of angiogenesis. Mindin may function as a potential biomarker or therapeutic target post MI.

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:OTU.1807/27546
Date02 June 2011
CreatorsMoon, Mark
ContributorsLiu, Peter
Source SetsLibrary and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada
Languageen_ca
Detected LanguageEnglish
TypeThesis

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