Implantation of a novel biodegradable PEUU patch onto a subacute myocardial infarction promoted contractile phenotype smooth muscle tissue formation and improved cardiac remodeling and contractile function at the chronic stage. Our findings suggest a new therapeutic option against post-infarct cardiac failure.

Our findings suggest that VEGF is essential for the induction of angiogenesis and functional improvements observed after MDSC transplantation for infarct repair.

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Objective The aim was to evaluate the therapeutic potential of human skeletal muscle-derived myoendothelial cells for myocardial infarct repair. Background We have recently identified and purified a novel population of myoendothelial cells from human skeletal muscle. These cells co-express myogenic and endothelial cell markers and produce robust muscle regeneration when injected into cardiotoxin-injured skeletal muscle. Methods Myoendothelial cells were isolated from biopsies of human skeletal muscle using a fluorescence-activated cell sorter along with populations of regular myoblasts and endothelial cells. Acute myocardial infarction was induced in male immune-deficient mice, and cells were directly injected into the ischemic area. Cardiac function was assessed by echocardiography, and donor cell engraftment, angiogenesis, scar tissue, endogenous cardiomyocyte proliferation and apoptosis were all evaluated by immunohistochemistry. Results A greater improvement in left ventricular function was observed after intramyocardial injection of myoendothelial cells when compared to hearts injected with myoblast or endothelial cells. Transplanted myoendothelial cells generated robust engraftments within the infarcted myocardium, and also stimulated angiogenesis, attenuation of scar tissue and proliferation and survival of endogenous cardiomyocytes more effectively than transplanted myoblasts or endothelial cells. Conclusions Our findings suggest that myoendothelial cells represent a novel cell population from human skeletal muscle that may hold promise for cardiac repair.

Momoi N, Tinney JP, Liu LJ, Elshershari H, Hoffmann PJ, Ralphe JC, Keller BB, Tobita K. Modest maternal caffeine exposure affects developing embryonic cardiovascular function and growth. Am J Physiol Heart Circ Physiol 294: H2248-H2256, 2008. First published March 21, 2008 doi:10.1152/ajpheart.91469.2007.-Caffeine consumption during pregnancy is reported to increase the risk of in utero growth restriction and spontaneous abortion. In the present study, we tested the hypothesis that modest maternal caffeine exposure affects in utero developing embryonic cardiovascular (CV) function and growth without altering maternal hemodynamics. Caffeine (10 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 subcutaneous) was administered daily to pregnant CD-1 mice from embryonic days (EDs) 9.5 to 18.5 of a 21-day gestation. We assessed maternal and embryonic CV function at baseline and at peak maternal serum caffeine concentration using high-resolution echocardiography on EDs 9.5, 11.5, 13.5, and 18.5. Maternal caffeine exposure did not influence maternal body weight gain, maternal CV function, or embryo resorption. However, crownrump length and body weight were reduced in maternal caffeine treated embryos by ED 18.5 (P Ͻ 0.05). At peak maternal serum caffeine concentration, embryonic carotid artery, dorsal aorta, and umbilical artery flows transiently decreased from baseline at ED 11.5 (P Ͻ 0.05). By ED 13.5, embryonic aortic and umbilical artery flows were insensitive to the peak maternal caffeine concentration; however, the carotid artery flow remained affected. By ED 18.5, baseline embryonic carotid artery flow increased and descending aortic flow decreased versus non-caffeine-exposed embryos. Maternal treatment with the adenosine A 2A receptor inhibitor reproduced the embryonic hemodynamic effects of maternal caffeine exposure. Adenosine A 2A receptor gene expression levels of ED 11.5 embryo and ED 18.5 uterus were decreased. Results suggest that modest maternal caffeine exposure has adverse effects on developing embryonic CV function and growth, possibly mediated via adenosine A 2A receptor blockade. adenosine A 2A receptor; cardiovascular development; carotid artery; pregnancy CAFFEINE IS A NATURALLY OCCURRING compound contained in many beverages, foods, and medications and is frequently consumed as a central nervous system stimulant. Human caffeine intake has increased in all age groups for the last two decades and 68 -74% of pregnant women consume caffeine at an average intake of 125-193 mg/day (14). Caffeine metabolism becomes slower in pregnancy, and ingested caffeine easily crosses the placenta (1,11,18). Although it has been suggested that the risk of fetal toxicity from caffeine in humans is low, several studies have shown that moderate to heavy caffeine consumption increases the risk of spontaneous abortion or low fetal birth weight (13,17,21,22,26,32,36). Moreover, recent studies identified a dose-dependent increase in the risk of spontaneous abortion in women who ingested at least 100 mg of caffeine daily (9, 45).The pharmacokinetics of ...