Fig. 1: Myeloid-specific LRP5, but not LRP6, KO, leads to increased myocardial ischemia-reperfusion injury and NET formation.

Mice lacking LRP5 (Lrp5^M, (a)) or LRP6 (Lrp6^M, (b)) in myeloid cells and their corresponding wildtype (WT) littermate control mice were subjected to myocardial ischemia-reperfusion injury. Infarction area (I) normalized against risk area (R) and Ejection Fractions before and after myocardial ischemia-reperfusion injury are shown. The ratios of risk area (R) to total area (T) are also shown. Each datum point represents one mouse (n = 8 for WT and n = 10 for Lrp5^M in (a). n = 7 for WT and n = 7 for Lrp6^M in (b)). Data were combined from three independent experiments. c Representative heart section images stained with triphenyl tetrazolium chloride from mice subjected to myocardial ischemia-reperfusion injury for (a, b). d Neutrophil presence in injured hearts determined by flowcytometry. Each datum point represents one mouse (n = 10 for WT and n = 8 for Lrp5^M). Data were combined from three independent experiments. e Pearson’s coefficients of co-localization of MPO and citrullinated histone (c-His) in the injured heart sections. Each datum point is one section. Three independent sections per mouse and five mice per group were analyzed. f Representative images of heart sections stained with anti-MPO and anti-citrullinated histone (Cit-His). g, h LRP5-deificient (KO) and wildtype (WT) neutrophils were subjected to Western analysis to examine citrullinated histone or ELISA to detect extracellular DNA. Each datum point represents one mouse (n = 3 for WT and n = 3 for KO). Data were combined from three independent experiments. Data in this figure are all presented as mean ± sem with p values (Student’s t-test, Two-tailed, unpaired).