Anti-integrin α

Animals Cells, Cultured Drug Evaluation, Preclinical Fibrosis Integrin alphaV / drug effects Kruppel-Like Transcription Factors / analysis Male Mice Mice, Inbred C57BL Myocardial Infarction / drug therapy Myocardium / pathology Myocytes, Cardiac / metabolism RNA, Messenger / biosynthesis Single-Cell Analysis Snake Venoms / pharmacology Stromal Cells / chemistry Transforming Growth Factor beta1 / pharmacology

Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
09 07 2020
Historique:
received: 14 02 2020
accepted: 19 06 2020
entrez: 11 7 2020
pubmed: 11 7 2020
medline: 1 1 2021
Statut: epublish

Résumé

There is currently no therapy to limit the development of cardiac fibrosis and consequent heart failure. We have recently shown that cardiac fibrosis post-myocardial infarction (MI) can be regulated by resident cardiac cells with a fibrogenic signature and identified by the expression of PW1 (Peg3). Here we identify αV-integrin (CD51) as an essential regulator of cardiac PW1

Identifiants

DOI: 10.1038/s41598-020-68223-8 PMID: 32647159 PMC: PMC7347632
pubmed: 32647159
doi: 10.1038/s41598-020-68223-8
pii: 10.1038/s41598-020-68223-8
pmc: PMC7347632
doi:

Substances chimiques

Integrin alphaV 0
Kruppel-Like Transcription Factors 0
Peg3 protein, mouse 0
RNA, Messenger 0
Snake Venoms 0
Transforming Growth Factor beta1 0
Cilengitide 4EDF46E4GI

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

11404

Références

Maggioni, A. P. et al. EURObservational Research Programme: Regional differences and 1-year follow-up results of the Heart Failure Pilot Survey (ESC-HF Pilot). Eur. J. Heart. Fail. 15, 808–817. https://doi.org/10.1093/eurjhf/hft050 (2013).
doi: 10.1093/eurjhf/hft050 pubmed: 23537547
Roger, V. L. et al. Heart disease and stroke statistics—2012 update: A report from the American Heart Association. Circulation 125, e2–e220. https://doi.org/10.1161/CIR.0b013e31823ac046 (2012).
doi: 10.1161/CIR.0b013e31823ac046 pubmed: 22179539
Seferovic, P. M. et al. Organization of heart failure management in European Society of Cardiology member countries: survey of the Heart Failure Association of the European Society of Cardiology in collaboration with the Heart Failure National Societies/Working Groups. Eur. J. Heart. Fail. 15, 947–959. https://doi.org/10.1093/eurjhf/hft092 (2013).
doi: 10.1093/eurjhf/hft092 pubmed: 23787723
Ponikowski, P. et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur. Heart J. 37, 2129–2200. https://doi.org/10.1093/eurheartj/ehw128 (2016).
doi: 10.1093/eurheartj/ehw128 pubmed: 27206819
Savarese, G. & Lund, L. H. Global public health burden of heart failure. Cardiac. Fail. Rev. 3, 7–11. https://doi.org/10.15420/cfr.2016:25:2 (2017).
doi: 10.15420/cfr.2016:25:2
Dunlay, S. M., Roger, V. L. & Redfield, M. M. Epidemiology of heart failure with preserved ejection fraction. Nat. Rev. Cardiol. 14, 591–602. https://doi.org/10.1038/nrcardio.2017.65 (2017).
doi: 10.1038/nrcardio.2017.65 pubmed: 28492288
Lewis, G. A. et al. Biological Phenotypes of Heart Failure With Preserved Ejection Fraction. J Am Coll Cardiol 70, 2186–2200. https://doi.org/10.1016/j.jacc.2017.09.006 (2017).
doi: 10.1016/j.jacc.2017.09.006 pubmed: 29050567
Gyongyosi, M. et al. Myocardial fibrosis: biomedical research from bench to bedside. Eur. J. Heart. Fail. 19, 177–191. https://doi.org/10.1002/ejhf.696 (2017).
doi: 10.1002/ejhf.696 pubmed: 28157267 pmcid: 5299507
Schelbert, E. B., Fonarow, G. C., Bonow, R. O., Butler, J. & Gheorghiade, M. Therapeutic targets in heart failure: Refocusing on the myocardial interstitium. J. Am. Coll. Cardiol. 63, 2188–2198. https://doi.org/10.1016/j.jacc.2014.01.068 (2014).
doi: 10.1016/j.jacc.2014.01.068 pubmed: 24657693
Li, A. H., Liu, P. P., Villarreal, F. J. & Garcia, R. A. Dynamic changes in myocardial matrix and relevance to disease: Translational perspectives. Circ. Res. 114, 916–927. https://doi.org/10.1161/CIRCRESAHA.114.302819 (2014).
doi: 10.1161/CIRCRESAHA.114.302819 pubmed: 24577970
Gourdie, R. G., Dimmeler, S. & Kohl, P. Novel therapeutic strategies targeting fibroblasts and fibrosis in heart disease. Nat. Rev. Drug Discov. 15, 620–638. https://doi.org/10.1038/nrd.2016.89 (2016).
doi: 10.1038/nrd.2016.89 pubmed: 27339799 pmcid: 5152911
Travers, J. G., Kamal, F. A., Robbins, J., Yutzey, K. E. & Blaxall, B. C. Cardiac fibrosis: The fibroblast awakens. Circ. Res. 118, 1021–1040. https://doi.org/10.1161/CIRCRESAHA.115.306565 (2016).
doi: 10.1161/CIRCRESAHA.115.306565 pubmed: 26987915 pmcid: 4800485
Kramann, R. et al. Perivascular Gli1+ progenitors are key contributors to injury-induced organ fibrosis. Cell Stem Cell 16, 51–66. https://doi.org/10.1016/j.stem.2014.11.004 (2015).
doi: 10.1016/j.stem.2014.11.004 pubmed: 25465115
Kalluri, R. The biology and function of fibroblasts in cancer. Nat. Rev. Cancer 16, 582–598. https://doi.org/10.1038/nrc.2016.73 (2016).
doi: 10.1038/nrc.2016.73 pubmed: 27550820
Teekakirikul, P. et al. Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-beta. J. Clin. Invest. 120, 3520–3529. https://doi.org/10.1172/JCI42028 (2010).
doi: 10.1172/JCI42028 pubmed: 20811150 pmcid: 2947222
Olivey, H. E., Mundell, N. A., Austin, A. F. & Barnett, J. V. Transforming growth factor-beta stimulates epithelial–mesenchymal transformation in the proepicardium. Dev. Dyn. 235, 50–59. https://doi.org/10.1002/dvdy.20593 (2006).
doi: 10.1002/dvdy.20593 pubmed: 16245329 pmcid: 3160345
Duan, J. et al. Wnt1/betacatenin injury response activates the epicardium and cardiac fibroblasts to promote cardiac repair. EMBO J. 31, 429–442. https://doi.org/10.1038/emboj.2011.418 (2012).
doi: 10.1038/emboj.2011.418 pubmed: 22085926
Humphreys, B. D. et al. Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis. Am. J. Pathol. 176, 85–97. https://doi.org/10.2353/ajpath.2010.090517 (2010).
doi: 10.2353/ajpath.2010.090517 pubmed: 20008127 pmcid: 2797872
Yaniz-Galende, E. et al. Fibrogenic potential of PW1/Peg3 expressing cardiac stem cells. J. Am. Coll. Cardiol. 70, 728–741. https://doi.org/10.1016/j.jacc.2017.06.010 (2017).
doi: 10.1016/j.jacc.2017.06.010 pubmed: 28774379
Besson, V. et al. PW1 gene/paternally expressed gene 3 (PW1/Peg3) identifies multiple adult stem and progenitor cell populations. Proc. Natl. Acad. Sci. USA 108, 11470–11475. https://doi.org/10.1073/pnas.1103873108 (2011).
doi: 10.1073/pnas.1103873108 pubmed: 21709251
Mitchell, K. J. et al. Identification and characterization of a non-satellite cell muscle resident progenitor during postnatal development. Nat. Cell Biol. 12, 257–266. https://doi.org/10.1038/ncb2025 (2010).
doi: 10.1038/ncb2025 pubmed: 20118923
Henderson, N. C. et al. Targeting of alphav integrin identifies a core molecular pathway that regulates fibrosis in several organs. Nat. Med. 19, 1617–1624. https://doi.org/10.1038/nm.3282 (2013).
doi: 10.1038/nm.3282 pubmed: 24216753
Chen, C., Li, R., Ross, R. S. & Manso, A. M. Integrins and integrin-related proteins in cardiac fibrosis. J. Mol. Cell. Cardiol. 93, 162–174. https://doi.org/10.1016/j.yjmcc.2015.11.010 (2016).
doi: 10.1016/j.yjmcc.2015.11.010 pubmed: 26562414
Salven, P., Mustjoki, S., Alitalo, R., Alitalo, K. & Rafii, S. VEGFR-3 and CD133 identify a population of CD34+ lymphatic/vascular endothelial precursor cells. Blood 101, 168–172. https://doi.org/10.1182/blood-2002-03-0755 (2003).
doi: 10.1182/blood-2002-03-0755 pubmed: 12393704
Skelly, D. A. et al. Single-cell transcriptional profiling reveals cellular diversity and intercommunication in the mouse heart. Cell Rep. 22, 600–610 (2018).
doi: 10.1016/j.celrep.2017.12.072
Dierick, F. et al. Resident PW1+ progenitor cells participate in vascular remodeling during pulmonary arterial hypertension. Circ. Res. 118, 822–833. https://doi.org/10.1161/CIRCRESAHA.115.307035 (2016).
doi: 10.1161/CIRCRESAHA.115.307035 pubmed: 26838788
Sojoodi, M. et al. The zinc finger transcription factor PW1/PEG3 restrains murine beta cell cycling. Diabetologia 59, 1474–1479. https://doi.org/10.1007/s00125-016-3954-z (2016).
doi: 10.1007/s00125-016-3954-z pubmed: 27130279 pmcid: 4901110
Besson, V. et al. Expression analysis of the stem cell marker Pw1/Peg3 reveals a CD34 negative progenitor population in the hair follicle. Stem Cells 35, 1015–1027. https://doi.org/10.1002/stem.2540 (2017).
doi: 10.1002/stem.2540 pubmed: 27862634
Korf-Klingebiel, M. et al. Myeloid-derived growth factor (C19orf10) mediates cardiac repair following myocardial infarction. Nat. Med. 21, 140–149. https://doi.org/10.1038/nm.3778 (2015).
doi: 10.1038/nm.3778 pubmed: 25581518
Furtado, M. B. et al. Cardiogenic genes expressed in cardiac fibroblasts contribute to heart development and repair. Circ. Res. 114, 1422–1434. https://doi.org/10.1161/CIRCRESAHA.114.302530 (2014).
doi: 10.1161/CIRCRESAHA.114.302530 pubmed: 24650916 pmcid: 4083003
Sun, Y. & Weber, K. T. Infarct scar: A dynamic tissue. Cardiovasc. Res. 46, 250–256 (2000).
doi: 10.1016/S0008-6363(00)00032-8
Lorchner, H. et al. Myocardial healing requires Reg3beta-dependent accumulation of macrophages in the ischemic heart. Nat. Med. 21, 353–362. https://doi.org/10.1038/nm.3816 (2015).
doi: 10.1038/nm.3816 pubmed: 25751817
Reed, N. I. et al. The alphavbeta1 integrin plays a critical in vivo role in tissue fibrosis. Sci. Transl. Med. 7, 288ra279. https://doi.org/10.1126/scitranslmed.aaa5094 (2015).
doi: 10.1126/scitranslmed.aaa5094
Conroy, K. P., Kitto, L. J. & Henderson, N. C. alphav integrins: key regulators of tissue fibrosis. Cell Tissue Res. 365, 511–519. https://doi.org/10.1007/s00441-016-2407-9 (2016).
doi: 10.1007/s00441-016-2407-9 pubmed: 27139180 pmcid: 5010580
Murray, I. R. et al. Alphav integrins on mesenchymal cells regulate skeletal and cardiac muscle fibrosis. Nat. Commun. 8, 1118. https://doi.org/10.1038/s41467-017-01097-z (2017).
doi: 10.1038/s41467-017-01097-z pubmed: 29061963 pmcid: 5653645
Nisato, R. E., Tille, J. C., Jonczyk, A., Goodman, S. L. & Pepper, M. S. alphav beta 3 and alphav beta 5 integrin antagonists inhibit angiogenesis in vitro. Angiogenesis 6, 105–119. https://doi.org/10.1023/B:AGEN.0000011801.98187.f2 (2003).
doi: 10.1023/B:AGEN.0000011801.98187.f2 pubmed: 14739617
Denizot, A. L. et al. A novel mutant allele of Pw1/Peg3 does not affect maternal behavior or nursing behavior. PLoS Genet. 12, e1006053. https://doi.org/10.1371/journal.pgen.1006053 (2016).
doi: 10.1371/journal.pgen.1006053 pubmed: 27187722 pmcid: 4871489
Lasinska, I. & Mackiewicz, J. Integrins as a new target for cancer treatment. Anticancer Agents Med. Chem. https://doi.org/10.2174/1871520618666181119103413 (2018).
doi: 10.2174/1871520618666181119103413
Mas-Moruno, C., Rechenmacher, F. & Kessler, H. Cilengitide: the first anti-angiogenic small molecule drug candidate design, synthesis and clinical evaluation. Anticancer Agents Med. Chem. 10, 753–768 (2010).
doi: 10.2174/187152010794728639
Chen, C., Khaleel, S. S., Huang, H. & Wu, C. H. Software for pre-processing Illumina next-generation sequencing short read sequences. Source Code Biol. Med. 9, 8. https://doi.org/10.1186/1751-0473-9-8 (2014).
doi: 10.1186/1751-0473-9-8 pubmed: 24955109 pmcid: 4064128
Li, B. & Dewey, C. N. RSEM: Accurate transcript quantification from RNA-Seq data with or without a reference genome. BMC Bioinform. 12, 323. https://doi.org/10.1186/1471-2105-12-323 (2011).
doi: 10.1186/1471-2105-12-323
Yates, A. et al. Ensembl 2016. Nucleic Acids Res. 44, D710-716. https://doi.org/10.1093/nar/gkv1157 (2016).
doi: 10.1093/nar/gkv1157 pubmed: 26687719
Butler, A., Hoffman, P., Smibert, P., Papalexi, E. & Satija, R. Integrating single-cell transcriptomic data across different conditions, technologies, and species. Nat. Biotechnol. 36, 411–420. https://doi.org/10.1038/nbt.4096 (2018).
doi: 10.1038/nbt.4096 pubmed: 29608179 pmcid: 6700744
R Foundation for Statistical Computing. A Language and Environment for Statistical Computing (R Foundation for Statistical Computing, Vienna, 2018).

Auteurs

Marion Bouvet (M)

Université de Paris, PARCC, INSERM, 56 Rue Leblanc, 75015, Paris, France.

Olivier Claude (O)

Université de Paris, PARCC, INSERM, 56 Rue Leblanc, 75015, Paris, France.

Maguelonne Roux (M)

Sorbonne Université, UPMC Univ Paris 06, INSERM, Institute of Cardio Metabolism and Nutrition (ICAN), Paris, France.

Dan Skelly (D)

The Jackson Laboratory, Bar Harbor, ME, USA.

Nihar Masurkar (N)

Université de Paris, PARCC, INSERM, 56 Rue Leblanc, 75015, Paris, France.

Nathalie Mougenot (N)

Sorbonne Université, UPMC Univ Paris 06, PECMV, UMS28, Paris, France.

Sophie Nadaud (S)

Sorbonne Université, UPMC Univ Paris 06, INSERM, Institute of Cardio Metabolism and Nutrition (ICAN), Paris, France.

Catherine Blanc (C)

Sorbonne Université, Inserm, UMS Omique, Plateforme Post-génomique de la Pitié-Salpêtrière, P3S, 75013, Paris, France.

Clément Delacroix (C)

Université de Paris, PARCC, INSERM, 56 Rue Leblanc, 75015, Paris, France.

Solenne Chardonnet (S)

Sorbonne Université, Inserm, UMS Omique, Plateforme Post-génomique de la Pitié-Salpêtrière, P3S, 75013, Paris, France.

Cédric Pionneau (C)

Sorbonne Université, Inserm, UMS Omique, Plateforme Post-génomique de la Pitié-Salpêtrière, P3S, 75013, Paris, France.

Claire Perret (C)

Sorbonne Université, UPMC Univ Paris 06, INSERM, Institute of Cardio Metabolism and Nutrition (ICAN), Paris, France.

Elisa Yaniz-Galende (E)

Sorbonne Université, UPMC Univ Paris 06, INSERM, Institute of Cardio Metabolism and Nutrition (ICAN), Paris, France.

Nadia Rosenthal (N)

The Jackson Laboratory, Bar Harbor, ME, USA.

David-Alexandre Trégouët (DA)

Sorbonne Université, UPMC Univ Paris 06, INSERM, Institute of Cardio Metabolism and Nutrition (ICAN), Paris, France.
INSERM UMR_S 1219, Bordeaux Population Health Research Center, University of Bordeaux, Bordeaux, France.

Giovanna Marazzi (G)

Université de Paris, PARCC, INSERM, 56 Rue Leblanc, 75015, Paris, France.

Jean-Sébastien Silvestre (JS)

Université de Paris, PARCC, INSERM, 56 Rue Leblanc, 75015, Paris, France.

David Sassoon (D)

Université de Paris, PARCC, INSERM, 56 Rue Leblanc, 75015, Paris, France.

Jean-Sébastien Hulot (JS)

Université de Paris, PARCC, INSERM, 56 Rue Leblanc, 75015, Paris, France. jean-sebastien.hulot@aphp.fr.

Articles similaires

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female

Evaluation of Low-Value Services Across Major Medicare Advantage Insurers and Traditional Medicare.

Ciara Duggan, Adam L Beckman, Ishani Ganguli et al.
1.00
Humans United States Aged Cross-Sectional Studies Medicare Part C

Effectiveness of Virtual Yoga for Chronic Low Back Pain: A Randomized Clinical Trial.

Hallie Tankha, Devyn Gaskins, Amanda Shallcross et al.
1.00
Humans Yoga Low Back Pain Female Male

Meal Timing and Anthropometric and Metabolic Outcomes: A Systematic Review and Meta-Analysis.

Hiu Yee Liu, Ashley A Eso, Nathan Cook et al.
1.00
Humans Meals Time Factors Female Adult

Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Anti-integrin α
questionsmedicales.fr › Cellules › Cellules cultivées › Anti-integrin α
questionsmedicales.fr › Techniques d'investigation › Évaluation préclinique de médicament › Anti-integrin α
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Fibrose › Anti-integrin α
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs immunologiques › Intégrines › Intégrines alpha › Intégrine alphaV › Anti-integrin α
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Facteurs de transcription › Facteurs de transcription Krüppel-like › Anti-integrin α
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Anti-integrin α
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Lignées consanguines de souris › Souris de lignée C57BL › Anti-integrin α
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Nécrose › Infarctus › Infarctus du myocarde › Anti-integrin α
questionsmedicales.fr › Tissus › Muscles › Muscle strié › Myocarde › Anti-integrin α
questionsmedicales.fr › Cellules › Cellules musculaires › Myocytes cardiaques › Anti-integrin α
questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Acides nucléiques › ARN › ARN messager › Anti-integrin α
questionsmedicales.fr › Techniques d'investigation › Techniques cytologiques › Analyse sur cellule unique › Anti-integrin α
questionsmedicales.fr › Facteurs biologiques › Toxines biologiques › Venins › Venins de serpent › Anti-integrin α
questionsmedicales.fr › Cellules › Cellules du tissu conjonctif › Cellules stromales › Anti-integrin α
questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Protéines de la superfamille du TGF bêta › Facteur de croissance transformant bêta › Facteur de croissance transformant bêta-1 › Anti-integrin α