Transplantation of periaortic adipose tissue inhibits atherosclerosis in apoE mice by evoking TGF-β1-mediated anti-inflammatory response in transplanted graft.

Perivascular adipose tissue (PAT) is associated with vascular homeostasis; however, its causal effect on atherosclerosis currently remains undefined. Here, we investigated the effect of experimental PAT transplantation on atherosclerosis. The thoracic periaortic adipose tissue (tPAT) was dissected from 16-week-old wild-type mice and transplanted over the infrarenal aorta of 20-week-old apoE deficient (apoE) mice fed high-cholesterol diet for 3 months.

Adrenergic receptor-mediated activation of FGF-21-adiponectin axis exerts atheroprotective effects in brown adipose tissue-transplanted apoE mice.

Brown adipose tissue (BAT) has been found as an endocrine organ that maintains metabolic homeostasis; however, the effects on atherosclerosis remain undefined. Here, we investigated the effect of experimental BAT transplantation on atherosclerosis. Interscapular BAT was dissected from wild-type mice and transplanted into the visceral cavity of 12-week-old apoE mice.

Dipeptidyl peptidase-4 inhibitor sitagliptin improves pancreatic β-cell function in hypertensive diabetic patients treated with angiotensin receptor blockers.

Introduction: Dipeptidyl peptidase (DPP)-4 inhibitors, a novel oral anti-diabetic agents, exert a protective effect on pancreatic β-cell function in patients with type 2 diabetic mellitus (T2DM). However, their beneficial effect in hypertensive T2DM patients treated with angiotensin receptor blockers (ARBs) has not been investigated.

Methods: In this open-label multicenter randomized study, a total of 55 hypertensive T2DM patients treated with ARBs were randomly assigned to receive the DPP-4 inhibitor sitagliptin or sulfonylurea (SU).

Maternal high-fat diet exaggerates atherosclerosis in adult offspring by augmenting periaortic adipose tissue-specific proinflammatory response.

Objective: Maternal obesity elicits offspring's metabolic disorders via developmental modifications of visceral adipose tissue; however, its effect on atherogenesis remains undefined. Perivascular adipose tissue has recently been implicated in vascular remodeling and vasoreactivity. We hypothesize that developmental modifications of perivascular adipose tissue by maternal high-fat diet (HFD) exposure promotes atherosclerosis in adult offspring.

Bone marrow angiotensin AT2 receptor deficiency aggravates atherosclerosis development by eliminating macrophage liver X receptor-mediated anti-atherogenic actions.

Background: Bone marrow (BM) Angiotensin II (Ang II) type 1 (AT1) receptor plays a crucial role in atherosclerosis development; however, the effect of BM Ang II type 2 (AT2) receptor on atherogenesis remains undefined.

Methods And Results: We generated BM chimera apoE-deficient (apoE(-/-)) mice whose BM cells were repopulated with AT2-deficient (Agtr2(-/-)) or wild-type (Agtr2(+/+)) cells. After 2 months of a high-cholesterol diet, the atherosclerotic lesion area was significantly increased in the apoE(-/-)/BM-Agtr2(-/-) mice compared with the apoE(-/-)/BM-Agtr2(+/+) mice (51%, P < 0.

Transplantation of periaortic adipose tissue from angiotensin receptor blocker-treated mice markedly ameliorates atherosclerosis development in apoE-/- mice.

Background: Perivascular adipose tissue is implicated in vasoreactivity; however, its effect on atherosclerosis remains undefined.

Methods And Results: We examined the effect of a high-cholesterol diet (HCD) on phenotypic alterations of the thoracic periaortic adipose tissue (tPAT) in apoE-deficient (apoE(-/-)) mice. Gene expression of the components of the renin angiotensin system and that of macrophage markers were significantly higher in apoE(-/-) mice fed an HCD than in those fed a chow diet (CD).

Periaortic adipose tissue-specific activation of the renin-angiotensin system contributes to atherosclerosis development in uninephrectomized apoE-/- mice.

Chronic kidney disease (CKD) is an independent risk factor for the development of cardiovascular disease. The perivascular adipose tissue is closely implicated in the development of atherosclerosis; however, the contribution to CKD-associated atherogenesis remains undefined. Eight-week-old apoE-deficient mice were uninephrectomized and fed a high-cholesterol diet starting at 12 wk of age.

Vascular angiotensin II type 2 receptor attenuates atherosclerosis via a kinin/NO-dependent mechanism.

Introduction: The angiotensin II (Ang II) type 1 receptor exerts pro-atherogenic action by augmenting oxidative stress, whereas the Ang II type 2 receptor (AT2)-mediated effect on atherosclerosis remains controversial.

Materials And Methods: AT2 transgenic (AT2-Tg) mice, which overexpress AT2 in their vascular smooth muscle cells, were crossed with apoE-deficient (apoE(-/-)) mice to generate AT2 transgenic apoE(-/-) mice (AT2-Tg/apoE(-/-)).

Results: A subpressor dose of Ang II infusion exaggerated atherosclerosis development in apoE(-/-) mice, which was markedly suppressed in AT2-Tg/apoE(-/-) mice.

Bone marrow AT1 augments neointima formation by promoting mobilization of smooth muscle progenitors via platelet-derived SDF-1{alpha}.

Objective: Bone marrow (BM)-derived endothelial progenitor cells (EPCs) and vascular smooth muscle progenitor cells (VPCs) contribute to neointima formation, whereas the angiotensin II (Ang II) type 1 receptor (AT(1))-mediated action on BM-derived progenitors remains undefined.

Methods And Results: A wire-induced vascular injury was performed in the femoral artery of BM-chimeric mice whose BM was repopulated with AT(1)-deficient (BM-Agtr1(-/-)) or wild-type (BM-Agtr1(+/+)) cells. Neointima formation was profoundly reduced by 38% in BM-Agtr1(-/-) mice.

Bone marrow angiotensin AT1 receptor regulates differentiation of monocyte lineage progenitors from hematopoietic stem cells.

Background: The angiotensin II (Ang II) type 1 (AT(1)) receptor is expressed in bone marrow (BM) cells, whereas it remains poorly defined how Ang II regulates differentiation/proliferation of monocyte-lineage cells to exert proatherogenic actions.

Methods And Results: We generated BM chimeric apoE(-/-) mice repopulated with AT(1)-deficient (Agtr1(-/-)) or wild-type (Agtr1(+/+)) BM cells. The atherosclerotic development was significantly reduced in apoE(-/-)/BM-Agtr1(-/-) mice compared with apoE(-/-)/BM-Agtr1(+/+) mice, accompanied by decreased numbers of BM granulocyte/macrophage progenitors (GMP:c-Kit(+)Sca-1(-)Lin(-)CD34(+)CD16/32(+)) and peripheral blood monocytes.

Clinical utility of evaluating intracranial artery stenosis and silent brain infarction to predict the presence of subclinical coronary artery disease in ischemic stroke patients.

Objective: We have recently reported the prevalence of subclinical cardiovascular diseases and the association between the presence of subclinical coronary artery disease (CAD) and vascular risk factors in ischemic stroke patients. The relationship between the presence of subclinical CAD and elements of brain ischemia including intracranial artery stenosis, silent brain infarction (SBI), and white matter lesions remains unclear. We determined the usefulness of elements of brain ischemia to predict the presence of subclinical CAD in ischemic stroke patients.

Prevalence of coronary artery disease in Japanese patients with cerebral infarction: impact of metabolic syndrome and intracranial large artery atherosclerosis.

Background: Patients with cerebral infarction have a high prevalence of asymptomatic coronary artery disease (CAD) and other vascular diseases, but there is a lack of such data for Japanese patients, so the present study investigated the prevalence of cardiovascular disease (CVD) in Japanese patients and determined the predictors of CAD.

Methods And Results: The study group comprised 104 patients with cerebral infarction who had no history of CVD. All patients underwent coronary computed tomographic angiography, and systematic evaluation was done on the basis of the presence of other vascular diseases, CVD risk markers, and the degree of atherosclerosis.

[Prevention of contrast-induced nephropathy using cardiac catheterization combined with hydration, oral N-acetylcysteine, sodium bicarbonate and iso-osmolar contrast agents].

Objectives: Contrast-induced nephropathy (CIN) after coronary angiography is a serious complication with an unfavorable prognosis. If CIN is persistent in the chronic phase, the prognosis is much worsened. We evaluated the efficacy of a new clinical therapy consisting of cardiac catheterization combined with hydration, oral N-acetylcysteine, sodium bicarbonate and iso-osmolar contrast agents.

[Survivor of blow out type of free wall rupture: multislice computed tomographic detection of myocardial rupture in a case of small myocardial infarction].

A 73-year-old man was admitted to the emergency room because of shock and loss of consciousness. Electrocardiography and echocardiography revealed myocardial infarction of the inferoposterior wall and cardiac tamponade. However, laboratory data showed mild inflammation without elevation of any cardiac enzymes.