15408-Conway, Simon

Simon J. Conway, PhD

Professor of Pediatrics

R4 W402F
Indianapolis, IN
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Simon J. Conway, PhD is a Professor of Pediatrics, holds secondary appointments in Departments of Anatomy & Cell Biology, Medical & Molecular Genetics, Biochemistry & Molecular Biology, is a member of the IU Simon Cancer Center and has been elected a Fellow of the American Heart Association. He is a geneticist and developmental biologist who uses transgenic mouse models to understand congenital and acquired birth defects and ameliorate cardiopulmonary neonatal and postnatal responses to heart and lung injury.  His research has been continually funded via NIH and is internationally acclaimed.

Key Publications

Stalmans I, Lambrechts D, Desmet F, Jansen S, Wang J, Maity S, Kneer PL, von der Ohe M,  Swillen A, Maes C, Gewillig M, Molin D, Hellings P, Boetel T, Haardt M, Compernolle V, Dewerchin M, Vlietinck R, Emanuel B, Gittenberger-de Groot AC, Esguerra C, Scambler P, Morrow B, Drisco, D, Moons L, Carmeliet G, Behn-Krappa A, Devriendt K, Collen D, Conway SJ* and Carmeliet P.* (2003). VEGF: a modifier of the del22q11 (DiGeorge) syndrome?   Nature Medicine, 9: 173-182.  [* joint corresponding authors]

Snider P, Hinton R, Moreno-Rodriguez, R, Wang J, Rogers R, Lindsley A, Li F, Ingram D, Menick D, Field LJ, Firulli AB, Molkentin JD, Markwald R and Conway SJ. (2008) Periostin is required for maturation and ECM stabilization of the cardiac skeleton.  Circ Res. 102:752-60.

Lepper C, Conway SJ, and Fan CM. (2009) Adult satellite cells and embryonic muscle progenitors have distinct genetic requirements.  Nature, 460:627-31.   

Snider P, Standley KN, Wang J, Azhar M, Doetschman T and Conway SJ. (2009) Origin of Cardiac Fibroblasts and the Role of Periostin.  Circ Res. 105:934-47.

Takeda N, Manabe I, Uchino Y, Shindo T, Sano M, Otsu K, Snider P, Conway SJ and Nagai R. (2009). Cardiac fibroblasts are essential for the adaptive response of the heart to pressure overload.  J Clin Invest. 120:254-65.

Olaopa M, Zhou HM, Snider P, Wang J, Schwartz, RJ, Moon A and Conway SJ. (2011) Pax3 is essential for normal cardiac neural crest morphogenesis but is not required during migration nor outflow tract septation.  Dev Biol. 356(2):308-22.

Qian L, Huang Y, Spencer I, Foley A, Vedantham V, Liu L, Conway SJ, Fu J and Srivastava D. (2012). In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytes. Nature, 485(7400):593-8.

Lajiness J, Snider P, Wang J, Feng GS, Krenz M and Conway SJ. (2014). SHP-2 deletion in post-migratory neural crest cells results in impaired cardiac sympathetic innervation.  Proc Natl Acad Sci USA., 111:E1374-82.  

Simmons O, Snider P, Wang J, Schwartz RJ, Chen YP and Conway SJ. (2015). Persistent Noggin arrests cardiomyocyte morphogenesis and results in early in utero lethality.  Dev. Dyn. 244(3):457-67.

Ahlfeld SK, Wang J, Gao Y, Snider P and Conway SJ. (2016). Initial TGFβ signaling suppression and loss of TGFBI causes early alveolar structural defects resulting in bronchopulmonary dysplasia.  Am J Pathol. 186(4):777-93.

Zhou HM and Conway SJ. (2016). Restricted Pax3 deletion in the neural tube results in congenital hydrocephalus.  J. Dev. Biol. 4(1), 7; doi:10.3390/jdb4010007   

Poulsen ET, Runager K, Nielsen N, Thomsen K, Snider P, Simmons O, Vorum H, Conway SJ* and Enghild JL*. (2017). Proteomic profiling of Tgfbi-null mouse corneas reveals only minor changes in matrix composition supportive of TGFBI knockdown as therapy against TGFBI-linked corneal dystrophies.  FEBS, 285:101-114 [* joint corresponding authors] 

de Lageneste O, Julien A, Abou-Khalil R, Frangi G, Carvalho C, Cagnard N, Cordier C, Conway SJ and Colnot C. (2018). Periosteum contains skeletal stem cells with high bone regenerative potential controlled by Periostin.  Nat Comm. 9(1):773.

Titles & Appointments

  • Professor of Pediatrics
  • Adjunct Professor of Anatomy, Cell Biology & Physiology
  • Adjunct Professor of Medical & Molecular Genetics
  • Professor of Biochemistry & Molecular Biology
  • Member of IU Simon Cancer Center
  • Education
    1996 FEL Institute of Child Health, Great Ormond Street Children's Hospital, University College London
    1993 PhD University College London
    1989 BSC University of Essex
  • Research

    Our lab’s focus is elucidating the underlying mechanisms of impaired cardiopulmonary and nervous system dysfunction in health and disease. Lack of formation of a separate aorta and pulmonary artery often results in neonatal lethality, and we have established in neural crest-associated Pax3/7 mutants that this is due to diminished cardiac innervation/bradycardia and associated respiratory failure as there is inappropriate mixing of oxygenated and de-oxygenated circulations postnatally. We are now examining key neural crest effectors that regulate morphogenesis prior to progenitor emigration to the heart. Moreover, these congenital heart defects frequently result in abnormal lung alveolar formation leading to Bronchopulmonary dysplasia (BPD). Using a hyperoxia-induced mouse model of BPD and both Periostin and Tgfbi knockout mice, our lab is examining how initial suppression of TGFb superfamily signaling instigates BPD pathogenesis. To test the consequences of TGFb inhibition and identify specific pathway effectors, we employ in vivo inducible caNoggin and caSmad7 transgenic as well as Tgfb ligand/receptor conditional knockout approaches; to either block all TGFb signaling and then compare these data when only BMP signaling or a single TGFb effector is blocked. Abnormal elevated TGFb signaling is routinely observed in response to injury and during postnatal cardiopulmonary fibrosis. Significantly, we have shown a partial Periostin element is uniquely capable of driving reporter expression in activated cardiac myofibroblasts, providing us with a unique in vivo tool for genetic manipulation of injury-site myofibroblasts. Thus, we seek to identify the molecular initiators of fibroblast-to-myofibroblast transition in fibrotic lungs and failing hearts and examine whether these pathological switches can be reversed in vivo. Using genetically-defined mouse models we seek to uncover novel therapeutic approaches for the diagnosis and treatment of patients.

  • Professional Organizations
    American Association of Anatomists
    American Heart Association (AHA)
    American Society for Cell Biology
    Genetics Society of America
    International Society for Heart Research
    Society for Developmental Biology
  • Awards
    Org: March of Dimes Defects Foundation
    Desc: Basil O’Connor Starter Scholar Award
    Org: School of Medicine, MCG
    Desc: Outstanding Young Faculty & Distinguished Research Awards
    Org: International Society for Heart Research
    Desc: Winner of Young Investigators Award (USA)
    Org: IUPUI
    Desc: Outstanding Faculty & Staff Award
    Org: NHLBI
    Desc: Cardiovascular Differentiation & Development Study Section Charter Member
    Org: Council on CV Sciences
    Desc: Elected Fellow of the American Heart Association
    Org: Medical University of South Carolina
    Desc: Awarded the Elsie Taber Lectureship in Human Development

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