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• W2972065720 abstract "Cardiac remodeling is the process established by the left ventricle (LV) to respond to different challenging stimuli. Although immunity has been clearly shown to participate to LV remodeling in myocardial infarction, how immune response participates to hypertensive chronic stress is poorly understood. We found that Placental Growth Factor (PlGF), belonging to the VEGF family, is necessary for adaptive remodeling to pressure overload and modulates the recruitment of innate immune cells in the LV. Here we asked where PlGF does exert its effects: i) directly in the myocardium or ii) by modulating immune organs? As TAC induced PlGF both in cardiac tissue and in the spleen, we devised a strategy to assess the contribution of these two tissues. We generated chimeric mice by spleen transplantation between WT and KO mice, obtaining: 1) WT mice with PlGF KO spleen and 2) PlGF KO mice with WT spleen (EF% 78 ± 0,7), finding that only mice with PlGF expressed in the spleen (EF% 68 ± 1,5) established adaptive remodeling to pressure overload, as assessed by echocardiography (p<0.01). Since in the absence of PlGF we observed a consistent reduction of LV macrophages, we characterized the subsets of innate immune cells by flow cytometry. While WT mice subjected to TAC showed early LV recruitment of non resident CD11b + CD64 + Timd4 - CCR2 low CX 3 CR1 hi macrophages, PlGF KO mice failed to show this response. To investigate the potential relevance of the spleen as reservoir of myeloid cells with adaptive/reparative functions for LV, we induced TAC in splenectomized mice, finding that they didn’t develop adaptive remodeling, exhibiting early HFrEF. To investigate the role of reparative macrophages, that are mostly characterized by the expression of the CX 3 CR1 receptor, and of pro-inflammatory monocytes that express high levels and accumulate through CCR2, we also subjected CCR2 KO and CX 3 CR1 KO mice to TAC. While CCR2 KO behaved similarly to WT mice, CX 3 CR1 KO were unable to establish adaptive remodeling and early developed HFrEF similarly to mice deprived of the spleen and to PlGF KO mice. Overall our results indicate that pressure overload induces PlGF in the spleen as an immunomodulator capable to deploy reparative macrophages that sustain adaptive remodeling of the LV." @default.
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• W2972065720 date "2019-09-01" @default.
• W2972065720 modified "2023-10-05" @default.
• W2972065720 title "Abstract 094: Adaptive Cardiac Remodeling to Chronic Pressure Overload Requires the Expression of Placental Growth Factor in the Spleen to Recruit Reparative Macrophages to the Left Ventricle" @default.
• W2972065720 doi "https://doi.org/10.1161/hyp.74.suppl_1.094" @default.
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