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Henar Cuervo, Ph.D.

January 1, 2018

Assistant Professor
Department of Physiology and Biophysics
University of Illinois at Chicago
Chicago, IL

Primary Research:

Our current research work is focused on understanding the signaling pathways regulating the functions of perivascular cells (pericytes and smooth muscle cells) in developmental, physiological and pathological conditions. We are especially interested in the role of pericytes in tumor angiogenesis, vascular retinopathies, arteriovenous malformations, and fibrosis.

Lab Web Site:

Members of the laboratory:

Taliha Nadeem (Master Student)
Jonathan Cothran (Research Specialist)
Jordan Fauser (Rotating Graduate Student)

Dr. Cuervo and Lab members

Recent Publications:

  • Cuervo, H., Pereira, B., Nadeem, T., Lin, M., Lee, F., Kitajewski, J., and Lin, C.S. (2017). PDGFRbeta-P2A-CreER(T2) mice: a genetic tool to target pericytes in angiogenesis. Angiogenesis 20, 655-662.
  • Cuervo, H., Nielsen, C.M., Simonetto, D.A., Ferrell, L., Shah, V.H., and Wang, R.A. (2016). Endothelial notch signaling is essential to prevent hepatic vascular malformations in mice. Hepatology 64, 1302-1316.
  • Tattersall, I.W., Du, J., Cong, Z., Cho, B.S., Klein, A.M., Dieck, C.L., Chaudhri, R.A., Cuervo, H., Herts, J.H., and Kitajewski, J. (2016). In vitro modeling of endothelial interaction with macrophages and pericytes demonstrates Notch signaling function in the vascular microenvironment. Angiogenesis 19, 201-215.
  • Kofler, N.M., Cuervo, H., Uh, M.K., Murtomaki, A., and Kitajewski, J. (2015). Combined deficiency of Notch1 and Notch3 causes pericyte dysfunction, models CADASIL, and results in arteriovenous malformations. Sci Rep 5, 16449.
  • Kangsamaksin, T., Murtomaki, A., Kofler, N.M., Cuervo, H., Chaudhri, R.A., Tattersall, I.W., Rosenstiel, P.E., Shawber, C.J., and Kitajewski, J. (2015). NOTCH decoys that selectively block DLL/NOTCH or JAG/NOTCH disrupt angiogenesis by unique mechanisms to inhibit tumor growth. Cancer Discov 5, 182-197.
  • Nielsen, C.M., Cuervo, H., Ding, V.W., Kong, Y., Huang, E.J., and Wang, R.A. (2014). Deletion of Rbpj from postnatal endothelium leads to abnormal arteriovenous shunting in mice. Development 141, 3782-3792.