Bonnie Blazer-Yost, Ph.D.

Image of Dr. Blazer Yost

Professor of Biology

Adjunct Professor Cellular and Integrative Physiology

Co-director Center for Developmental and Regenerative Biology School of Science

Indiana University-Purdue University Indianapolis

723 W. Michigan Street

Indianapolis, IN 46204

Phone: (317) 278-1145

Fax: (317) 274-2846


Bonnie Blazer-Yost is a Professor in the Department of Biology at IUPUI with joint appointments in the Department of Integrative and Cellular Physiology and the Department of Anatomy and Cell Biology in the Indiana University School of Medicine. The main focus of her laboratory is the physiology and pathophysiology of barrier epithelial cells. Her group studies how various hormones and other effectors regulate transepithelial ion transport in renal, airway and brain cells. The major projects in the laboratory are directed toward understanding and treating diseases such as polycystic kidney disease, hypertension, metabolic syndrome and hydrocephalus.

One of the current projects is a study of potential drugs to treat autosomal dominant polycystic kidney disease (ADPKD). This is a genetic disease that affects over 1 in 1,000 people. The cystic kidneys grow slowly throughout the patient’s life, causing pressure and pain and eventually in middle to old age result in renal failure in over half the patients. At the time of renal failure, the kidneys can be the size of footballs causing pain and distention of the abdomen. There are no drugs to treat ADPKD and the only thing that can be done for the patients is to aspirate the largest of the cysts to relieve that pain and dialyze or transplant the patients when their kidneys fail. Due to a serendipitous observation that insulin sensitizing agents of the PPARγ class of compounds have the unexpected effect of inhibiting the synthesis of the CFTR Cl- channel in cultured renal cells, the investigators have examined the potential for these agents to inhibit cyst growth in animal models of PKD. The positive results in pre-clinical models suggest that FDA-approved PPAR agonists such as pioglitazone and rosiglitazone may be effective agents for long-term therapy in PKD patients. This research is the culmination of a bench to bedside series of experiments that may result in a new treatment for ADPKD. The clinical trial using pioglitazone to treat ADPKD are funded and initiated in 2016. Other, more preliminary studies to explore new and innovative therapies for the treatment of late-stage PKD are ongoing.

The other major project in the Blazer-Yost laboratory is the study of a pressure- and osmotic-sensitive cation channel known as TRPV4. An unexpected observation has led to the discovery that TRPV4 antagonists relieve hydrocephalus, or “water on the brain” in a rat model of pediatric hydrocephalus. Hydrocephalus is a devastating disease which affects nearly 1 in 1000 births, and has medical costs over $1 billion per year. The accumulating cerebrospinal fluid results in increased hydrostatic pressure causing pain and neuronal destruction and can ultimately cause permanent damage or death. Currently, there are no drugs to treat this disease, with the only viable treatment being surgical intervention. The standard of care is the placement of cerebral shunts to drain the excess fluid, however this approach often results in a less than optimal outcome. Shunt failures due to blockage, infection, and other causes are as high as 50% even in major medical centers which specialize in these procedures. Two chemically distinct forms of TRPV4 antagonists have been shown to be effective in decreasing the hydrocephalus in the rat model. The laboratory members are currently studying the mechanism of action of these compounds using tissue culture and preclinical animal models.


    Blazer-Yost, B.L. Chapter 25 ADPKD Channel – The Polycystins. In Ion Channels and Transporters of Epithelia in Health and Disease. Editors K.L. Hamilton, D.C. Devor, B.J. Harvey. Springer, 2015
    Banga, A., S. Flaig, S. Lewis, S. Winfree, B. L. Blazer-Yost. Epinephrine stimulation of anion secretion in the Calu-3 serous cell model. Am. J. Physiol. Lung Mol. Physiol. 306:L937-L946, 2014
    Li, P., X. Lai, F. Witzmann, B.L. Blazer-Yost. Bioinformatic Analysis of Differential Protein Expression in Calu-3 Cells Exposed to Carbon Nanotubes. Proteomes 1:219-239 doi: 10.3390/proteomes 1030219, 2013.
    Lai, X., B.L. Blazer-Yost, J.W. Clack, S.L. Fears, S. Mitra, S.A. Ntim, H.N. Ringham and F.A. Witzmann. Protein expression profiles of intestinal epithelial co-cultures: Effect of functionalized carbon nanotube exposure. Int. J. Biomed. Nanosci. Nanotech. 3:127-162, 2013.
    Banga, A. F.A. Witzmann, H. Petrache, and B.L. Blazer-Yost. Functional effects of nanoparticle exposure on Calu-3 airway epithelial cells. Cell. Physiol. Biochem. 29: 197-212, 2012.
    Blazer-Yost, B.L., A. J. Banga, A. Amos, E. Chernoff, X. Lai, C. Li, S. Mitra and F.A. Witzmann. Effect of carbon nanoparticles on barrier function of renal epithelial cells. Nanotoxicology 5: 354-371, 2011
    Blazer-Yost, B. L., B. J. Blacklock, S. Flaig, R. L. Bacallao and V. Gattone. Lysophosphatidic Acid is a Modulator of Cyst Growth in Autosomal Dominant Polycystic Kidney Disease. Cell. Physiol. Biochem. 278: 1255-1264, 2011
    Blazer-Yost, B.L. PPARγ Agonists – Blood Pressure and Edema. PPAR Research Volume 2010, Article ID 785369, 5 pages doi:10.1155/2010/785369, 2010.
    Blazer-Yost, B.L., J. Haydon, T. Eggleston-Gulyas, J-H. Chen, X. Wang, V. Gattone and V.E. Torres. Pioglitazone attenuates cystic burden in the PCK rodent model of polycystic kidney disease. PPAR Research. Article ID 274376, 8 pages doi:10.1155/2010/274376, 2010
    Menniti, M., R. Iuliano, M. Sopjani, M. Foller, S. Mariggio, C. Nofziger, A.M. Perri, R. Amato, B. Blazer-Yost, D. Corda, F. Lang and N. Perrotti. 60 kDa lysophospholipase, a new Sgk1 molecular partner involved in the regulation of ENaC. Cell. Physiol. Biochem. 26:587-596, 2010