Mitochondria-targeted heme oxygenase-1 decreases oxidative stress in renal epithelial cells

Bolisetty, Subhashini; Traylor, Amie M.; Zarjou, Abolfazl; Johnson, Michelle S.; Benavides, Gloria A.; Ricart, Karina; Boddu, Ravindra; Moore, Ray; Landar, Aimee; Barnes, Stephen; Darley‐Usmar, Victor; Agarwal, Anupam

doi:10.1152/ajprenal.00160.2013

Cited by 59 publications

(48 citation statements)

References 38 publications

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“…In the absence of such a phenomenon, the bioenergetics might be more severely compromised. A recent study indicated that expression of HO-1 targeted to mitochondria attenuated oxidative stress (43). These observations, taken together, suggest that mitochondrial translocation of HO-1 could serve as a cytoprotective mechanism against possible mitochondrial dysfunction induced by oxidative or metabolic insults (32).…”

Section: Effect Of Oxidized Hb Exposure On E10 Cellsmentioning

confidence: 87%

Oxidized Ferric and Ferryl Forms of Hemoglobin Trigger Mitochondrial Dysfunction and Injury in Alveolar Type I Cells

Chintagari

Jana

Alayash

2016

Am J Respir Cell Mol Biol

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Lung alveoli are lined by alveolar type (AT) 1 cells and cuboidal AT2 cells. The AT1 cells are likely to be exposed to cell-free hemoglobin (Hb) in multiple lung diseases; however, the role of Hb redox (reduction-oxidation) reactions and their precise contributions to AT1 cell injury are not well understood. were reversed by the addition of scavenger proteins, haptoglobin and hemopexin. Collectively, these data establish, for the first time, a central role for cell-free Hb in lung epithelial injury, and that these effects are mediated through the redox transition of Hb to higher oxidation states.

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Section: Effect Of Oxidized Hb Exposure On E10 Cellsmentioning

confidence: 87%

Oxidized Ferric and Ferryl Forms of Hemoglobin Trigger Mitochondrial Dysfunction and Injury in Alveolar Type I Cells

Chintagari

Jana

Alayash

2016

Am J Respir Cell Mol Biol

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“…While HO-1 localizes predominantly to the endoplasmic reticulum, expression in the nuclear (18,82), mitochondrial (17,21), and secretory (83, 151) subcellular compartments has been reported. In the setting of hypoxia-or heme-mediated oxidative stress in vitro, HO-1 localized to the nucleus and modulated transcription of oxidative stress response genes (82).…”

Section: Cellular Localization Of Ho-1mentioning

confidence: 99%

“…HO-1 targeted to mitochondria was protective against hypoxia-induced oxidative damage in human embryonic kidney cells. Protection was superior in mitochondrial-targeted HO-1 overexpressing cells compared with cytoplasmic overexpression (21). Bindu et al found mitochondrial expression of HO-1 in a rat model of gastric mucosal injury, which protected from mitochondrial stress, improved cellular respiratory function, and prevented apoptosis (17).…”

Section: Cellular Localization Of Ho-1mentioning

confidence: 99%

Heme Oxygenase-1 in Kidney Health and Disease

Lever

Boddu

George

et al. 2016

Antioxidants & Redox Signaling

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117

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“…While mitochondrial fission is orchestrated by the dynamin-related protein 1 (DRP1) and the mitochondrial fission 1 (Fis1) protein [34], [35], the fusion process is controlled by the autosomal dominant optic atrophy 1 (OPA1) protein, together with the mitochondrial fusion proteins mitofusion 1 and 2 (Mfn 1 and 2), located on the mitochondrial outer membrane, [36], [37]. As HO-1/HO-2 are known regulators of mitochondrial integrity and function [38], [39], [40], [41], we hypothesized that adipose HO-1 gene is essential for increased mitochondrial fusion that may result in an increase in the beige cell population within adipose tissue or conversion of white adipose function populations and white adipose function that include expression of PGC1α levels and thermogenic genes.…”

Section: Introductionmentioning

confidence: 99%

Ablation of adipose-HO-1 expression increases white fat over beige fat through inhibition of mitochondrial fusion and of PGC1α in female mice

Singh

Grant

Meissner

et al. 2017

Hormone Molecular Biology and Clinical Investigation

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Abstract:Background: Hmox1 plays an important role in the regulation of mitochondrial bioenergetics and function by regulating cellular heme-derived CO and bilirubin. Previous studies have demonstrated that global disruption of HO-1 in humans and mice resulted in severe organ dysfunction. Methods: We investigated the potential role of adipose-specific-HO-1 genetic ablation on adipose tissue function, mitochondrial quality control and energy expenditure by generating an adipo-HO-1 knockout mouse model (Adipo-HO-1 −/− ) and, in vitro, adipocyte cells in which HO activity was inhibited. Adiposity, signaling proteins, fasting glucose and oxygen consumption were determined and compared to adipocyte cultures with depressed levels of both HO-1/HO-2. Results: Adipo-HO-1 −/− female mice exhibited increased adipocyte size, and decreases in the mitochondrial fusion to fission ratio, PGC1, and SIRT3. Importantly, ablation of HO-1 in adipose tissue resulted in fat acquiring many properties of visceral fat such as decreases in thermogenic genes including pAMPK and PRDM16. Deletion of HO-1 in mouse adipose tissue led to complete metabolic dysfunction, an increase in white adipose tissue, a reduction of beige fat and associated increases in FAS, aP2 and hyperglycemia. Mechanistically, genetic deletion of HO-1 in adipose tissues decreased the mitochondrial fusion to fission ratio; disrupted the activity of the PGC1 transcriptional axis and thermogenic genes both in vitro and in vivo. Conclusion: Ablation of adipose tissue-HO-1 abridged PGC1 expression promoted mitochondrial dysfunction and contributed to an increase of pro-inflammatory visceral fat and abrogated beige-cell like phenotype.

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Mitochondria-targeted heme oxygenase-1 decreases oxidative stress in renal epithelial cells

Abstract: . Mitochondria-targeted heme oxygenase-1 decreases oxidative stress in renal epithelial cells.

Cited by 59 publications

References 38 publications

Oxidized Ferric and Ferryl Forms of Hemoglobin Trigger Mitochondrial Dysfunction and Injury in Alveolar Type I Cells

Oxidized Ferric and Ferryl Forms of Hemoglobin Trigger Mitochondrial Dysfunction and Injury in Alveolar Type I Cells

Heme Oxygenase-1 in Kidney Health and Disease

Ablation of adipose-HO-1 expression increases white fat over beige fat through inhibition of mitochondrial fusion and of PGC1α in female mice

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