What we've been up to
ASN 2017- Kidney Week in New Orleans
Andrea discussing her research
20th Annual Undergraduate
Shankland Lab Research featured on cover of Kidney International
Dr. Mariya Sweetwyne's paper accepted to Kidney International
"Mitochondrial-targeted peptide, SS-31, improves glomerular architecture in mice of advanced age"
link to PubMed
New Funding for FSGS Research
FY 2015 Investigator-Initiated Research Award – Partnering PI Option
NIH/NIA (Shankland) 08/15/2016-03/31/2021
Reduced Glomerular Progenitors Impair Regeneration in Aged Kidney
The grant will define how the decline in podocyte number with advancing age cannot adequately be replaced by their neighboring parietal
epithelial cell progenitors, which leads to kidney scarring.
DOD PR151175 (Shankland and Pun) 09/30/2016-04/30/2019
New podocyte-targeted treatments for focal segmental glomerulosclerosis (FSGS)
We propose the development of two synergistic kidney-targeting technologies: (i) “passive” targeting, kidney-accumulating polymers and (ii)
“active” targeting podocyte-specific peptide
DOD PR151965 (Shankland and Pun) 6/15/2016-12/14/2018
Development of Cell Therapies for FSGS
The major goal of this proposal is to develop urine-derived renal progenitor cells as a cell therapy for treatment of FSGS
NIH/NIDDK 1 UH2 DK107343-01 (Shankland and Zheng) 07/01/2015-06/30/2020
Rebuilding the glomerular filtration barrier by regenerating adult podocytes
Podocytes are cells in the kidney’s glomerular filtering units that limit the passage of proteins from the blood in to the urine. As adults, they
cannot proliferate to replace , and therefore they are reliant on other stem cells for their regeneration. In this grant, we will study such stem
cells in podocyte repair to rebuild a kidney.
NIH/NIDDK 1 R01 DK097598-01A1 (Shankland) PI 07/01/2014-06/30/2019
Juxta-glomerular cells serve as glomerular epithelial cell progenitors in glomerular disease
The purpose of this proposal is to study the existing problem of age-related podocyte depletion in a completely new context. The goal is to
prove that with advancing age, kidney regeneration, and thus repair, is inadequate because progenitors are unable to replace and restore
glomerular podocytes. We anticipate that the results will provide compelling evidence for a new paradigm in aging kidneys in which recently
identified progenitors are unable to adequately regenerate to replace podocytes, which leads to glomerulosclerosis and reduced kidney
NIH/NIDDK 5 T32 DL07467-31 (Shankland) 7/15/1993-6/30/2019
Training in Renal Disease
This is a training grant that supports research training for three M.D. post-graduate fellows who undergoperiods of both renal and basic
science research training.
NIH R01 5 R01 DK093493-02 (Shankland) PI 9/03/2012-6/30/2017
Pericyte-endothelial cross talk in vascular stability after kidney injury
These studies will investigate the mechanisms by which pericytes nurture kidney blood vessels and the mechanisms by which they detach in
response to injury and thereafter fail to nurture. In understanding these processes we hope to develop new therapies to treat kidney diseases.
Multi-Clonal Population of Cells of Renin Lineage (CoRL) Transdifferentiate into Podocytes and PECs in Experimental FSGS
RAS Inhibition Enhances Proliferation and Migration of Cells of Renin Lineage (CoRL) as Progenitors in Experimental FSGS
2017 American Society of Nephrology Annual Meeting, New Orleans, LA
“Podocyte Regeneration from Renin Lineage Cells”
2015 American Society of Nephrology Annual Meeting, San Diego, CA
"What is Aging Nephropathy?"
"Role of Parietal Cells Following Glomerular Injury"
The Lab Gang