Amandeep Bajwa

University of Tennessee Health Science Center

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Mark D. Okusa

University of Virginia

Bijay Bisunke

Institut thématique Génétique, génomique et bioinformatique

Diane L. Rosin

University of Udine

Manjul Rana

University of Tennessee Health Science Center

Jun Yang

St. Jude Children's Research Hospital

Jie Fang

St. Jude Children's Research Hospital

Evan S. Glazer

Ben-Gurion University of the Negev

David Shibata

University of Tennessee Health Science Center

Rita G. Kansal

University of Tennessee Health Science Center

Hong Ye

Yichang Central People's Hospital

Cooperative Institutions

University of Virginia

University of Tennessee Health Science Center

The Ohio State University

University of Virginia Health System

Harvard University

Immunité et Cancer

University of Tennessee at Knoxville

Boston Children's Hospital

University of Toronto

The University of Tokyo

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Supplementary Figure Legends from Bromo- and Extra-Terminal Domain Inhibitors Induce Mitochondrial Stress in Pancreatic Ductal Adenocarcinoma

Manjul Rana Rita G. Kansal Bijay Bisunke Jie Fang David Shibata

<p>Supplementary Figure Legends</p>

10.1158/1535-7163.27036136

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Epithelial and Endothelial Pannexin1 Channels Mediate AKI

Journal of the American Society of Nephrology (2018)

Jakub Jankowski Heather M. Perry Christopher B. Medina Liping Huang Junlan Yao

Background Pannexin1 (Panx1), an ATP release channel, is present in most mammalian tissues, but the role of Panx1 in health and disease is not fully understood. Panx1 may serve to modulate AKI; ATP is a precursor to adenosine and may function to block inflammation, or ATP may act as a danger-associated molecular pattern and initiate inflammation. Methods We used pharmacologic and genetic approaches to evaluate the effect of Panx1 on kidney ischemia-reperfusion injury (IRI), a mouse model of AKI. Results Pharmacologic inhibition of gap junctions, including Panx1, by administration of carbenoxolone protected mice from IRI. Furthermore, global deletion of Panx1 preserved kidney function and morphology and diminished the expression of proinflammatory molecules after IRI. Analysis of bone marrow chimeric mice revealed that Panx1 expressed on parenchymal cells is necessary for ischemic injury, and both proximal tubule and vascular endothelial Panx1 tissue-specific knockout mice were protected from IRI. In vitro , Panx1 -deficient proximal tubule cells released less and retained more ATP under hypoxic stress. Conclusions Panx1 is involved in regulating ATP release from hypoxic cells, and reducing this ATP release may protect kidneys from AKI.

Carbenoxolone

Proinflammatory cytokine

Knockout mouse

10.1681/asn.2017121306

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Identification of APOL1 with Probe-Independent Polymerase Chain Reaction (PCR) Method

Journal of the American Society of Nephrology (2023)

Murat Doğan Anshul Bhalla Amandeep Bajwa Canan Kuscu Cem Kuscu

Identification

10.1681/asn.20233411s11152c

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Obesity Has Opposing Effects on Acute vs. Chronic Kidney Disease

Journal of the American Society of Nephrology (2020)

Thomas Rousselle James D. Eason Daniel G. Maluf Valeria R. Mas Amandeep Bajwa

Rousselle, Thomas V.; Eason, James D.; Maluf, Daniel; Mas, Valeria R.; Bajwa, Amandeep Author Information

10.1681/asn.20203110s159c

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Mesenchymal stem cells induce Foxp3-Tregs to suppress effector T cells and protect against retinal ischemic injury

Investigative Ophthalmology & Visual Science (2021)

Rajashekhar Gangaraju Mona Agrawal Pratheepa Kumari Rasiah Amandeep Bajwa Johnson Rajasingh

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QW-1624F2-2, a synthetic analogue of 1,25-dihydroxyvitamin D3, enhances the response to other deltanoids and suppresses the invasiveness of human metastatic breast tumor cells

Molecular Cancer Therapeutics (2006)

Sujatha Sundaram Matthew J. Beckman Amandeep Bajwa Jeffrey Wei Kathleen M. Smith

The enzyme 24-hydroxylase, also known as CYP24, metabolizes 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] and is an established marker of vitamin D activity. Our studies evaluated the influence of a low-calcemic 1,25(OH)(2)D(3) analogue, QW-1624F2-2 (QW), on the regulation of CYP24 expression in MKL-4 cells, a metastatic mammary tumor cell model. 1,25(OH)(2)D(3) and its analogue, EB 1089, stimulated CYP24 induction at both protein and transcript levels. In contrast, QW failed to produce a sustained stimulation of CYP24, due, in large part, to a reduction in the stability of the CYP24 message. QW enhanced the capacity of 1,25(OH)(2)D(3) and EB 1089 to inhibit tumor cell proliferation by approximately 2-fold. QW also blocked the sustained induction of CYP24 expression by 1,25(OH)(2)D(3) and EB 1089, increased the potency of 1,25(OH)(2)D(3) and EB 1089, and inhibited breast tumor cell proliferation and invasion.

10.1158/1535-7163.mct-06-0092

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Role of Mitochondrial Therapy for Ischemic-Reperfusion Injury and Acute Kidney Injury

The Nephron journals/Nephron journals (2021)

Navjotsingh Pabla Amandeep Bajwa

Acute kidney injury (AKI) is a common clinical disorder associated with decline in renal function because of ischemic and nephrotoxic insults. The pathophysiology of AKI involves multiple cellular mechanisms, such as kidney parenchymal cell (epithelial and endothelial) dysfunction and immune-cell infiltration. Mitochondrial injury which causes ATP depletion and triggers apoptosis and necrosis is at the heart of ischemia reperfusion injury (IRI). Pharmacological (SS-31 or MitoQ), cellular (dendritic cells or mesenchymal stem cells), or genetic strategies that either directly or indirectly preserve mitochondrial integrity and function have been shown to mitigate IRI-linked AKI in preclinical models. Interestingly, isolated mitochondria have been recently shown to be taken up by various mammalian cells resulting in incorporation of transplanted mitochondria into the endogenous mitochondrial network of recipient cells and contributing to protection from ischemic injury in various preclinical models of ischemia including the heart, liver, and kidneys. The mini review summarizes the current available therapeutic strategies that improve kidney function by targeting mitochondria health.

Cell therapy

10.1159/000520698

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Mitochondrial transplantation by intra-arterial injection for acute kidney injury

AJP Renal Physiology (2020)

Ilias P. Doulamis Alvise Guariento Thomas Duignan Takashi Kido Arzoo Orfany

Acute kidney injury is a common clinical disorder and one of the major causes of morbidity and mortality in the postoperative period. In this study, the safety and efficacy of autologous mitochondrial transplantation by intra-arterial injection for renal protection in a swine model of bilateral renal ischemia-reperfusion injury were investigated. Female Yorkshire pigs underwent percutaneous bilateral temporary occlusion of the renal arteries with balloon catheters. Following 60 min of ischemia, the balloon catheters were deflated and animals received either autologous mitochondria suspended in vehicle or vehicle alone, delivered as a single bolus to the renal arteries. The injected mitochondria were rapidly taken up by the kidney and were distributed throughout the tubular epithelium of the cortex and medulla. There were no safety-related issues detected with mitochondrial transplantation. Following 24 h of reperfusion, estimated glomerular filtration rate and urine output were significantly increased while serum creatinine and blood urea nitrogen were significantly decreased in swine that received mitochondria compared with those that received vehicle. Gross anatomy, histopathological analysis, acute tubular necrosis scoring, and transmission electron microscopy showed that the renal cortex of the vehicle-treated group had extensive coagulative necrosis of primarily proximal tubules, while the mitochondrial transplanted kidney showed only patchy mild acute tubular injury. Renal cortex IL-6 expression was significantly increased in vehicle-treated kidneys compared with the kidneys that received mitochondrial transplantation. These results demonstrate that mitochondrial transplantation by intra-arterial injection provides renal protection from ischemia-reperfusion injury, significantly enhancing renal function and reducing renal damage.

Renal cortex

Acute tubular necrosis

Blood urea nitrogen

Renal ischemia

10.1152/ajprenal.00255.2020

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Sphingosine Kinase 2 Deficiency Attenuates Kidney Fibrosis via IFN-γ

Journal of the American Society of Nephrology (2016)

Amandeep Bajwa Liping Huang Elvira Kurmaeva Ye Hong Krishna R. Dondeti

Maladaptive repair after AKI may lead to progressive fibrosis and decline in kidney function. Sphingosine 1-phosphate has an important role in kidney injury and pleiotropic effects in fibrosis. We investigated the involvement of sphingosine kinase 1 and 2 (SphK1 and SphK2), which phosphorylate sphingosine to produce sphingosine 1-phosphate, in kidney fibrosis induced by folic acid (FA) or unilateral ischemia-reperfusion injury. Analysis of Masson trichrome staining and fibrotic marker protein and mRNA expression 14 days after AKI revealed that wild-type (WT) and Sphk1-/- mice exhibited more kidney fibrosis than Sphk2-/- mice. Furthermore, kidneys of FA-treated WT and Sphk1-/- mice had greater immune cell infiltration and expression of fibrotic and inflammatory markers than kidneys of FA-treated Sphk2-/- mice. In contrast, kidneys of Sphk2-/- mice exhibited greater expression of Ifng and IFN-γ-responsive genes (Cxcl9 and Cxcl10) than kidneys of WT or Sphk1-/- mice did at this time point. Splenic T cells from untreated Sphk2-/- mice were hyperproliferative and produced more IFN-γ than did those of WT or Sphk1-/- mice. IFN-γ blocking antibody administered to Sphk2-/- mice or deletion of Ifng (Sphk2-/-Ifng-/- mice) blocked the protective effect of SphK2 deficiency in fibrosis. Moreover, adoptive transfer of Sphk2-/- (but not Sphk2-/-Ifng-/- ) CD4 T cells into WT mice blocked FA-induced fibrosis. Finally, a selective SphK2 inhibitor blocked FA-induced kidney fibrosis in WT mice. These studies demonstrate that SphK2 inhibition may serve as a novel therapeutic approach for attenuating kidney fibrosis.

Sphingosine kinase 1

Sphingosine Kinase

10.1681/asn.2016030306

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SOX9 promotes stress-responsive transcription of VGF nerve growth factor inducible gene in kidney epithelial cells

bioRxiv (Cold Spring Harbor Laboratory) (2020)

JY Kim Yuntao Bai Laura A. Jayne Ferdos Abdulkader Megha Gandhi

Abstract Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, as well as cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxic, cytotoxic, and inflammatory insults to renal tubular epithelial cells (RTECs) resulting in the onset of AKI. To uncover stress-responsive disease-modifying genes, here we have carried out renal transcriptome profiling in three distinct murine models of AKI. We find that Vgf nerve growth factor inducible gene upregulation is a common transcriptional stress response in RTECs to ischemia, cisplatin, and rhabdomyolysis-associated renal injury. The Vgf gene encodes a secretory peptide precursor protein that has critical neuro-endocrine functions; however, its role in the kidneys remains unknown. Our functional studies show that RTEC-specific Vgf gene ablation exacerbates ischemia, cisplatin, and rhabdomyolysis-associated AKI in vivo and cisplatin-induced RTEC cell death in vitro. Importantly, addback experiments showed that aggravation of cisplatin-induced renal injury caused by Vgf gene ablation is partly reversed by TLQP-21, a Vgf-derived peptide. Finally, in vitro and in vivo mechanistic studies showed that injury-induced Vgf upregulation in RTECs is driven by the transcriptional regulator Sox9. These findings reveal a crucial downstream target of the Sox9-directed transcriptional program and identify Vgf as a stress-responsive protective gene in kidney epithelial cells.

10.1101/2020.07.06.189829

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Citations (1)