We are analyzing https://link.springer.com/article/10.1007/s00395-017-0623-4.

Title:
Dissecting the role of myeloid and mesenchymal fibroblasts in age-dependent cardiac fibrosis | Basic Research in Cardiology
Description:
Aging is associated with increased cardiac interstitial fibrosis and diastolic dysfunction. Our previous study has shown that mesenchymal fibroblasts in the C57BL/6J (B6J) aging mouse heart acquire an inflammatory phenotype and produce higher levels of chemokines. Monocyte chemoattractant protein-1 (MCP-1) secreted by these aged fibroblasts promotes leukocyte uptake into the heart. Some of the monocytes that migrate into the heart polarize into M2a macrophages/myeloid fibroblasts. The number of activated mesenchymal fibroblasts also increases with age, and consequently, both sources of fibroblasts contribute to fibrosis. Here, we further investigate mechanisms by which inflammation influences activation of myeloid and mesenchymal fibroblasts and their collagen synthesis. We examined cardiac fibrosis and heart function in three aged mouse strains; we compared C57BL/6J (B6J) with two other strains that have reduced inflammation via different mechanisms. Aged C57BL/6N (B6N) hearts are protected from oxidative stress and fibroblasts derived from them do not develop an inflammatory phenotype. Likewise, these mice have preserved diastolic function. Aged MCP-1 null mice on the B6J background (MCP-1KO) are protected from elevated leukocyte infiltration; they develop moderate but reduced fibrosis and diastolic dysfunction. Based on these studies, we further delineated the role of resident versus monocyte-derived M2a macrophages in myeloid-dependent fibrosis and found that the number of monocyte-derived M2a (but not resident) macrophages correlates with age-related fibrosis and diastolic dysfunction. In conclusion, we have found that ROS and inflammatory mediators are necessary for activation of fibroblasts of both developmental origins, and prevention of either led to better functional outcomes.
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Keywords {🔍}

pubmed, article, google, scholar, cas, heart, central, cardiac, fibroblasts, fibrosis, entman, trial, mesenchymal, aging, inflammation, diastolic, inflammatory, res, taffet, cieslik, macrophages, dysfunction, cell, cardiol, physiol, monocyte, cells, basic, role, stem, circ, left, function, research, mouse, chemoattractant, protein, aged, mice, access, mol, murine, ventricular, privacy, cookies, content, myeloid, activation, agerelated, failure,

Topics {✒️}

angiotensin-ii-induced cardiac hypertrophy angiotensin-ii-induced cardiac inflammation immune-inflammatory dysregulation modulates month download article/chapter nicotinamide nucleotide transhydrogenase interleukin-6-dependent phenotypic modulation age-dependent cardiac fibrosis spleen-derived murine fibrocytes ly-6chigh monocytes depend cell-type-specific responses mesenchymal stem cells article basic research m2a macrophages/myeloid fibroblasts monocyte-derived m2a age-related diastolic dysfunction reactive oxygen species blood-derived macrophages c57bl/6n mouse strains macrophage m1 polarization fibroblast progenitors contributes matrix metalloproteinase activity cardiac inflammation contributes cieslik ka il-6-dependent mechanism monocyte chemoattractant protein-1 full article pdf left ventricular structure age-related fibrosis m2 macrophage activation gene expression profile tumor necrosis factor cardiac ageing signature monocyte chemoattractant assay privacy choices/manage cookies ventricular compliance accounts examined cardiac fibrosis aged mouse strains c57bl/6 mouse substrains aging mouse heart elevated leukocyte infiltration activated mesenchymal fibroblasts inflammation influences activation fibroblast collagen myeloid-dependent fibrosis pronounced inflammatory reaction defective myofibroblast formation ampk pathway swirski fk splenic reservoir monocytes conditions privacy policy

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         description:Aging is associated with increased cardiac interstitial fibrosis and diastolic dysfunction. Our previous study has shown that mesenchymal fibroblasts in the C57BL/6J (B6J) aging mouse heart acquire an inflammatory phenotype and produce higher levels of chemokines. Monocyte chemoattractant protein-1 (MCP-1) secreted by these aged fibroblasts promotes leukocyte uptake into the heart. Some of the monocytes that migrate into the heart polarize into M2a macrophages/myeloid fibroblasts. The number of activated mesenchymal fibroblasts also increases with age, and consequently, both sources of fibroblasts contribute to fibrosis. Here, we further investigate mechanisms by which inflammation influences activation of myeloid and mesenchymal fibroblasts and their collagen synthesis. We examined cardiac fibrosis and heart function in three aged mouse strains; we compared C57BL/6J (B6J) with two other strains that have reduced inflammation via different mechanisms. Aged C57BL/6N (B6N) hearts are protected from oxidative stress and fibroblasts derived from them do not develop an inflammatory phenotype. Likewise, these mice have preserved diastolic function. Aged MCP-1 null mice on the B6J background (MCP-1KO) are protected from elevated leukocyte infiltration; they develop moderate but reduced fibrosis and diastolic dysfunction. Based on these studies, we further delineated the role of resident versus monocyte-derived M2a macrophages in myeloid-dependent fibrosis and found that the number of monocyte-derived M2a (but not resident) macrophages correlates with age-related fibrosis and diastolic dysfunction. In conclusion, we have found that ROS and inflammatory mediators are necessary for activation of fibroblasts of both developmental origins, and prevention of either led to better functional outcomes.
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      description:Aging is associated with increased cardiac interstitial fibrosis and diastolic dysfunction. Our previous study has shown that mesenchymal fibroblasts in the C57BL/6J (B6J) aging mouse heart acquire an inflammatory phenotype and produce higher levels of chemokines. Monocyte chemoattractant protein-1 (MCP-1) secreted by these aged fibroblasts promotes leukocyte uptake into the heart. Some of the monocytes that migrate into the heart polarize into M2a macrophages/myeloid fibroblasts. The number of activated mesenchymal fibroblasts also increases with age, and consequently, both sources of fibroblasts contribute to fibrosis. Here, we further investigate mechanisms by which inflammation influences activation of myeloid and mesenchymal fibroblasts and their collagen synthesis. We examined cardiac fibrosis and heart function in three aged mouse strains; we compared C57BL/6J (B6J) with two other strains that have reduced inflammation via different mechanisms. Aged C57BL/6N (B6N) hearts are protected from oxidative stress and fibroblasts derived from them do not develop an inflammatory phenotype. Likewise, these mice have preserved diastolic function. Aged MCP-1 null mice on the B6J background (MCP-1KO) are protected from elevated leukocyte infiltration; they develop moderate but reduced fibrosis and diastolic dysfunction. Based on these studies, we further delineated the role of resident versus monocyte-derived M2a macrophages in myeloid-dependent fibrosis and found that the number of monocyte-derived M2a (but not resident) macrophages correlates with age-related fibrosis and diastolic dysfunction. In conclusion, we have found that ROS and inflammatory mediators are necessary for activation of fibroblasts of both developmental origins, and prevention of either led to better functional outcomes.
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