Ang Guo, PhD

Portrait
Research Assistant Professor of Internal Medicine - Cardiovascular Medicine

Contact Information

Office: 2269 CBRB
319-335-0044

Education

PhD, Physiology, Molecular Cardiology, Shanghai Institute of Health Sciences

Postdoctoral Fellow, Molecular Cardiology and Physiology, University of Iowa College of Medicine

Center, Program and Institute Affiliations

Cardiovascular Research Center

Research Summary

Ca2+ is the most ubiquitous 2nd messenger in cell signaling. It regulates very different biological processes. My long-term curiosity is that how cells convert Ca2+, such a diffusible and universal signal, into specific commands that control different cellular responses and biological functions. I have been focusing on the Ca2+ signaling in cardiomyocytes, in which Ca2+ signals not only control the cell contraction and heart rhythm, but also affect the physiological and pathological changes of cardiomyocytes in response to stresses and stimulations. Therefore, mechanisms must exist to distinguish Ca2+ signals relevant to different functions. Understanding the Ca2+ signaling mechanisms in heart muscle cells would have major implications in both basic biology as well as potential novel therapies. My research interests are centered on four related areas of investigations: 1). Discovering novel components in Ca2+ regulated signaling networks; 2). Revealing the subcellular microdomains specialized for localized Ca2+ events, which are essential for coding of Ca2+ signaling related to diseases; 3). Discovering the molecular mechanism of Ca2+ dependent regulation of chromatin remodeling. 4). Translating mechanistic insights into novel therapies in disease models.

Publications

Guo, A., Hall, D., Zhang, C., Peng, T., Miller, J. D., Kutschke, W., Grueter, C. E., Johnson, F. L., Lin, R. Z. & Song, L. S. (2015). Molecular Determinants of Calpain-dependent Cleavage of Junctophilin-2 protein in cardiomyocytes. Journal of Biological Chemistry, 290(29), 17946-55.

Chen, W., Wang, R., Chen, B., Kong, H., Zhou, Q., Xie, C., Tian, X., Guo, A., Bai, Y., Jones, P. P., O'Mara, M., Zhang, L., Bolstead, J., Semeniuk, L., Cheng, H., Chen, J., Tieleman, D. P., Gillis, A. M., Duff, H. J., Fill, M., Song, L. S. & Chen, S. R. (2014). A store Ca2+ sensing gate controls Ca2+ waves and Ca2+ triggered arrhythmias. Nature Medicine, 20(2), 184-92.

Guo, A., Song, L. S. (2014). AutoTT: Automated Detection and Analysis of T-Tubule Architecture in Cardiomyocytes. Biophysical Journal, 106(12), 2729-36.

Guo, A., Zhang, X. Y., Iyer, V. R., Chen, B., Zhang, C., Kutschke, W., Weiss, R. M., Franzini-Armstrong, C. & Song, L. S. (2014). Overexpression of junctophilin-2 does not enhance baseline cardiac function but attenuates the development of heart failure following cardiac stress. Proc Natl Acad Sci USA, 111(33), 12240-5.

Zhang, C., Chen, B., Guo, A., Zhu, Y., Miller, J., Kutschke, W., Zimmerman, K., Weiss, R. M., Wehrens, X. H., Hong, J., Johnson, F. L., Santana, L. F., Anderson, M. E. & Song, L. S. (2014). Microtubule-mediated defects in junctophilin-2 trafficking contribute to myocyte T-tubule remodeling and Ca2+ handling dysfunction in heart failure. Circulation, 129(17), 1742-50.

Chen, B., Guo, A., Zhang, C., Chen, R., Zhu, Y., Hong, J., Kutschke, W., Zimmerman, K., Weiss, R. M., Zingman, L., Anderson, M. E., Wehrens, X. H. & Song, L. S. (2013). Critical roles of Junctophilin-2 in T-tubule and excitation-contraction coupling maturation during postnatal development. (Vols. 100). (1), pp. 54-62. Cardiovascular Research.

Guo, A., Zhang, C., Chen, B. & Song, L. S. (2013). Emerging mechanisms of T-tubule remodelling in heart failure. Cardiovascular Research, 98(2), 204-15.

Guo, A., Cala, S. E. & Song, L. S. (2012). Calsequestrin Accumulation in Rough Endoplasmic Reticulum Promotes Perinuclear Ca2+ Release and Myocyte Hypertrophy. Journal of Biological Chemistry, 287(20), 16670-80.

Wei, S., Guo, A., Chen, B., Kutschke, W., Xie, Y. P., Zimmerman, K., Weiss, R. M., Anderson, M. E., Cheng, H. & Song, L. S. (2010). T-tubule remodeling during transition from hypertrophy to heart failure. (Vols. 107). (4), pp. 520-31. Circulation Research.

Guo, A., Yang, H. T. (2009). Ca2+ removal mechanisms in mouse embryonic stem cell-derived cardiomyocytes. American Journal of Physiology Cell Physiol, 297(3), C732-41.