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Commercial antibodies are used widely to quantify and localize the alpha1-adrenergic receptor (AR) subtypes, alpha1A, alpha1B, and alpha1D. We tested ten antibodies, from abcam and Santa Cruz, using western blot with heart and brain tissue from wild-type (WT) mice and mice with systemic knockout (KO) of one or all three subtypes. We found that none of the(More)
OBJECTIVES The goal was to identify alpha-1-adrenergic receptor (AR) subtypes in human coronary arteries. BACKGROUND The alpha1-ARs regulate human coronary blood flow. The alpha1-ARs exist as 3 molecular subtypes, alpha1A, alpha1B, and alpha1D, and the alpha1D subtype mediates coronary vasoconstriction in the mouse. However, the alpha1A is thought to be(More)
OBJECTIVE Matrix metalloproteinase-2 (MMP-2) plays a major role in dysfunctional ventricular remodeling following myocardial injury induced by ischemia/reperfusion and heart failure. To directly assess the role of MMP-2 in the absence of superimposed injury, we generated cardiac-specific, constitutively active MMP-2 transgenic mice. METHODS Morphologic(More)
BACKGROUND alpha1-adrenergic receptors (alpha1-ARs) play adaptive roles in the heart and protect against the development of heart failure. The 3 alpha1-AR subtypes, alpha1A, alpha1B, and alpha1D, have distinct physiological roles in mouse heart, but very little is known about alpha1 subtypes in human heart. Here, we test the hypothesis that the alpha1A and(More)
Phosphatidylinositol transfer protein alpha (PITPalpha) selectively transports and promotes exchange of phosphatidylinositol (PI) and phosphatidylcholine (PC) between lipid bilayers. In higher eukaryotes PITPalpha is required for cellular functions such as phospholipase C-mediated signaling, regulated exocytosis, and secretory vesicle formation. We have(More)
Catecholamines and alpha(1)-adrenergic receptors (alpha(1)-ARs) cause cardiac hypertrophy in cultured myocytes and transgenic mice, but heart size is normal in single KOs of the main alpha(1)-AR subtypes, alpha(1A/C) and alpha(1B). Here we tested whether alpha(1)-ARs are required for developmental cardiac hypertrophy by generating alpha(1A/C) and alpha(1B)(More)
The left ventricle (LV) and right ventricle (RV) have differing hemodynamics and embryological origins, but it is unclear whether they are regulated differently. In particular, no previous studies have directly compared the LV versus RV myocardial inotropic responses to alpha(1)-adrenergic receptor (alpha(1)-AR) stimulation. We compared alpha(1)-AR inotropy(More)
An alpha1-adrenergic receptor (alpha1-AR) antagonist increased heart failure in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), but it is unknown whether this adverse result was due to alpha1-AR inhibition or a nonspecific drug effect. We studied cardiac pressure overload in mice with double KO of the 2 main(More)
BACKGROUND In many cell types, including neutrophils and HL60 cells, there is an absolute requirement for a GTP-dependent step to elicit Ca(2+)-regulated secretion. Neutrophils and HL60 cells secrete lysosomal enzymes from azurophilic granules; this secretion is inhibited by 1% ethanol, indicating that phosphatidate (PA) produced by phospholipase D (PLD)(More)
Global activation of MAP kinases has been reported in both human and experimental heart failure. Chronic remodeling of the surviving ventricular wall after myocardial infarction (MI) involves both myocyte loss and fibrosis; we hypothesized that this cardiomyopathy involves differential shifts in pro- and anti-apoptotic MAP kinase signaling in cardiac(More)