Chronic infection with HP may be involved in the development of the atherosclerosis via endothelial dysfunction and systemic and vascular inflammation.

Mature lymphoid cells express the transcription repressor Bach2, which imposes regulation on humoral and cellular immunity. Here we found critical roles for Bach2 in the development of cells of the B lineage, commencing from the common lymphoid progenitor (CLP) stage, with Bach1 as an auxiliary. Overexpression of Bach2 in pre-pro-B cells deficient in the transcription factor EBF1 and single-cell analysis of CLPs revealed that Bach2 and Bach1 repressed the expression of genes important for myeloid cells ('myeloid genes'). Bach2 and Bach1 bound to presumptive regulatory regions of the myeloid genes. Bach2(hi) CLPs showed resistance to myeloid differentiation even when cultured under myeloid conditions. Our results suggest that Bach2 functions with Bach1 and EBF1 to promote B cell development by repressing myeloid genes in CLPs.

Bach1 is a transcriptional repressor of heme oxygenase-1 gene ( Hmox-1 ) and β β β β -globin gene. Heme oxygenase (HO)-1 is an inducible cytoprotective enzyme that degrades pro-oxidant heme to carbon monoxide (CO) and biliverdin/bilirubin, which are thought to mediate anti-inflammatory and anti-oxidant actions of HO-1. In the present study, we investigated the role of Bach1 in tissue protection against myocardial ischemia/reperfusion (I/R) injury in vivo using mice lacking the Bach1 gene ( Bach1

Abstract-The aim of this study was to determine the role of the AT2 receptor (AT2R) in left ventricular (LV) remodeling after myocardial infarction (MI). The left anterior descending arteries were ligated in AT2R gene knockout (Agtr2-) and wild-type (Agtr2ϩ) mice. The LV remodeling was evaluated by echocardiography and histology over a period of 2 weeks after MI. The infarct sizes in hearts excised from Agtr2ϩ and Agtr2-mice on day 1 were similar. The mortality rate of Agtr2-mice (62.9%) on day 14 after MI was significantly (PϽ0.05) higher than that of Agtr2ϩ mice (39.7%). Accordingly, LV/body weight ratios (3.7Ϯ0.2 versus 3.0Ϯ0.1 on day 14) and LV end-diastolic (4.8Ϯ0.3 versus 3.9Ϯ0.4 mm on day 7) and end-systolic (4.4Ϯ0.3 versus 3.2Ϯ0.6 mm on day 7) dimensions evaluated by echocardiography were significantly greater in Agtr2-than in Agtr2ϩ mice. The rates of ventricular arrhythmia, rates of cardiac rupture, and blood pressures in the 2 strains were similar after MI. Myocyte cross-sectional areas were increased after MI, but the magnitudes were similar in Agtr2ϩ and Agtr2-mice, indicating the greater increases in LV dimensions and weight in Agtr2-mice are due to elongation of myocyte length and/or an increase in the interstitial weight (including vasculatures, infiltrated cells, and interstitial fluid). Interstitial fibrosis in remote myocardium was not evident in either strain. These results indicate AT2R plays a significant role in the protection against early development of LV dilation, thereby reducing the early mortality rate after MI. Key Words: mice Ⅲ myocardial infarction Ⅲ receptors, angiotensin Ⅲ remodeling M yocardial infarction induces global changes in ventricular architecture, called post-myocardial infarction (MI) left ventricular (LV) remodeling, which involves LV dilation, myocyte hypertrophy, and interstitial fibrosis, leading to a deterioration in LV function that is associated with increased rate of mortality. 1,2 A substantial body of evidence 1,3-5 has suggested that angiotensin II (Ang II) plays a critical role in the development of post-MI LV remodeling. Ang II has 2 major receptor subtypes, AT1 receptor (AT1R) and AT2R, both of which are expressed in the heart. 6 It has been suggested that AT1R signaling mediates vasoconstriction, aldosterone secretion, cardiomyocyte hypertrophy, proliferation of fibroblasts, interstitial collagen deposition, and catecholamine release, all of which are implicated in progression of LV remodeling. 7,8 Harada et al 3 recently reported that AT1R gene-knockout mice had less LV remodeling and improved survival after MI. A deletion of AT1R or a blockade of AT1R with specific antagonists may result in selective binding of Ang II to the AT2R, indicating that the effect of AT1R blockade could be in part mediated by the effect of AT2R. 7 However, little is known about the role played by AT2R in post-MI LV remodeling. The AT2R is thought to have opposite effect to AT1R and has been shown to suppress myocardial hypertrophy, 9 -11 fibroblast proliferation, 10,12 and ...