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article, pubmed, cells, google, scholar, cas, heart, hypertrophy, chen, central, dendritic, inflammation, cdc, fibrosis, cardiac, hypertension, research, role, wang, bone, fassett, left, kwak, dysfunction, dcs, myocardial, access, remodeling, circulation, doicirculationaha, failure, privacy, cookies, content, basic, marrowderived, overloadinduced, ventricular, bache, tcell, regulatory, cell, res, usa, university, data, publish, search, systolic, liu,

Topics {✒️}

angiotensin-ii-induced cardiac hypertrophy month download article/chapter angiotensin ii-induced hypertension bone marrow chimeras professional antigen-presenting cells hypertension-induced vascular inflammation dendritic cells maximize chronic pressure overload t-cell activation contribute increased t-cell infiltration modulating t-cell function congestive heart failure article basic research dendritic cells hypertensive myocardial fibrosis induced lv fibrosis full article pdf left ventricular remodeling cd11c+ cells cardiovascular research building privacy choices/manage cookies article wang activated effector cd8+cd44+ lillehei heart institute research grant 09grnt2260175 heart failure progression left ventricular american heart association pressure-mediated hypertrophy maintain compensative hypertrophy orchestrate immune responses cd11b+ cells anzai shanghai tenth people cardiac hypertrophy immune activation caused european economic area recent studies demonstrated transverse aortic constriction de los santos de faria ap cytokine hypothesis revisited ethics declarations sources article log conditions privacy policy mann dl van den borne minnesota medical school check access electronic supplementary material

Questions {❓}

• Kuwahara F, Kai H, Tokuda K, Takeya M, Takeshita A, Egashira K, Imaizumi T (2004) Hypertensive myocardial fibrosis and diastolic dysfunction: another model of inflammation?

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      description:Inflammatory responses play an important role in the development of left ventricular (LV) hypertrophy and dysfunction. Recent studies demonstrated that increased T-cell infiltration and T-cell activation contribute to LV hypertrophy and dysfunction. Dendritic cells (DCs) are professional antigen-presenting cells that orchestrate immune responses, especially by modulating T-cell function. In this study, we investigated the role of bone marrow-derived CD11c+ DCs in transverse aortic constriction (TAC)-induced LV fibrosis and hypertrophy in mice. We observed that TAC increased the number of CD11c+ cells and the percentage of CD11c+ MHCII+ (major histocompatibility complex class II molecule positive) DCs in the LV, spleen and peripheral blood in mice. Using bone marrow chimeras and an inducible CD11c+ DC ablation model, we found that depletion of bone marrow-derived CD11c+ DCs significantly attenuated LV fibrosis and hypertrophy in mice exposed to 24 weeks of moderate TAC. CD11c+ DC ablation significantly reduced TAC-induced myocardial inflammation as indicated by reduced myocardial CD45+ cells, CD11b+ cells, CD8+ T cells and activated effector CD8+CD44+ T cells in LV tissues. Moreover, pulsing of autologous DCs with LV homogenates from TAC mice promoted T-cell proliferation. These data indicate that bone marrow-derived CD11c+ DCs play a maladaptive role in hemodynamic overload-induced cardiac inflammation, hypertrophy and fibrosis through the presentation of cardiac self-antigens to T cells.
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