Honors & Awards

  • Graduate Research Fellowship, National Science Foundation (2014-2017)
  • Predoctoral Graduate Research Fellowship, American Heart Association (2013-2015)
  • Graduate Student Travel Grant, Stanford Biosciences Office of Graduate Education (2014)

Education & Certifications

  • Certificate, Stanford Graduate School of Business, Stanford Ignite (2014)
  • Bachelor of Science, Duke University, Biology (2012)

Service, Volunteer and Community Work

  • Program Assistant, Stanford Summer Research Program (SSRP) (6/1/2013 - Present)


    Stanford University

Research & Scholarship

Current Research and Scholarly Interests

My research focuses on the molecular mechanisms driving cardiovascular development, disease, and regeneration. I am also interested in utilizing induced pluripotent stem cells for the in-vitro modeling of cardiovascular disorders and for high-throughput drug screening/discovery.

Lab Affiliations


Journal Articles

  • IGF promotes cardiac lineage induction in vitro by selective expansion of early mesoderm. Stem cells (Dayton, Ohio) Engels, M. C., Rajarajan, K., Feistritzer, R., Sharma, A., Nielsen, U. B., Schalij, M. J., de Vries, A. A., Pijnappels, D. A., Wu, S. M. 2014


    A thorough understanding of the developmental signals that direct pluripotent stem cells (PSCs) towards a cardiac fate is essential for translational applications in disease modeling and therapy. We screened a panel of 44 cytokines/signaling molecules for their ability to enhance Nkx2.5(+) cardiac progenitor cell (CPC) formation during in vitro embryonic stem cell (ESC) differentiation. Treatment of murine ESCs with insulin or insulin-like growth factors (IGF1/2) during early differentiation increased mesodermal cell proliferation and, consequently, CPC formation. Furthermore, we show that downstream mediators of IGF signaling (e.g. phospho-Akt and mTOR) are required for this effect. These data support a novel role for IGF family ligands to expand the developing mesoderm and promote cardiac differentiation. Insulin or IGF treatment could provide an effective strategy to increase the PSC-based generation of CPCs and cardiomyocytes for applications in regenerative medicine. Stem Cells 2014.

    View details for DOI 10.1002/stem.1660

    View details for PubMedID 24496962

  • Induced pluripotent stem cell-derived cardiomyocytes for cardiovascular disease modeling and drug screening STEM CELL RESEARCH & THERAPY Sharma, A., Wu, J. C., Wu, S. M. 2013; 4

    View details for DOI 10.1186/scrt380

    View details for Web of Science ID 000329186900001

    View details for PubMedID 24476344

  • Screening drug-induced arrhythmia events using human induced pluripotent stem cell-derived cardiomyocytes and low-impedance microelectrode arrays. Circulation Navarrete, E. G., Liang, P., Lan, F., Sanchez-Freire, V., Simmons, C., Gong, T., Sharma, A., Burridge, P. W., Patlolla, B., Lee, A. S., Wu, H., Beygui, R. E., Wu, S. M., Robbins, R. C., Bers, D. M., Wu, J. C. 2013; 128 (11): S3-13


    Drug-induced arrhythmia is one of the most common causes of drug development failure and withdrawal from market. This study tested whether human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) combined with a low-impedance microelectrode array (MEA) system could improve on industry-standard preclinical cardiotoxicity screening methods, identify the effects of well-characterized drugs, and elucidate underlying risk factors for drug-induced arrhythmia. hiPSC-CMs may be advantageous over immortalized cell lines because they possess similar functional characteristics as primary human cardiomyocytes and can be generated in unlimited quantities.Pharmacological responses of beating embryoid bodies exposed to a comprehensive panel of drugs at 65 to 95 days postinduction were determined. Responses of hiPSC-CMs to drugs were qualitatively and quantitatively consistent with the reported drug effects in literature. Torsadogenic hERG blockers, such as sotalol and quinidine, produced statistically and physiologically significant effects, consistent with patch-clamp studies, on human embryonic stem cell-derived cardiomyocytes hESC-CMs. False-negative and false-positive hERG blockers were identified accurately. Consistent with published studies using animal models, early afterdepolarizations and ectopic beats were observed in 33% and 40% of embryoid bodies treated with sotalol and quinidine, respectively, compared with negligible early afterdepolarizations and ectopic beats in untreated controls.We found that drug-induced arrhythmias can be recapitulated in hiPSC-CMs and documented with low impedance MEA. Our data indicate that the MEA/hiPSC-CM assay is a sensitive, robust, and efficient platform for testing drug effectiveness and for arrhythmia screening. This system may hold great potential for reducing drug development costs and may provide significant advantages over current industry standard assays that use immortalized cell lines or animal models.

    View details for DOI 10.1161/CIRCULATIONAHA.112.000570

    View details for PubMedID 24030418

  • Autophagy - the friendly fire in endothelial cell regeneration. Focus on "Autophagy in endothelial progenitor cells is cytoprotective in hypoxic conditions" AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY Sharma, A., Wu, S. M. 2013; 304 (7): C614-C616

    View details for DOI 10.1152/ajpcell.00046.2013

    View details for Web of Science ID 000316995700003

    View details for PubMedID 23407881

  • Of Fish and Men Clonal Lineage Analysis Identifies Divergence in Myocardial Development CIRCULATION RESEARCH Sharma, A., Wu, S. M. 2013; 112 (4): 583-585
  • Endoglin regulates PI3-kinase/Akt trafficking and signaling to alter endothelial capillary stability during angiogenesis MOLECULAR BIOLOGY OF THE CELL Lee, N. Y., Golzio, C., Gatza, C. E., Sharma, A., Katsanis, N., Blobe, G. C. 2012; 23 (13): 2412-2423


    Endoglin (CD105) is an endothelial-specific transforming growth factor ? (TGF-?) coreceptor essential for angiogenesis and vascular homeostasis. Although endoglin dysfunction contributes to numerous vascular conditions, the mechanism of endoglin action remains poorly understood. Here we report a novel mechanism in which endoglin and G?-interacting protein C-terminus-interacting protein (GIPC)-mediated trafficking of phosphatidylinositol 3-kinase (PI3K) regulates endothelial signaling and function. We demonstrate that endoglin interacts with the PI3K subunits p110? and p85 via GIPC to recruit and activate PI3K and Akt at the cell membrane. Opposing ligand-induced effects are observed in which TGF-?1 attenuates, whereas bone morphogenetic protein-9 enhances, endoglin/GIPC-mediated membrane scaffolding of PI3K and Akt to alter endothelial capillary tube stability in vitro. Moreover, we employ the first transgenic zebrafish model for endoglin to demonstrate that GIPC is a critical component of endoglin function during developmental angiogenesis in vivo. These studies define a novel non-Smad function for endoglin and GIPC in regulating endothelial cell function during angiogenesis.

    View details for DOI 10.1091/mbc.E11-12-0993

    View details for Web of Science ID 000306287400003

    View details for PubMedID 22593212

  • Xenotransplantation: Weighing the Risks and Benefits of a Controversial Procedure Penn Bioethics Journal A. Sharma 2010; 6 (2): 25-29

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