Syndecan-1 (Syn1) has been implicated in angiogenesis during tumor formation and wound healing. To investigate the unknown role of Syn1 in cardiac healing, remodeling and function, acute myocardial infarction (AMI) was performed in Syn1-deficient (Syn1KO) and wild type (WT) mice.

Cardiac function and structure did not differ between sham-operated WT and Syn1KO mice at 14 days. However, significantly less necrotic cardiomyocytes remained in the infarct of Syn1KO versus WT mice (% necrotic cardiomyocytes; 16±4.1 in WT vs 1.3±0.1 in KO, n = 5, p < 0.05) suggesting accelerated infarct healing in absence of Syn1 at 14 days. Increased number of CD45-staining leukocytes and CD31 staining capillaries in Syn1KO versus WT mice (CD45; 1068±283 in WT vs 2076±193 in KO; CD31; 138±5.9 in WT vs 233±19 in KO, n = 5, p < 0.05) confirmed accelerated infarct healing in absence of Syn1. Cardiac contractility was significantly depressed in Syn1KO as compared to WT mice in response to dobutamine (dP/dtmax, mmHg/s; 9080±830 in WT vs 5550±1140 in KO, n = 5, p < 0.05). Decreased fractional shortening and increased end-diastolic dimensions in Syn1KO versus WT mice at echocardiography (%FS: 19±2.5 in WT vs 11±1.3 in KO; EDD, mm: 5.6±1.2 in WT vs 6.6±0.3 in KO, n = 5, p < 0.05) confirmed depressed cardiac function in Syn1KO mice, resulting in a 70% higer lung to body weight index in Syn1KO as compared to WT mice.

In conclusion, absence of Syn1 results in increased inflammation, angiogenesis and accelerated healing after AMI, leading to increased dilatation and decreased cardiac function.