Macrophages Promote Aortic Valve Cell Calcification and Alter STAT3 Splicing

Objective: Macrophages have been described in calcific aortic valve disease, but it is unclear if they promote or counteract calcification. We aimed to determine how macrophages are involved in cal...

[1]  Brian A. Aguado,et al.  Transcatheter aortic valve replacements alter circulating serum factors to mediate myofibroblast deactivation , 2019, Science Translational Medicine.

[2]  B. Haagmans,et al.  ADAR1: “Editor-in-Chief” of Cytoplasmic Innate Immunity , 2019, Front. Immunol..

[3]  Michael A. Raddatz,et al.  Adaptive Immune Cells in Calcific Aortic Valve Disease. , 2019, American journal of physiology. Heart and circulatory physiology.

[4]  E. Aikawa,et al.  Roles and Regulation of Extracellular Vesicles in Cardiovascular Mineral Metabolism , 2018, Front. Cardiovasc. Med..

[5]  G. Booz,et al.  Recent Developments on the Crosstalk Between STAT3 and Inflammation in Heart Function and Disease , 2018, Front. Immunol..

[6]  M. Bersi,et al.  Cadherin-11 as a regulator of valve myofibroblast mechanobiology. , 2018, American journal of physiology. Heart and circulatory physiology.

[7]  Joshua D. Hutcheson,et al.  Spatiotemporal Multi-Omics Mapping Generates a Molecular Atlas of the Aortic Valve and Reveals Networks Driving Disease , 2018, Circulation.

[8]  Katherine A. Gallagher,et al.  Murine macrophage chemokine receptor CCR2 plays a crucial role in macrophage recruitment and regulated inflammation in wound healing , 2018, European journal of immunology.

[9]  D. Harrison,et al.  Hypertension and increased endothelial mechanical stretch promote monocyte differentiation and activation: roles of STAT3, interleukin 6 and hydrogen peroxide , 2018, Cardiovascular research.

[10]  D. Bau,et al.  Interleukin-32 plays an essential role in human calcified aortic valve cells , 2018, European Cytokine Network.

[11]  K. Yutzey,et al.  Macrophage Transitions in Heart Valve Development and Myxomatous Valve Disease , 2018, Arteriosclerosis, thrombosis, and vascular biology.

[12]  Jihye Song,et al.  Tissue-specific Role of CX3CR1 Expressing Immune Cells and Their Relationships with Human Disease , 2018, Immune network.

[13]  R. Horch,et al.  Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis , 2017, Nature Communications.

[14]  E. Horwitz,et al.  Contribution of Extra‐Cardiac Cells in Murine Heart Valves is Age‐Dependent , 2017, Journal of the American Heart Association.

[15]  Cynthia R. Clark,et al.  Targeting Cadherin-11 Prevents Notch1-Mediated Calcific Aortic Valve Disease. , 2017, Circulation.

[16]  Fei Li,et al.  The shift of macrophages toward M1 phenotype promotes aortic valvular calcification , 2017, The Journal of thoracic and cardiovascular surgery.

[17]  M. Dweck,et al.  End stage renal disease‐induced hypercalcemia may promote aortic valve calcification via Annexin VI enrichment of valve interstitial cell derived‐matrix vesicles , 2017, Journal of cellular physiology.

[18]  Lior Goldberg,et al.  Alternative Splicing of STAT3 Is Affected by RNA Editing. , 2017, DNA and cell biology.

[19]  Teng Wang,et al.  M1 macrophages promote aortic valve calcification mediated by microRNA-214/TWIST1 pathway in valvular interstitial cells. , 2016, American journal of translational research.

[20]  C. Otto,et al.  Calcific aortic stenosis , 2016, Nature Reviews Disease Primers.

[21]  Joseph Chen,et al.  Notch1 Mutation Leads to Valvular Calcification Through Enhanced Myofibroblast Mechanotransduction , 2015, Arteriosclerosis, thrombosis, and vascular biology.

[22]  I. Perrotta,et al.  HIF-1α and VEGF: Immunohistochemical Profile and Possible Function in Human Aortic Valve Stenosis , 2015, Ultrastructural pathology.

[23]  S. Xiong,et al.  The chemotaxis of M1 and M2 macrophages is regulated by different chemokines , 2015, Journal of leukocyte biology.

[24]  J. Lincoln,et al.  Isolation of Murine Valve Endothelial Cells , 2014, Journal of visualized experiments : JoVE.

[25]  Li V. Yang,et al.  In vitro cell migration and invasion assays. , 2014, Journal of visualized experiments : JoVE.

[26]  J. Albina,et al.  The Monocyte to Macrophage Transition in the Murine Sterile Wound , 2014, PloS one.

[27]  Hong Wang,et al.  Monocyte and macrophage differentiation: circulation inflammatory monocyte as biomarker for inflammatory diseases , 2014, Biomarker Research.

[28]  A. Undas,et al.  Interleukin-6 receptor Asp358Ala gene polymorphism is associated with plasma C-reactive protein levels and severity of aortic valve stenosis , 2013, Clinical chemistry and laboratory medicine.

[29]  Y. Bossé,et al.  Inflammation Is Associated with the Remodeling of Calcific Aortic Valve Disease , 2013, Inflammation.

[30]  Thomas A. Wynn,et al.  Macrophage biology in development, homeostasis and disease , 2013, Nature.

[31]  J. Cleveland,et al.  Cross-Talk Between the Toll-Like Receptor 4 and Notch1 Pathways Augments the Inflammatory Response in the Interstitial Cells of Stenotic Human Aortic Valves , 2012, Circulation.

[32]  A. Cope,et al.  Monocytes Induce STAT3 Activation in Human Mesenchymal Stem Cells to Promote Osteoblast Formation , 2012, PloS one.

[33]  Nan Li,et al.  Notch Signal Suppresses Toll-like Receptor-triggered Inflammatory Responses in Macrophages by Inhibiting Extracellular Signal-regulated Kinase 1/2-mediated Nuclear Factor κB Activation* , 2011, The Journal of Biological Chemistry.

[34]  R. Markwald,et al.  Recruitment of bone marrow-derived valve interstitial cells is a normal homeostatic process. , 2011, Journal of molecular and cellular cardiology.

[35]  Javier Bermejo,et al.  Diet-Induced Aortic Valve Disease in Mice Haploinsufficient for the Notch Pathway Effector RBPJK/CSL , 2011, Arteriosclerosis, thrombosis, and vascular biology.

[36]  Craig A Simmons,et al.  Cell–Matrix Interactions in the Pathobiology of Calcific Aortic Valve Disease: Critical Roles for Matricellular, Matricrine, and Matrix Mechanics Cues , 2011, Circulation research.

[37]  J. J. Higgins,et al.  The aligned rank transform for nonparametric factorial analyses using only anova procedures , 2011, CHI.

[38]  F. Ohsuzu,et al.  Deficiency of Interleukin-1 Receptor Antagonist Induces Aortic Valve Disease in BALB/c Mice , 2010, Arteriosclerosis, thrombosis, and vascular biology.

[39]  Markus G. Manz,et al.  Development of Monocytes, Macrophages, and Dendritic Cells , 2010, Science.

[40]  M. Simionescu,et al.  Effect of depletion of monocytes/macrophages on early aortic valve lesion in experimental hyperlipidemia , 2009, Cell and Tissue Research.

[41]  Jae-Hoon Choi,et al.  Brief Definitive Report Identifi Cation of Antigen-presenting Dendritic Cells in Mouse Aorta and Cardiac Valves , 2022 .

[42]  Xia Zhang,et al.  The Isolation and Characterization of Murine Macrophages , 2008, Current protocols in immunology.

[43]  Michael S Sacks,et al.  Synergistic effects of cyclic tension and transforming growth factor-beta1 on the aortic valve myofibroblast. , 2007, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.

[44]  M. Mack,et al.  Critical roles for CCR2 and MCP-3 in monocyte mobilization from bone marrow and recruitment to inflammatory sites. , 2007, The Journal of clinical investigation.

[45]  B. Lüderitz,et al.  Cells of primarily extra-valvular origin in degenerative aortic valves and bioprostheses. , 2005, European heart journal.

[46]  D. Srivastava,et al.  Mutations in NOTCH1 cause aortic valve disease , 2005, Nature.

[47]  A. Papavassiliou,et al.  Growth Hormone Attenuates the Transcriptional Activity of Runx2 by Facilitating Its Physical Association With Stat3β , 2004, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[48]  R. de Caterina,et al.  Neoangiogenesis, T-lymphocyte infiltration, and heat shock protein-60 are biological hallmarks of an immunomediated inflammatory process in end-stage calcified aortic valve stenosis. , 2004, Journal of the American College of Cardiology.

[49]  S. Dewilde,et al.  The STAT3 isoforms α and β have unique and specific functions , 2004, Nature Immunology.

[50]  Steffen Jung,et al.  Blood monocytes consist of two principal subsets with distinct migratory properties. , 2003, Immunity.

[51]  I. Bernstein,et al.  Notch signalling in hematopoiesis. , 2003, Seminars in cell & developmental biology.

[52]  D. Scadden,et al.  Notch1 activation increases hematopoietic stem cell self-renewal in vivo and favors lymphoid over myeloid lineage outcome. , 2002, Blood.

[53]  L. Miele,et al.  Human Notch-1 Inhibits NF-κB Activity in the Nucleus Through a Direct Interaction Involving a Novel Domain1 , 2001, The Journal of Immunology.

[54]  Emile R. Mohler,et al.  Bone Formation and Inflammation in Cardiac Valves , 2001, Circulation.

[55]  A. Bigas,et al.  Notch1 and Notch2 Inhibit Myeloid Differentiation in Response to Different Cytokines , 1998, Molecular and Cellular Biology.

[56]  J. Lammers,et al.  STAT3β, a Splice Variant of Transcription Factor STAT3, Is a Dominant Negative Regulator of Transcription* , 1996, The Journal of Biological Chemistry.

[57]  A. Gown,et al.  Characterization of the Early Lesion of ‘Degenerative’ Valvular Aortic Stenosis: Histological and Immunohistochemical Studies , 1994, Circulation.

[58]  R M Nerem,et al.  The application of a homogeneous half-space model in the analysis of endothelial cell micropipette measurements. , 1988, Journal of biomechanical engineering.

[59]  P. Murray.  Macrophage Polarization. , 2017, Annual review of physiology.

[60]  Meghan A Bowler,et al.  In vitro models of aortic valve calcification: solidifying a system. , 2015, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.

[61]  R Core Team,et al.  R: A language and environment for statistical computing. , 2014 .

[62]  F. Guilak,et al.  Correlation between heart valve interstitial cell stiffness and transvalvular pressure: implications for collagen biosynthesis. , 2006, American journal of physiology. Heart and circulatory physiology.

[63]  F. Guilak,et al.  The role of the cytoskeleton in the viscoelastic properties of human articular chondrocytes. , 2004, Journal of orthopaedic research : official publication of the Orthopaedic Research Society.

[64]  R. Hochmuth,et al.  Micropipette aspiration of living cells. , 2000, Journal of biomechanics.