ArticleProceedings of the National Academy of Sciences of the United States of America2008
Fc receptor engagement mediates differentiation of cardiac fibroblast precursor cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 91 citations in OpenAlex.
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- Flow Cytometry-Based Quantification and Analysis of Myocardial B-cells.Journal of visualized experiments : JoVE · 2022Article
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- Exploring the cardiac ECM during fibrosis: A new era with next-gen proteomics.Frontiers in molecular biosciences · 2022Review
- Cancer-associated fibroblasts in acute leukemia.Frontiers in oncology · 2022Review
- Research Progress of Myocardial Fibrosis and Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022Review
- Immunomodulatory Treatment Strategies Targeting B Cells for Heart Failure.Frontiers in pharmacology · 2022Review
- Fcγ receptor activation mediates vascular inflammation and abdominal aortic aneurysm development.Clinical and translational medicine · 2021Article
- Controlling cardiac fibrosis through fibroblast state space modulation.Cellular signalling · 2021Review
- Serum Amyloid P inhibits single stranded RNA-induced lung inflammation, lung damage, and cytokine storm in mice.PloS one · 2021Article
- The role of B cells in heart failure and implications for future immunomodulatory treatment strategies.ESC heart failure · 2020Review
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- Serum Amyloid P and a Dendritic Cell-Specific Intercellular Adhesion Molecule-3-Grabbing Nonintegrin Ligand Inhibit High-Fat Diet-Induced Adipose Tissue and Liver Inflammation and Steatosis in Mice.The American journal of pathology · 2019Article
- Elevation of pulmonary CD163Journal of thoracic disease · 2019Article
- The Development of Serum Amyloid P as a Possible Therapeutic.Frontiers in immunology · 2018Review
- Protective effect of human serum amyloid P on CCl4-induced acute liver injury in mice.International journal of molecular medicine · 2017Article
- Monocyte differentiation and macrophage priming are regulated differentially by pentraxins and their ligands.BMC immunology · 2017Article
- Reversal of maladaptive fibrosis and compromised ventricular function in the pressure overloaded heart by a caveolin-1 surrogate peptide.Laboratory investigation; a journal of technical methods and pathology · 2017Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
We previously described a critical role for a fibroblast precursor population in the development of a murine fibrotic cardiomyopathy model (I/RC). These precursors arose from circulating bone marrow-derived cells of monocytic origin. Administration of serum amyloid P (SAP) prevented the presence of this cell population in the heart and the cardiomyopathy. Because SAP binds to Fc receptors (FcRs) expressed on monocytes, we investigated the involvement of FcR signaling. We chose mice lacking the FcRgamma chain protein (FcRgamma(-/-)), a common membrane-signaling component of activating FcRs. Like wild-type mice, FcRgamma(-/-) mice developed fibrosis and cardiac dysfunction when subjected to I/RC. However, unlike wild-type mice, SAP in FcRgamma(-/-) mice failed to inhibit the development of fibrosis and cardiac dysfunction and did not diminish the numbers of alpha-smooth muscle actin(+) and CD34(+), CD45(+) fibroblasts that were typical for I/RC. To further examine the role of SAP in monocyte-to-fibroblast transition, we performed in vitro assays in which human peripheral blood mononuclear cells (PBMCs) migrated through human umbilical vein endothelial cells (HUVECs). We found that MCP-1-dependent transendothelial migration of monocytes markedly accelerated their differentiation into fibroblasts. This monocyte differentiation to fibroblasts was eliminated when SAP was added to the PBMC suspension before endothelial transmigration. Adding SAP to cells after successful migration did not inhibit fibroblast maturation. These data indicate that SAP inhibits the differentiation of a blood-borne, myeloid cell population into fibroblasts by signaling through activating FcRs before transendothelial migration has occurred. We suggest that FcR activation of circulating precursor cells may represent a new treatment target for adverse remodeling and cardiac fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.