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Renal Group

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Overview of research program

The laboratory's key aim is to unravel the molecular mechanisms underpinning progressive kidney disease. Renal disease is now considered the single most important factor predisposing to vascular disease (ie heart attack and stroke) in the community. However the majority of renal disease is entirely asymptomatic. In general more that 70% of kidney function is lost before any symptoms appear and usually once kidney function is lost it is not reversible and dialysis remains the only option for the majority of patients. Diabetes mellitus now accounts for the majority of kidney failure in our population. Hence the main focus of The Renal Research Group is primarily on diabetic kidney disease.

The laboratory uses a number of approaches to achieve this aim, including studying the single cell, cells in culture, animal models of diabetes through to studies on people with diabetes. This approach allow us to determine the molecular abnormalities present at a cellular level, the interaction between cells that go to make up the kidney and then the response of the kidney to the metabolic, biochemical, physiological and molecular abnormalities that occur in the ‘whole body’ as a response to diabetes mellitus. As vascular disease goes hand in hand with diabetes a further component of our work focuses on determining the molecular mechanisms that drive vascular pathology in patients with diabetes mellitus. Once the molecular mechanisms are defined we then look for novel mechanisms that can arrest progressive disease or promote renal repair and regeneration that may act as future therapeutic targets. Our work has highlighted the parallels between developmental biology and cancer cell biology in progressive kidney disease. In 2007 a key focus of our work has been to elucidate the cellular abnormalities inherent in epithelial to mesenchymal transition (common to cancer cell biology) and the recapitulation of developmental signaling processes in kidney disease.

Our current projects are:

  • The isoform specific effects of transforming growth factorβ (TGFβ)and in diabetic nephropathy.
  • Differentiating the inflammatory vs the profibrotic component of progressive renal disease in diabetic nephropathy.
  • The role of the Kruppel like family of transcription factors in mediating progressive renal fibrosis.
  • The role of macrophage migration inhibitory factor and Kruppel like factor 4 (KLF4) in diabetic nephropathy.
  • Signalling through the serine-threonine glucocorticoid pathway (SGK-1) pathway and convergence on the epidermal growth factor receptor (EGF-R) as a unifying factor mediating salt and water retention (and consequently high blood pressure) and kidney scarring in diabetic nephropathy.
  • Stimulation of the peroxisome proliferator agonist receptors as a strategy to reduce progressive renal disease in kidney disease due to, and independent of, diabetes mellitus.
  • Mechanisms of renal repair with a focus on the BMP-7 signalling pathways
  • The consequences of statins on renal tubular function.
  • Hypoxia inducible genes and diabetic nephropathy
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Major funding sources

  • NHMRC
  • The Hillcrest Foundation
  • Pharmaceutical companies
  • Philanthropic donations
  • Australian Research Council
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Selected publications

Holian J, Qi W, Kelly DJ, Zhang Y, Mreich E, Pollock CA, Chen XM. The Role of Kruppel-like factor 6 in Transforming Growth Factor-Beta-1-induced Epithelial-Mesenchymal Transition of Proximal Tubule Cells. Am J Physiol Renal Physiol. 2008 Aug 27.

Mather A, Chen XM, McGinn S, Field MJ, Sumual S, Mangiafico S, Zhang Y, Kelly DJ, Pollock CA. High glucose induced endothelial cell growth inhibition is associated with an increase in TGFbeta(1) secretion and inhibition of Ras prenylation via suppression of the mevalonate pathway. Int J Biochem Cell Biol. 2008 Jul 25.

Saad S, Chen XM, Stevens V, Pollock C. The role of Sgk-1 in the upregulation of transport proteins by PPARgamma agonists in human proximal tubule cells. Nephrol Dial Transplant. Unique ID: GFN614, In Press 2008.

Stevens VA, Saad S, Poronnik P, Fenton-Lee CA, Polhill TS, Pollock CA. The role of SGK-1 in angiotensin II-mediated sodium reabsorption in human proximal tubular cells. Nephrol Dial Transplant. 2008 Jun;23(6):1834-43.

Panchapakesan U, Chen XM, Pollock CA. Drug insight: thiazolidinediones and diabetic nephropathy–relevance to renoprotection. Nat Clin Pract Nephrol. 2005 Nov;1(1):33-43. Review. PMID: 16932362

Qi W, Chen X, Poronnik P, Pollock CA.Transforming growth factor-beta/connective tissue growth factor axis in the kidney. Int J Biochem Cell Biol. 2008;40(1):9-13.

Panchapakesan U, Sumual S, Pollock C. Nanomedicines in the treatment of anemia in renal disease: focus on CERA (Continuous Erythropoietin Receptor Activator). Int J Nanomedicine. 2007;2(1):33-8. Review. PMID: 17722510

Qi W, Chen X, Gilbert RE, Zhang Y, Waltham M, Schache M, Kelly DJ, Pollock CA. High glucose-induced thioredoxin-interacting protein in renal proximal tubule cells is independent of transforming growth factor-beta1. Am J Pathol. 2007 Sep;171(3):744-54. PMID: 17675577

Pollock CA, Poronnik P. Albumin transport and processing by the proximal tubule: physiology and pathophysiology. Curr Opin Nephrol Hypertens. 2007 Jul;16(4):359-64. Review.

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Major collaborations

  • University of Melbourne
  • The Millenium Institute at Westmead Hospital, Sydney
  • University of Queensland
  • St Vincents Institute of Medical Research, University of Melbourne
  • University of Toronto, Canada
  • Kings College London, England
  • The Department of Physiology Tubingen, Germany
  • Sundaram Medical Foundation and Memorial Hospital, India.
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