The Basile Lab seeks to better understand the pathophysiology of kidney disease.

Basile Lab

The laboratory of Dr. David Basile seeks to better understand the pathophysiology of kidney disease with a focus on alterations vascular function, remodeling and immune cell activity. Areas of research include are primarily focused on a number of hypotheses related to how acute kidney injury (AKI) may link to progression of chronic kidney disease (CKD). The group utilizes a number of different experimental models of kidney injury to define the cellular and molecular alterations in immune response as well as integrative approaches to evaluate alterations in kidney hemodynamics and vascular remodeling.

Work in my laboratory has been directed toward elucidating the pathophysiology of acute kidney injury (AKI) and chronic kidney disease (CKD). Since 2001, my lab has focused on studying the functional chronic consequences of acute kidney injury with particular questions related to the altered vasculature and immune function. Our projects span the use of pre-clinical models of kidney injury, strategies to focus on cellular and pathophysiological events leading to renal damage and the application of novel therapies. The major areas of research in my laboratory are summarized below:

  1. Causes of CKD following AKI
    My laboratory is well-versed with the models and methodologies related to the establishment of renal injury, the measurements of CKD and fibrosis, evaluation of capillary structure and the isolation and culture of endothelial cells from kidney and other organs. We are also capable of whole animal physiological measurements including measurements of blood flow and blood pressure by telemetry and multiple molecular biological and imaging techniques geared at measuring gene and protein expression. Recent studies in this area have focused on how renal injury alters the profile of lymphocytes with potential pro-inflammatory and renal hemodynamic consequences.
  2. Influences of mitochondrial adaptations on resistance to ischemic injury
    Work in collaboration with Dr. Bacallao in the Division of Nephrology have focused on how adaptations in the mitochondrial proteome may provide resistance to injury following renal ischemia reperfusion. These studies involve investigation of experimental and genetic models of AKI resistance, methods to over express mitochondrial genes in kidney in vivo, investigation of mitochondrial responses using respiratory and microscopy methodologies.
  3. Investigation into renal endothelial stem and progenitor cells
    In collaboration with Dr. Mervin Yoder in the Department of Pediatrics, we have successfully established long term cultures of renal derived endothelial cells from rats and mice. These studies are focused on the long term goal of re-establishing renal vascularization by using either ECFC based cell-therapy or determining ways to improve endogenous renal endothelial proliferative capacity. We have investigated the unique cellular properties of renal derived endothelial cells and demonstrated and identified ABCG2 as a potential marker of the ECFCs and are investigating the role of these cells in the setting of renal development and repair. We have also conducted studies using ECFC as potential therapeutic treatment in kidney injury. 

Current Research Funding

1RO1 DK 063114 PI-Basile 10/1/17-6/30/22 (No cost ext)

Long-term effects of acute renal failure
This application was originally funded in 2003 to investigate the pathophysiological mechanisms predisposing the development of AKI-to-CKD. In the most recent project period, the goals of the application were to 1) determine how Th17 cell activity alters renal function predisposing kidney injury, 2) to investigate the potential role of store-operated Ca2+ in Th17 activation, 3) to investigate levels of IL17A in clinical samples from patients with AKI with or without subsequent CKD.

VA- 1 IO BX00518401 PI-Bacallao (Role: Co-I) 4/1/20-3/31/25

Mitochondrial functions modified by sulfotransferase 1C2
The goals of this project are to investigate the potential role of sulfotransferase 1C2 on the protection of mitochondrial function in the setting of kidney injury, with particular emphasis on alterations mitochondrial membrane cholesterol

1R37CA262238-01 PI-Lautenschlaeger (Role: Co-I) 7/1/21-6/30/27

Urine based circulating tumor DNA analysis
The goals of this project are to evaluate the potential of using tumor based circulating DNA as diagnostic measure of tumor recurrence in blood and urine. Studies in animal models evaluate the renal handling of circulating DNA.

Indiana CTSI/CTR Co-PIs (Basile, D & Schlader, Z) 5/1/21-4/30/23

Heat waves, aging and the kidneys
The pilot funded project with Dr. Schlader at IU-Bloomington seeks to develop an animal model of heat stress induced-kidney injury in aging rats with the goal of investigating interventional treatments to mitigate kidney damage in aging populations in the face of heat waves.

Recently Completed Research

1R43DK125142-01A1 Singh, Jaipal (Vasculonics) (Role: PI of IU component) 9/1/20-8/31/21

A Potential DDAH-Biotherapeutic to Preserve Kidney Function in Cardiac Surgery Patients
The major goals of this project are to evaluate novel modified DDAH as means to lower renal and circulating ADMA levels to mitigate acute kidney injury.

NIH-R41-115357    Coleman (Theratome) (PI; IU component) 10/1/18-9/30/19 

Mitigation of acute and chronic kidney injury by systemic infusion of adipose derived soluble therapeutic factor
This application is designed to investigate the potential therapeutic benefit of the secretome of adipose stromal cells (ASC) on renal injury in a pre-clinical model of acute renal ischemia reperfusion injury.

17GRNT33671036 Basile/Yoder Co PI 7/1/2017-6/30/19

American Heart Association
Role of endothelial side population as a source of endothelial progenitor cells during growth or response to injury
The role of this project is to test the hypothesis that endothelial side population represents an enriched population of cells in progenitor activity.  The studies will explore with renal side population cells have lower progenitor potential than cells from other beds and will explore whether these cells are activated in response to renal injury. 

Recent Publications

Ullah, MM and Basile DP.  Role of renal hypoxia in the progression from acute kidney injury to chronic kidney disease. Semin Nephrol. 2019, 39:567-580.  PMID: 31836039; PubMed Central PMCID: PMC6917038 

Basile DP, Collett JA, Yoder MC. Endothelial colony-forming cells and pro-angiogenic cells: clarifying definitions and their potential role in mitigating acute kidney injury. Acta Physiol (Oxf). 2017 Jun 28;PubMed PMID: 28656611.

Kolb AL, Corridon PR, Zhang S, Xu W, Witzmann FA, Collett JA, Rhodes GJ, Winfree S, Bready D, Pfeffenberger ZJ, Pomerantz JM, Hato T, Nagami GT, Molitoris BA, Basile DP, Atkinson SJ, Bacallao.  Exogenous gene transmission of isocitrate dehydrogenase 2 mimics ischemic preconditioning protection.  J. Am Soc Nephrol 29:1154-64, 2018.  PMCID: PMC5875948

Mehrotra P, Sturek MS, Neyra JA, Basile DP.  Calcium channel Orai1 promotes lymphocyte IL17 expression and progressive kidney injury. J. Clin Invest, 129:4951-61, 2019. PubMed PMID: 31415242; PubMed Central PMCID: PMC6819116

Collett JA, Ortiz-Soriano VM, Li X, Flannery AH, Toto RD, Moe OW, Basile DP, and Neyra JA.  IL-17 levels are higher in patients with AKI and associate with mortality and major adverse kidney events. Critical Care 26:107, 2022. PMCID: PMC9008961

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