Education & Training
- MD, University of Western Ontario, 2001
- MSc, Developmental Biology, University of Toronto, 1997
- BSc, Genetics, University of Western Ontario, 1995
Research Interest Summary
Chronic kidney disease (CKD) is a growing public health burden that results in significant morbidity and increased risk of mortality for individual patients. In the United States alone, the cost of care for CKD, kidney transplant and dialysis is over 40 billion dollars annually. At present, there are limited therapies available to ameliorate the progressive loss of renal function in CKD, and this ultimately leads to dialysis or transplant for these patients. Thus, there is an urgent need to develop novel tools and resources that may lead to innovative strategies to enhance renal repair and promote the generation of new nephrons in future.
In the pediatric population, renal dysplasia/hypoplasia is a leading cause of renal failure in children, and the risk of chronic kidney disease is linked to decreased renal reserve as a result of the formation of fewer and/or abnormal nephrons during kidney development. Furthermore, decreased congenital nephron endowment is associated with adult onset hypertension, a common health problem that leads to decreased life expectancy. Understanding the molecular mechanisms that control nephron number and formation is critical to making an impact on these diseases.
My laboratory is focused on understanding how microRNAs (miRNAs) regulate kidney development and disease. MiRNAs are small, non-coding RNA molecules that function largely as negative regulators of gene expression, and while they have been implicated in stem cell biology and the development of other organs, little is known about their role in the kidney [3, 4]. Nephron progenitors represent a population of self-renewing, multipotent progenitor cells that give rise to all the epithelial components of the nephron, the functional unit of the kidney. To make an impact on patients with CKD, we are studying the role of miRNAs in nephron progenitors, as a means of both understanding how nephron number and formation is determined during kidney development, and how one might propagate and manipulate nephron progenitors for novel renal regenerative therapies.
Shalaby F, Ho J, Stanford WL, Schwartz L, Fischer K-D, Bernstein A, Rossant J. A requirement for Flk1 in primitive and definitive hematopoiesis. Cell 1997; 89: 981- 990. PMID: 9200616.
Uyttendaele H, Ho J, Rossant J, Kitajewski J. Vascular patterning defects associated with expression of activated Notch4 in embryonic endothelium. Proc Natl Acad Sci USA 2001; 98(10): 5643-5648. PMID: 11344305.
Ho J, Ng KH, Rosen S, Dostal A, Gregory RI and Kreidberg JA. Podocyte-specific loss of functional miRNAs leads to rapid glomerular and tubular damage. J Am Soc Neph 2008; 19(11): 2069-2075. PMID: 18832437.
Pandey P, Qin S, Ho J. Zhou J and Kreidberg JA. Systems biology approach to identify transcriptome reprogramming and microRNA targets during the progression of Polycystic Kidney Disease. BMC Systems Biology 2011; 5(1): 56. PMID 21518438. *highly accessed
Ho J, Pandey P, Schatton T, Sims-Lucas S, Khalid M, Frank MH, Hartwig S and Kreidberg JA. The pro-apoptotic protein Bim is a microRNA target in kidney progenitor cells. J Am Soc Neph 2011; 22(6): 1053-1063. PMID 21546576.
Ho J and Kreidberg JA. The long and short of microRNAs. J Am Soc. Neph 2012; 23(3): 400-4. PMID 22302196.
Sims-Lucas S, Schaefer C, Bushnell D, Ho J, Logar A, Prochownik E, GIttes G and Bates CM. Endothelial progenitors exist within the kidney and lung mesenchyme. PLOS One 2013; Jun 18; 8(6):e65993. PMID 23823180.
Chu JYS, Sims-Lucas S, Bushnell DS, Bodnar AJ, Kreidberg J and Ho J. Dicer function is required in the metanephric mesenchyme in early kidney development. Am J Physiol Renal Physiol 2014; 306(7): F764-72. PMID 24500693.
Marrone AK, Stolz DB, Bastacky SI, Kostka D, Bodnar AJ and Ho J. miR-17~92 is required for nephrogenesis and renal function. J Am Soc Neph 2014; 25(7): 1440-1452. PMID 24511118.
Edinger, RS, Coronnello C, Bodnar AJ, LaFramboise WA, Benos PV, Ho J, Johnson JP and Butterworth MB. Aldosterone regulates microRNAs in the cortical collecting duct to alter sodium transport. J Am Soc Neph 2014; 25(11): 2445-2457. PMID 24744440.