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Article ; Online: Proximal Tubular Oxidative Metabolism in Acute Kidney Injury and the Transition to CKD.

Schaub, Jennifer A / Venkatachalam, Manjeri A / Weinberg, Joel M

Kidney360

2020 Volume 2, Issue 2, Page(s) 355–364

Abstract: The proximal tubule relies on oxidative mitochondrial metabolism to meet its energy needs and has limited capacity for glycolysis, which makes it uniquely susceptible to damage during AKI, especially after ischemia and anoxia. Under these conditions, ... ...

Abstract	The proximal tubule relies on oxidative mitochondrial metabolism to meet its energy needs and has limited capacity for glycolysis, which makes it uniquely susceptible to damage during AKI, especially after ischemia and anoxia. Under these conditions, mitochondrial ATP production is initially decreased by several mechanisms, including fatty acid-induced uncoupling and inhibition of respiration related to changes in the shape and volume of mitochondria. Glycolysis is initially insufficient as a source of ATP to protect the cells and mitochondrial function, but supplementation of tricarboxylic acid cycle intermediates augments anaerobic ATP production, and improves recovery of mitochondrial oxidative metabolism. Incomplete recovery is characterized by defects of respiratory enzymes and lipid metabolism. During the transition to CKD, tubular cells atrophy but maintain high expression of glycolytic enzymes, and there is decreased fatty acid oxidation. These metabolic changes may be amenable to a number of therapeutic interventions.
MeSH term(s)	Acute Kidney Injury/chemically induced ; Humans ; Kidney Tubules, Proximal/metabolism ; Mitochondria/metabolism ; Oxidative Stress ; Renal Insufficiency, Chronic/metabolism
Language	English
Publishing date	2020-12-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2641-7650
ISSN (online)	2641-7650
DOI	10.34067/KID.0004772020
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Article ; Online: Pericytes Preserve Capillary Integrity to Prevent Kidney Hypoxia.

Venkatachalam, Manjeri A / Weinberg, Joel M

Journal of the American Society of Nephrology : JASN

2016 Volume 28, Issue 3, Page(s) 717–719

MeSH term(s)	Capillaries ; Humans ; Hypoxia ; Kidney ; Kidney Diseases ; Kidney Tubules ; Pericytes ; Zinc Finger Protein GLI1
Chemical Substances	GLI1 protein, human ; Zinc Finger Protein GLI1
Language	English
Publishing date	2016-12-15
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2016111157
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Article ; Online: NO Synthesis but Not Apoptosis, Mitosis or Inflammation Can Explain Correlations between Flow Directionality and Paracellular Permeability of Cultured Endothelium.

Ghim, Mean / Yang, Sung-Wook / David, Kamilah R Z / Eustaquio, Joel / Warboys, Christina M / Weinberg, Peter D

International journal of molecular sciences

2022 Volume 23, Issue 15

Abstract: Haemodynamic wall shear stress varies from site to site within the arterial system and is thought to cause local variation in endothelial permeability to macromolecules. Our aim was to investigate mechanisms underlying the changes in paracellular ... ...

Abstract	Haemodynamic wall shear stress varies from site to site within the arterial system and is thought to cause local variation in endothelial permeability to macromolecules. Our aim was to investigate mechanisms underlying the changes in paracellular permeability caused by different patterns of shear stress in long-term culture. We used the swirling well system and a substrate-binding tracer that permits visualisation of transport at the cellular level. Permeability increased in the centre of swirled wells, where flow is highly multidirectional, and decreased towards the edge, where flow is more uniaxial, compared to static controls. Overall, there was a reduction in permeability. There were also decreases in early- and late-stage apoptosis, proliferation and mitosis, and there were significant correlations between the first three and permeability when considering variation from the centre to the edge under flow. However, data from static controls did not fit the same relation, and a cell-by-cell analysis showed that <5% of uptake under shear was associated with each of these events. Nuclear translocation of NF-κB p65 increased and then decreased with the duration of applied shear, as did permeability, but the spatial correlation between them was not significant. Application of an NO synthase inhibitor abolished the overall decrease in permeability caused by chronic shear and the difference in permeability between the centre and the edge of the well. Hence, shear and paracellular permeability appear to be linked by NO synthesis and not by apoptosis, mitosis or inflammation. The effect was mediated by an increase in transport through tricellular junctions.
MeSH term(s)	Endothelium, Vascular ; Humans ; Inflammation ; Mitosis ; Permeability ; Stress, Mechanical
Language	English
Publishing date	2022-07-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23158076
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Article ; Online: Mitochondrial biogenesis in kidney disease.

Weinberg, Joel M

Journal of the American Society of Nephrology : JASN

2011 Volume 22, Issue 3, Page(s) 431–436

Abstract: The transcriptional regulation of mitochondrial biogenesis by normal metabolic adaptation or injury has been clarified over the past decade. Mitochondrial biogenesis and its attendant processes enhance metabolic pathways such as fatty acid oxidation and ... ...

Abstract	The transcriptional regulation of mitochondrial biogenesis by normal metabolic adaptation or injury has been clarified over the past decade. Mitochondrial biogenesis and its attendant processes enhance metabolic pathways such as fatty acid oxidation and increase antioxidant defense mechanisms that ameliorate injury from aging, tissue hypoxia, and glucose or fatty acid overload, all of which contribute to the pathogenesis of acute and chronic kidney disease. There has been considerable interest in peroxisome proliferator-activated receptors (PPAR) in the kidney, which affect multiple processes in addition to mitochondrial biogenesis. As yet there is relatively little information focused specifically on mitochondrial biogenesis and its regulation by PPARγ coactivators and their modulators such as SIRT1. The available data indicate that these pathways will be fruitful areas for study in the modification of renal disease.
MeSH term(s)	Fatty Acids/metabolism ; Glucose/metabolism ; Humans ; Kidney/physiopathology ; Kidney Diseases/physiopathology ; Mitochondria/physiology ; PPAR gamma/physiology ; Sirtuin 1/physiology
Chemical Substances	Fatty Acids ; PPAR gamma ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2011-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2010060643
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Article ; Online: Bent pinkies: Quantifying fifth finger clinodactyly in a sample of U.S. adults.

Lee, Myoung Keun / Dahl, Zelda T / Anderton, Joel / Maurer, Jennifer L / Marazita, Mary L / Shaffer, John R / Weinberg, Seth M

PloS one

2022 Volume 17, Issue 7, Page(s) e0271734

Abstract: Mild curvature of the fifth finger (or clinodactyly) is a relatively common trait. While severe forms can cause functional impairment and are a feature of certain congenital syndromes, mild clinodactyly is considered a minor morphological variant. ... ...

Abstract	Mild curvature of the fifth finger (or clinodactyly) is a relatively common trait. While severe forms can cause functional impairment and are a feature of certain congenital syndromes, mild clinodactyly is considered a minor morphological variant. Despite exhibiting continuous variation, clinodactyly is rarely treated as a quantitative trait. Consequently, the degree of fifth finger curvature in the general population and the factors that impact this curvature are not well understood. In the present study, we measured fifth finger curvature in a sample of 1,295 U.S. adults and investigated the role of sex, age and body size. We found that clinodactyly exhibited a non-normal distribution. All participants displayed some degree of curvature, but it tended to be slight with an overall mean of 3.68 degrees (median: 3.58 degrees). In only 0.8% of cases did the curvature exceed the nominal 10-degree threshold for clinically meaningful clinodactyly. We did not find statically significant sex differences. Further, there was no meaningful relationship with height and only a weak positive relationship with age. We found that clinodactyly showed asymmetry; the curvature was greater on the left than on the right fifth finger (p < 2.2e-16), but this was not influenced by sex, age, or height. These results suggest the possibility that the kind of ubiquitous mild clinodactyly observed in the general population may be etiologically distinct from more rare and severe forms of the condition.
MeSH term(s)	Adult ; Female ; Fingers/abnormalities ; Hand Deformities, Congenital ; Humans ; Male
Language	English
Publishing date	2022-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0271734
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Article ; Online: Fibrosis without fibroblast TGF-β receptors?

Venkatachalam, Manjeri A / Weinberg, Joel M

Kidney international

2015 Volume 88, Issue 3, Page(s) 434–437

Abstract: A report by Neelisetty et al. suggests that TGFBR2 deletion from matrix-producing interstitial cells results in decreased transforming growth factor-β (TGF-β) signaling in the cells but does not decrease renal fibrosis after injury. Considered in the ... ...

Abstract	A report by Neelisetty et al. suggests that TGFBR2 deletion from matrix-producing interstitial cells results in decreased transforming growth factor-β (TGF-β) signaling in the cells but does not decrease renal fibrosis after injury. Considered in the context of TGF-β signaling in different cell types involved in renal fibrosis and the existence of other ligands that may produce fibrosis, these findings are provocative, but owing to technical issues of recombination efficiency in inducible models of Cre-lox gene deletion, further studies are needed.
MeSH term(s)	Animals ; Extracellular Matrix/metabolism ; Kidney/metabolism ; Kidney Diseases/metabolism ; Signal Transduction ; Transforming Growth Factor beta/metabolism
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2015.170
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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: TWEAK-Fn14 as a mediator of acute kidney injury.

Weinberg, Joel M

Kidney international

2010 Volume 79, Issue 2, Page(s) 151–153

Abstract: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible 14 (TWEAK-Fn14), are widely expressed and are involved in both injury and repair. Hotta et al. now demonstrate an important role for Fn14 in ...

Abstract	Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible 14 (TWEAK-Fn14), are widely expressed and are involved in both injury and repair. Hotta et al. now demonstrate an important role for Fn14 in the common clamp ischemia model of acute kidney injury. Their data suggest paracrine and autocrine effects in which TWEAK produced by tubule cells feeds back on them via upregulated Fn-14 receptors expressed downstream in the proximal tubule.
MeSH term(s)	Acute Kidney Injury/etiology ; Acute Kidney Injury/physiopathology ; Animals ; Autocrine Communication ; Cytokine TWEAK ; Feedback, Physiological ; Mice ; Paracrine Communication ; Receptors, Tumor Necrosis Factor/physiology ; TWEAK Receptor ; Tumor Necrosis Factors/physiology
Chemical Substances	Cytokine TWEAK ; Receptors, Tumor Necrosis Factor ; TWEAK Receptor ; Tnfrsf12a protein, mouse ; Tnfsf12 protein, mouse ; Tumor Necrosis Factors
Language	English
Publishing date	2010-12-29
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2010.435
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Article ; Online: NO Synthesis but Not Apoptosis, Mitosis or Inflammation Can Explain Correlations between Flow Directionality and Paracellular Permeability of Cultured Endothelium

Mean Ghim / Sung-Wook Yang / Kamilah R. Z. David / Joel Eustaquio / Christina M. Warboys / Peter D. Weinberg

International Journal of Molecular Sciences, Vol 23, Iss 8076, p

2022 Volume 8076

Abstract	Haemodynamic wall shear stress varies from site to site within the arterial system and is thought to cause local variation in endothelial permeability to macromolecules. Our aim was to investigate mechanisms underlying the changes in paracellular permeability caused by different patterns of shear stress in long-term culture. We used the swirling well system and a substrate-binding tracer that permits visualisation of transport at the cellular level. Permeability increased in the centre of swirled wells, where flow is highly multidirectional, and decreased towards the edge, where flow is more uniaxial, compared to static controls. Overall, there was a reduction in permeability. There were also decreases in early- and late-stage apoptosis, proliferation and mitosis, and there were significant correlations between the first three and permeability when considering variation from the centre to the edge under flow. However, data from static controls did not fit the same relation, and a cell-by-cell analysis showed that <5% of uptake under shear was associated with each of these events. Nuclear translocation of NF-κB p65 increased and then decreased with the duration of applied shear, as did permeability, but the spatial correlation between them was not significant. Application of an NO synthase inhibitor abolished the overall decrease in permeability caused by chronic shear and the difference in permeability between the centre and the edge of the well. Hence, shear and paracellular permeability appear to be linked by NO synthesis and not by apoptosis, mitosis or inflammation. The effect was mediated by an increase in transport through tricellular junctions.
Keywords	leaky junction ; cell death ; cell division ; FITC-avidin ; transport ; orbital shaker ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2022-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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