Calcification Induced by Type I Interferon in Human Aortic Valve Interstitial Cells Is Larger in Males and Blunted by a Janus Kinase Inhibitor

Arteriosclerosis, Thrombosis, and Vascular Biology
Iván Parra-IzquierdoCarmen García-Rodríguez

Abstract

Objective- Calcific aortic valve disease is the most prevalent valvulopathy in Western countries. An unanticipated pathogenetic clue involving IFN (interferon) was disclosed by the finding of constitutive type I IFN activity associated with aortic valve calcification in children with the atypical Singleton-Merten syndrome. On this basis, the role of type I IFN on inflammation and calcification in human aortic valve interstitial cells (AVIC) was examined. Approach and Results- IFN-α was weakly proinflammatory but potentiated lipopolysaccharide-mediated activation of NF (nuclear factor)-κB and the ensuing induction of proinflammatory molecules in human AVIC. Stimulation with IFN-α and in combination with lipopolysaccharide promoted osteoblast-like differentiation characterized by increased osteoblastic gene expression, BMP (bone morphogenetic protein)-2 secretion, and ectopic phosphatase activity. Sex differences were observed. Likewise, IFN-α treatment of human AVICs in osteogenic medium resulted in increased formation of calcific nodules. Strikingly, IFN-α-mediated calcification was significantly higher in AVICs from males, and was blocked by tofacitinib, a JAK (Janus kinase) inhibitor, and by a BMP antagonist. A female-specifi...Continue Reading

References

Feb 9, 2005·The Journal of Immunology : Official Journal of the American Association of Immunologists·Jukka SirénSampsa Matikainen
May 16, 2007·The Journal of Biological Chemistry·Nicole A de WeerdPaul J Hertzog
Sep 8, 2007·The American Journal of Pathology·Amber C LiuAvrum I Gotlieb
Nov 21, 2008·International Journal of Cardiology·Alexandros AlexopoulosHelen Papadaki
Dec 2, 2009·Advances in Experimental Medicine and Biology·Toshihisa Komori
Sep 15, 2010·The Journal of Experimental Medicine·Giorgio Trinchieri
Jan 21, 2011·International Journal of Cardiology·Javier LópezCarmen García-Rodríguez
May 28, 2011·Circulation Research·Jordan D MillerDonald D Heistad
Sep 18, 2012·Arteriosclerosis, Thrombosis, and Vascular Biology·Rui SongXianzhong Meng
Dec 13, 2012·Circulation. Cardiovascular Imaging·Shivani R AggarwalMaurice Enriquez-Sarano
Jan 19, 2013·Cell Death & Disease·N SévèreP J Marie
Feb 1, 2013·Epigenetics : Official Journal of the DNA Methylation Society·Eric HervouetRégis Delage-Mourroux
Dec 24, 2013·Nature Reviews. Immunology·Lionel B Ivashkiv, Laura T Donlin
Feb 4, 2014·Biology of Sex Differences·Salil Sharma, Mansoureh Eghbali
Mar 19, 2014·Journal of Molecular and Cellular Cardiology·Diala El HusseiniPatrick Mathieu
Mar 26, 2014·Arteriosclerosis, Thrombosis, and Vascular Biology·Linda L Demer, Yin Tintut
Oct 15, 2014·Nature Reviews. Cardiology·Huan WangKristi S Anseth
Oct 24, 2014·European Cells & Materials·M BrudererM J Stoddart
Jan 15, 2015·Annual Review of Medicine·John J O'SheaArian Laurence
Jan 27, 2015·American Journal of Human Genetics·Mi-Ae JangChang-Seok Ki
May 15, 2015·American Journal of Physiology. Cell Physiology·Sean MartinTechung Lee
May 21, 2015·The Journal of Surgical Research·Neil VenardosDavid A Fullerton
Jun 9, 2015·Nature Reviews. Immunology·Yanick J Crow, Nicolas Manel
Jun 13, 2015·Journal of Immunology Research·Patrick MathieuMarie-Chloé Boulanger
Aug 1, 2015·Journal of the American College of Cardiology·Tania A PawadeMarc R Dweck
Sep 21, 2015·Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology·Matthew TorrePaul A VanderLaan
Oct 9, 2015·Methods in Molecular Biology·Ricardo Villa-Bellosta, Magda R Hamczyk
Mar 22, 2016·Journal of Molecular and Cellular Cardiology·Jesper HjortnaesElena Aikawa
May 21, 2016·Arteriosclerosis, Thrombosis, and Vascular Biology·M Victoria Gomez-StallonsKatherine E Yutzey
Nov 4, 2016·Physiological Reviews·Vera Regitz-Zagrosek, Georgios Kararigas
Nov 7, 2017·Nature Medicine·Kevin R KingRalph Weissleder
Mar 30, 2018·Frontiers in Physiology·Carmen García-RodríguezMariano Sánchez Crespo

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Citations

Dec 24, 2019·Arteriosclerosis, Thrombosis, and Vascular Biology·Hong S LuAlan Daugherty
May 10, 2020·Journal of the American Heart Association·Martine VoisineMarie-Annick Clavel
Aug 5, 2019·World Journal of Pediatrics : WJP·Zhong-Xun Yu, Hong-Mei Song
Feb 19, 2020·Expert Review of Cardiovascular Therapy·Sahrai SaeedJohn Chambers
Aug 13, 2020·International Journal of Molecular Sciences·Volha I SummerhillVeronika A Myasoedova
Feb 9, 2019·Experimental Biology and Medicine·David H Wu, Antonis K Hatzopoulos
Oct 6, 2020·Frontiers in Cell and Developmental Biology·Kashif KhanAdel Schwertani
Jan 24, 2021·Pediatric Rheumatology Online Journal·Tingyan HeJun Yang
Feb 14, 2021·The Canadian Journal of Cardiology·Marie-Ange Fleury, Marie-Annick Clavel
Jul 6, 2019·Cell Calcium·Julien AnractThierry Capiod
May 28, 2021·Frontiers in Cardiovascular Medicine·Petra BüttnerFlorian Schlotter
Jun 25, 2021·Journal of Molecular and Cellular Cardiology·Cierra J WalkerLeslie A Leinwand
May 20, 2021·The FEBS Journal·Iván Parra-IzquierdoCarmen García-Rodríguez

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