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Article ; Online: Are Pax proteins potential therapeutic targets in kidney disease and cancer?

Grimley, Edward / Dressler, Gregory R

2018 Volume 94, Issue 2, Page(s) 259–267

Abstract: Pax genes encode developmental regulators that are expressed in a variety of tissues and control critical events in morphogenesis. In the kidney, Pax2 and Pax8 are expressed in embryonic development and in specific renal diseases associated with aberrant ...

Abstract	Pax genes encode developmental regulators that are expressed in a variety of tissues and control critical events in morphogenesis. In the kidney, Pax2 and Pax8 are expressed in embryonic development and in specific renal diseases associated with aberrant epithelial cell proliferation. Prior genetic and cell biological studies suggest that reducing the activity of Pax proteins in renal cancer or in polycystic kidney disease can slow the progression of these conditions. The Pax proteins may be critical for providing tissue and locus specificity to recruit epigenetic modifiers that control gene expression and chromatin structure. Although they are nuclear, targeting Pax proteins to inhibit function may be feasible with small molecules. Such inhibition of Pax protein function may provide novel therapies for subsets of renal disorders that are tissue- and cell type-specific and avoid systemic effects on non-Pax-expressing cells and tissues. Given the paucity of effective treatments for renal cancer and cystic disease, the Pax family of proteins represents new pharmaceutical targets that merit exploration and further development.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Disease Progression ; Epigenesis, Genetic/drug effects ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Gene Expression Regulation, Developmental/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Kidney/cytology ; Kidney/growth & development ; Kidney/metabolism ; Kidney Neoplasms/drug therapy ; Kidney Neoplasms/genetics ; Kidney Neoplasms/pathology ; Molecular Targeted Therapy/methods ; PAX2 Transcription Factor/antagonists & inhibitors ; PAX2 Transcription Factor/genetics ; PAX2 Transcription Factor/metabolism ; PAX8 Transcription Factor/antagonists & inhibitors ; PAX8 Transcription Factor/genetics ; PAX8 Transcription Factor/metabolism ; Polycystic Kidney Diseases/drug therapy ; Polycystic Kidney Diseases/genetics ; Polycystic Kidney Diseases/pathology ; Protein Domains/drug effects ; Urothelium/cytology ; Urothelium/drug effects ; Urothelium/metabolism ; Urothelium/pathology
Chemical Substances	Antineoplastic Agents ; PAX2 Transcription Factor ; PAX2 protein, human ; PAX8 Transcription Factor ; PAX8 protein, human
Language	English
Publishing date	2018-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2018.01.025
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Article ; Online: Renal-specific loss of ferroportin disrupts iron homeostasis and attenuates recovery from acute kidney injury.

Soofi, Abdul / Li, Vivie / Beamish, Jeffrey A / Abdrabh, Sham / Hamad, Mawieh / Das, Nupur K / Shah, Yatrik M / Dressler, Gregory R

American journal of physiology. Renal physiology

2023 Volume 326, Issue 2, Page(s) F178–F188

Abstract: Chronic kidney disease is increasing at an alarming rate and correlates with the increase in diabetes, obesity, and hypertension that disproportionately impact socioeconomically disadvantaged communities. Iron plays essential roles in many biological ... ...

Abstract	Chronic kidney disease is increasing at an alarming rate and correlates with the increase in diabetes, obesity, and hypertension that disproportionately impact socioeconomically disadvantaged communities. Iron plays essential roles in many biological processes including oxygen transport, mitochondrial function, cell proliferation, and regeneration. However, excess iron induces the generation and propagation of reactive oxygen species, which lead to oxidative stress, cellular damage, and ferroptosis. Iron homeostasis is regulated in part by the kidney through iron resorption from the glomerular filtrate and exports into the plasma by ferroportin (FPN). Yet, the impact of iron overload in the kidney has not been addressed. To test more directly whether excess iron accumulation is toxic to kidneys, we generated a kidney proximal tubule-specific knockout of FPN. Despite significant intracellular iron accumulation in FPN mutant tubules, basal kidney function was not measurably different from wild type kidneys. However, upon induction of acute kidney injury (AKI), FPN mutant kidneys exhibited significantly more damage and failed recovery, evidence for ferroptosis, and increased fibrosis. Thus, disruption of iron export in proximal tubules, leading to iron overload, can significantly impair recovery from AKI and can contribute to progressive renal damage indicative of chronic kidney disease. Understanding the mechanisms that regulate iron homeostasis in the kidney may provide new therapeutic strategies for progressive kidney disease and other ferroptosis-associated disorders.
MeSH term(s)	Humans ; Kidney/metabolism ; Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Iron/metabolism ; Iron Overload/metabolism ; Homeostasis/physiology ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/metabolism ; Cation Transport Proteins
Chemical Substances	metal transporting protein 1 ; Iron (E1UOL152H7) ; Cation Transport Proteins
Language	English
Publishing date	2023-11-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00184.2023
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Article ; Online: Patient-reported outcomes in a pilot clinical trial of twice-weekly hemodialysis start with adjuvant pharmacotherapy and transition to thrice-weekly hemodialysis vs conventional hemodialysis.

Murea, Mariana / Highland, Benjamin R / Yang, Wesley / Dressler, Emily / Russell, Gregory B

BMC nephrology

2022 Volume 23, Issue 1, Page(s) 322

Abstract: Background: Physical and emotional symptoms are prevalent in patients with kidney-dysfunction requiring dialysis (KDRD) and the rigors of thrice-weekly hemodialysis (HD) may contribute to deteriorated health-related quality of life. Less intensive HD ... ...

Abstract	Background: Physical and emotional symptoms are prevalent in patients with kidney-dysfunction requiring dialysis (KDRD) and the rigors of thrice-weekly hemodialysis (HD) may contribute to deteriorated health-related quality of life. Less intensive HD schedules might be associated with lower symptom and/or emotional burden. Methods: The TWOPLUS Pilot study was an individually-randomized trial conducted at 14 dialysis units, with the primary goal to assess feasibility and safety. Patients with incident KDRD and residual kidney function were assigned to incremental HD start (twice-weekly HD for 6 weeks followed by thrice-weekly HD) vs conventional HD (thrice-weekly HD). In exploratory analyses, we compared the two treatment groups with respect to three patient-reported outcomes measures. We analyzed the change from baseline in the score on Dialysis Symptom Index (DSI, range 0-150), Generalized Anxiety Disorder-7 (GAD-7, range 0-21), and Patient Health Questionnaire-9 (PHQ-9, range 0-27) at 6 (n = 20 in each treatment group) and 12 weeks (n = 21); with lower scores denoting lower symptom burden. Analyses were adjusted for age, race, gender, baseline urine volume, diabetes mellitus, and malignancy. Participants' views on the intervention were sought using a Patient Feedback Questionnaire (n = 14 in incremental and n = 15 in conventional group). Results: The change from baseline to week 6 in estimated mean score (standard error; P value) in the incremental and conventional group was - 9.7 (4.8; P = 0.05) and - 13.8 (5.0; P = 0.009) for DSI; - 1.9 (1.0; P = 0.07) and - 1.5 (1.4; P = 0.31) for GAD-7; and - 2.5 (1.1; P = 0.03) and - 3.5 (1.5; P = 0.02) for PHQ-9, respectively. Corresponding changes from week 6 to week 12 were - 3.1 (3.2; P = 0.34) and - 2.4 (5.5; P = 0.67) in DSI score; 0.5 (0.6; P = 0.46) and 0.1 (0.6; P = 0.87) in GAD-7 score; and - 0.3 (0.6; P = 0.70) and - 0.5 (0.6; P = 0.47) in PHQ-9 score, respectively. Majority of respondents felt their healthcare was not jeopardized and expressed their motivation for study participation was to help advance the care of patients with KDRD. Conclusions: This study suggests a possible mitigating effect of twice-weekly HD start on symptoms of anxiety and depression at transition from pre-dialysis to KDRD. Larger clinical trials are required to rigorously test clinically-matched incrementally-prescribed HD across diverse organizations and patient populations. Trial registration: Registered at ClinicalTrials.gov with study identifier NCT03740048, registration date 14/11/2018.
MeSH term(s)	Humans ; Kidney Failure, Chronic/therapy ; Patient Reported Outcome Measures ; Pilot Projects ; Quality of Life ; Renal Dialysis/methods
Language	English
Publishing date	2022-09-27
Publishing country	England
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	2041348-8
ISSN	1471-2369 ; 1471-2369
ISSN (online)	1471-2369
ISSN	1471-2369
DOI	10.1186/s12882-022-02946-w
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Article ; Online: Polarity and renal cystogenesis.

Dressler, Gregory R

Journal of the American Society of Nephrology : JASN

2011 Volume 23, Issue 1, Page(s) 4–5

MeSH term(s)	Animals ; Cell Polarity ; ErbB Receptors/metabolism ; Humans ; Kidney Tubules/embryology ; Receptor, ErbB-4
Chemical Substances	ERBB4 protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; Receptor, ErbB-4 (EC 2.7.10.1)
Language	English
Publishing date	2011-12-08
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2011111121
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Article ; Online: Patterning and early cell lineage decisions in the developing kidney: the role of Pax genes.

Dressler, Gregory R

Pediatric nephrology (Berlin, Germany)

2011 Volume 26, Issue 9, Page(s) 1387–1394

Abstract: Specification of the intermediate mesoderm and the epithelial derivatives that will make the mammalian kidney depends on the concerted action of many transcription factors and signaling proteins. Among the earliest genes expressed in the nephric duct and ...

Abstract	Specification of the intermediate mesoderm and the epithelial derivatives that will make the mammalian kidney depends on the concerted action of many transcription factors and signaling proteins. Among the earliest genes expressed in the nephric duct and surrounding mesenchyme is Pax2, whose function is essential for making and maintaining the epithelium. The Pax2 protein is subject to phosphorylation in response to signals that activate the c-Jun N-terminal kinase pathway, including Wnts and BMPs. In cell culture systems, Pax2 is know to recruit components of a histone H3 lysine 4 methyltransferase complex to specific DNA sites to alter the pattern of histone modifications and determine gene expression. This epigenetic function may underlie the ability of Pax2 and similar proteins to maintain cell lineages during development.
MeSH term(s)	Animals ; Body Patterning/genetics ; Cell Lineage/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Humans ; Kidney/embryology ; Kidney/metabolism ; PAX2 Transcription Factor/genetics ; PAX2 Transcription Factor/metabolism ; Signal Transduction/genetics
Chemical Substances	PAX2 Transcription Factor
Language	English
Publishing date	2011-01-11
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-010-1749-x
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Article: Pax Protein Depletion in Proximal Tubules Triggers Conserved Mechanisms of Resistance to Acute Ischemic Kidney Injury and Prevents Transition to Chronic Kidney Disease.

Beamish, Jeffrey A / Telang, Asha C / McElliott, Madison C / Al-Suraimi, Anas / Chowdhury, Mahboob / Ference-Salo, Jenna T / Otto, Edgar A / Menon, Rajasree / Soofi, Abdul / Weinberg, Joel M / Patel, Sanjeevkumar R / Dressler, Gregory R

bioRxiv : the preprint server for biology

2023

Abstract: Acute kidney injury (AKI) is a common condition that lacks effective treatments. In part this shortcoming is due to an incomplete understanding of the genetic mechanisms that control pathogenesis and recovery. Pax2 and Pax8 are homologous transcription ... ...

Abstract	Acute kidney injury (AKI) is a common condition that lacks effective treatments. In part this shortcoming is due to an incomplete understanding of the genetic mechanisms that control pathogenesis and recovery. Pax2 and Pax8 are homologous transcription factors with overlapping functions that are critical for kidney development and are re-activated in AKI. In this report, we examined the role of Pax2 and Pax8 in recovery from ischemic AKI. We found that Pax2 and Pax8 are upregulated after severe AKI and correlate with chronic injury. Surprisingly, we then discovered that proximal-tubule-selective deletion of Pax2 and Pax8 resulted in a less severe chronic injury phenotype. This effect was mediated by protection against the acute insult, similar to preconditioning. Prior to injury, Pax2 and Pax8 mutant mice develop a unique subpopulation of S3 proximal tubule cells that display features usually seen only in acute or chronic injury. The expression signature of these cells was strongly enriched with genes associated with other mechanisms of protection against ischemic AKI including caloric restriction, hypoxic preconditioning, and female sex. Taken together, our results identify a novel role for Pax2 and Pax8 in mature proximal tubules that regulates critical genes and pathways involved in both injury response and protection from ischemic AKI. Translational statement: Identifying the molecular and genetic regulators unique to the nephron that dictate vulnerability to injury and regenerative potential could lead to new therapeutic targets to treat ischemic kidney injury. Pax2 and Pax8 are two homologous nephron-specific transcription factors that are critical for kidney development and physiology. Here we report that proximal-tubule-selective depletion of Pax2 and Pax8 protects against both acute and chronic injury and induces an expression profile in the S3 proximal tubule with common features shared among diverse conditions that protect against ischemia. These findings highlight a new role for Pax proteins as potential therapeutic targets to treat AKI.
Language	English
Publishing date	2023-10-05
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.03.559511
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Article ; Online: Pax protein depletion in proximal tubules triggers conserved mechanisms of resistance to acute ischemic kidney injury preventing transition to chronic kidney disease.

Kidney international

2023 Volume 105, Issue 2, Page(s) 312–327

Abstract: Acute kidney injury (AKI) is a common condition that lacks effective treatments. In part, this shortcoming is due to an incomplete understanding of the genetic mechanisms that control pathogenesis and recovery. Identifying the molecular and genetic ... ...

Abstract	Acute kidney injury (AKI) is a common condition that lacks effective treatments. In part, this shortcoming is due to an incomplete understanding of the genetic mechanisms that control pathogenesis and recovery. Identifying the molecular and genetic regulators unique to nephron segments that dictate vulnerability to injury and regenerative potential could lead to new therapeutic targets to treat ischemic kidney injury. Pax2 and Pax8 are homologous transcription factors with overlapping functions that are critical for kidney development and are re-activated in AKI. Here, we examined the role of Pax2 and Pax8 in recovery from ischemic AKI and found them upregulated after severe AKI and correlated with chronic injury. Surprisingly, proximal-tubule-selective deletion of Pax2 and Pax8 resulted in a less severe chronic injury phenotype. This effect was mediated by protection against the acute insult, similar to pre-conditioning. Prior to injury, Pax2 and Pax8 mutant mice develop a unique subpopulation of proximal tubule cells in the S3 segment that displayed features usually seen only in acute or chronic injury. The expression signature of these cells was strongly enriched with genes associated with other mechanisms of protection against ischemic AKI including caloric restriction, hypoxic pre-conditioning, and female sex. Thus, our results identified a novel role for Pax2 and Pax8 in mature proximal tubules that regulates critical genes and pathways involved in both the injury response and protection from ischemic AKI.
MeSH term(s)	Animals ; Female ; Mice ; Acute Kidney Injury/complications ; Acute Kidney Injury/genetics ; Ischemia/complications ; Kidney Tubules, Proximal/pathology ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/genetics ; Reperfusion Injury/genetics ; PAX8 Transcription Factor/genetics ; PAX8 Transcription Factor/metabolism ; PAX2 Transcription Factor/genetics ; PAX2 Transcription Factor/metabolism
Chemical Substances	Pax2 protein, mouse ; Pax8 protein, mouse ; PAX8 Transcription Factor ; PAX2 Transcription Factor
Language	English
Publishing date	2023-11-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.10.022
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Article ; Online: Expression Profiling of Fibroblasts in Chronic and Acute Disease Models Reveals Novel Pathways in Kidney Fibrosis.

Higashi, Atsuko Y / Aronow, Bruce J / Dressler, Gregory R

Journal of the American Society of Nephrology : JASN

2018 Volume 30, Issue 1, Page(s) 80–94

Abstract: Background: Renal interstitial fibrosis results from activation and proliferation of fibroblasts to myofibroblasts, secretion and accumulation of extracellular matrix, and displacement of normal renal tubules. In contrast to chronic renal disease, acute ...

Abstract	Background: Renal interstitial fibrosis results from activation and proliferation of fibroblasts to myofibroblasts, secretion and accumulation of extracellular matrix, and displacement of normal renal tubules. In contrast to chronic renal disease, acute injury may be repaired, a process that includes a decrease in the number of myofibroblasts in the interstitium and degradation of the accumulated extracellular matrix, leaving little evidence of prior injury. Methods: To investigate whether activated fibroblasts demonstrate changes in gene expression that correspond with regression after acute injury but are not observed in chronic models of fibrosis, we used microarrays to analyze gene expression patterns among fibroblast populations at different stages of injury or repair. We then mined the data for signaling pathways in fibroblasts corresponding to the acute proliferative, regression, and chronic phases of renal injury. Results: We identified multiple gene clusters with changes that correlate with the three phases of renal injury, including changes in levels of receptors for the antifibrotic factor PGE2. In adult renal fibroblast cultures, PGE2 was able to upregulate many genes that are suppressed by the profibrotic cytokine TGF- Conclusions: Inherent gene expression changes in activated fibroblasts accompany the transition from AKI to repair and regeneration. In chronic models, however, activated fibroblasts are resistant to the antifibrotic effects of PGE2 due to suppression of a subset of PGE receptors.
MeSH term(s)	Acute Kidney Injury/genetics ; Acute Kidney Injury/pathology ; Animals ; Cell Differentiation/genetics ; Cells, Cultured ; Dinoprostone/pharmacology ; Disease Models, Animal ; Extracellular Matrix/metabolism ; Fibroblasts/cytology ; Fibrosis/genetics ; Fibrosis/pathology ; Gene Expression Profiling ; Gene Expression Regulation ; Immunohistochemistry ; Mice ; Myofibroblasts/cytology ; Real-Time Polymerase Chain Reaction/methods ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/pathology ; Signal Transduction/genetics
Chemical Substances	Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2018-12-13
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2018060644
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Article ; Online: Turning the page on epigenetic bookmarks.

Dressler, Gregory R

Developmental cell

2010 Volume 18, Issue 1, Page(s) 4–5

Abstract: Cells remember established patterns of gene expression through rounds of cell division despite dynamic changes in genomic chromatin structure. Two recent studies in Molecular Cell and Nature Medicine, broadly impacting on epigenetic gene regulation and ... ...

Abstract	Cells remember established patterns of gene expression through rounds of cell division despite dynamic changes in genomic chromatin structure. Two recent studies in Molecular Cell and Nature Medicine, broadly impacting on epigenetic gene regulation and disease, address how cells remember and suggest that both histone methyltransferases and locus specific DNA binding proteins can mark transcribed genes for reactivation after mitosis.
MeSH term(s)	Animals ; Binding Sites/genetics ; DNA Methylation/genetics ; DNA-Binding Proteins/genetics ; Drosophila Proteins/genetics ; Epigenesis, Genetic/genetics ; Gene Expression Regulation/genetics ; Hepatocyte Nuclear Factor 1-beta/genetics ; Histone Methyltransferases ; Histone-Lysine N-Methyltransferase/genetics ; Humans ; Mitosis/genetics ; Transcriptional Activation/genetics
Chemical Substances	DNA-Binding Proteins ; Drosophila Proteins ; Hepatocyte Nuclear Factor 1-beta (138674-15-4) ; Histone Methyltransferases (EC 2.1.1.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; PRC2 protein, Drosophila (EC 2.1.1.43)
Language	English
Publishing date	2010-01-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2010.01.004
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Article ; Online: High-throughput image analysis with deep learning captures heterogeneity and spatial relationships after kidney injury.

McElliott, Madison C / Al-Suraimi, Anas / Telang, Asha C / Ference-Salo, Jenna T / Chowdhury, Mahboob / Soofi, Abdul / Dressler, Gregory R / Beamish, Jeffrey A

Scientific reports

2023 Volume 13, Issue 1, Page(s) 6361

Abstract: Recovery from acute kidney injury can vary widely in patients and in animal models. Immunofluorescence staining can provide spatial information about heterogeneous injury responses, but often only a fraction of stained tissue is analyzed. Deep learning ... ...

Abstract	Recovery from acute kidney injury can vary widely in patients and in animal models. Immunofluorescence staining can provide spatial information about heterogeneous injury responses, but often only a fraction of stained tissue is analyzed. Deep learning can expand analysis to larger areas and sample numbers by substituting for time-intensive manual or semi-automated quantification techniques. Here we report one approach to leverage deep learning tools to quantify heterogenous responses to kidney injury that can be deployed without specialized equipment or programming expertise. We first demonstrated that deep learning models generated from small training sets accurately identified a range of stains and structures with performance similar to that of trained human observers. We then showed this approach accurately tracks the evolution of folic acid induced kidney injury in mice and highlights spatially clustered tubules that fail to repair. We then demonstrated that this approach captures the variation in recovery across a robust sample of kidneys after ischemic injury. Finally, we showed markers of failed repair after ischemic injury were correlated both spatially within and between animals and that failed repair was inversely correlated with peritubular capillary density. Combined, we demonstrate the utility and versatility of our approach to capture spatially heterogenous responses to kidney injury.
MeSH term(s)	Humans ; Mice ; Animals ; Deep Learning ; Kidney/blood supply ; Acute Kidney Injury ; Models, Animal ; Folic Acid
Chemical Substances	Folic Acid (935E97BOY8)
Language	English
Publishing date	2023-04-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-33433-3
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