Involvement of DJ-1 in ischemic preconditioning-induced delayed cardioprotection in vivo

Wang, Huan; Li, Yuanyuan; Qiu, Lingyu; Yan, Yu‐Feng; Liao, Zhangping; Chen, Heping

doi:10.3892/mmr.2016.6091

Cited by 10 publications

(8 citation statements)

References 33 publications

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“…DJ‐1 is known to be present in the heart and only recently has its cardioprotective role in myocardial I/R injury been uncovered through a DJ‐1‐antioxidative stress pathway . Notably, the important role of DJ‐1 as a potential mediator of IPC has been investigated in our recently published experimental studies . In the present study, this is again confirmed by the better cell viability with the less LDH release in DJ‐1 overexpressing H9c2 cells subjected to H/R and disappeared cardioprotection of DHP in DJ‐1 knockdown H9c2 cells.…”

Section: Discussionsupporting

confidence: 82%

“…31,32 Notably, the important role of DJ-1 as a potential mediator of IPC has been investigated in our recently published experimental studies. 9,10,33 In the present study, this is again confirmed by the better cell viability with the less LDH release in DJ-1 overexpressing H9c2 cells subjected to H/R and disappeared cardioprotection of DHP in DJ-1 knockdown H9c2 cells. Moreover, the present study also showed that DHP attenuated H/R-induced oxidative stress in a DJ-1-dependent way.…”

Section: Dj-1 Contributes To the Inhibitory Effect Of Dhp On H/r-insupporting

confidence: 83%

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DJ‐1 plays an obligatory role in the cardioprotection of delayed hypoxic preconditioning against hypoxia/reoxygenation‐induced oxidative stress through maintaining mitochondrial complex I activity

Ding

Wang

et al. 2018

Cell Biochemistry & Function

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DJ-1 was recently reported to mediate the cardioprotection of delayed hypoxic preconditioning (DHP) by suppressing hypoxia/reoxygenation (H/R)-induced oxidative stress, but its mechanism against H/R-induced oxidative stress during DHP is not fully elucidated. Here, using the well-established cellular model of DHP, we again found that DHP significantly improved cell viability and reduced lactate dehydrogenase release with concurrently up-regulated DJ-1 protein expression in H9c2 cells subjected to H/R. Importantly, DHP efficiently improved mitochondrial complex I activity following H/R and attenuated H/R-induced mitochondrial reactive oxygen species (ROS) generation and subsequent oxidative stress, as demonstrated by a much smaller decrease in reduced glutathione/oxidized glutathione ratio and a much smaller increase in intracellular ROS and malondialdehyde contents than that observed for the H/R group. However, the aforementioned effects of DHP were antagonized by DJ-1 knockdown with short hairpin RNA but mimicked by DJ-1 overexpression. Intriguingly, pharmacological inhibition of mitochondria complex I with Rotenone attenuated all the protective effects caused by DHP and DJ-1 overexpression, including maintenance of mitochondria complex I and suppression of mitochondrial ROS generation and subsequent oxidative stress. Taken together, this work revealed that preserving mitochondrial complex I activity and subsequently inhibiting mitochondrial ROS generation could be a novel mechanism by which DJ-1 mediates the cardioprotection of DHP against H/R-induced oxidative stress damage.

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Section: Discussionsupporting

confidence: 82%

Section: Dj-1 Contributes To the Inhibitory Effect Of Dhp On H/r-insupporting

confidence: 83%

DJ‐1 plays an obligatory role in the cardioprotection of delayed hypoxic preconditioning against hypoxia/reoxygenation‐induced oxidative stress through maintaining mitochondrial complex I activity

Ding

Wang

et al. 2018

Cell Biochemistry & Function

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“…At present, there is little basic research on the antioxidation system of shrimp. Pv DJ-1, in the previous work, has confirmed that it has significant antioxidant effects similar to vertebrates [ 9 , 29 , 30 ]. In this paper, cloning and functional studies reveal that Pv Kelch-like-1 in the Pv DJ-1 transcriptome occupies a position in the shrimp antioxidant system.…”

Section: Discussionmentioning

confidence: 81%

A Novel Kelch-Like-1 Is Involved in Antioxidant Response by Regulating Antioxidant Enzyme System in Penaeus vannamei

Qiao

Liang

Liu

et al. 2020

Genes

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Heavy metals are typical cumulative pollutants that can enter and poison the human body through the food chain. However, the molecular mechanism of heavy metal-induced oxidative stress is unclear. In this study, we characterize PvKelch-like-1 from P. vannamei and explore its antioxidant roles in immune regulation of crustaceans. PvKelch-like-1 full length contains 2107 nucleotides, consists of a 5′ untranslated region (UTR) of 79 bp, a 3′ UTR of 180 bp, and a ORF of 1848 encoded 615 amino acids, which contain a BTB, BACK and Kelch motif, putative molecular mass and isoelectric point were 69 KDa and 6.54. PvKelch-like-1 mRNA was ubiquitously expressed in all detected tissue of P. vannamei, and mRNA expression levels were significantly up-regulated from 6 to 24 h after cadmium stress and reached the highest level (3.2-fold) at 12 h in the hepatopancreas. Subcellular localization analysis revealed that PvKelch-like-1 was localized in the nucleus. Silencing PvKelch-like-1 significantly increased reactive oxygen species (ROS) (1.61-fold) production and DNA damage (1.32-fold) in the shrimp hemolymph, and significantly decreased total hemocyte counts (THC) (0.64-fold) at 6 h in hemolymph. Additionally, the antioxidant genes PvCAT (0.43-fold), PvMnSOD (0.72-fold), PvGST (0.31-fold) and PvGPx (0.59-fold) at 6 h were decreased significantly in PvKelch-like-1 silenced shrimp after cadmium stress. Overexpression of PvKelch-like-1 has the opposite results in enzyme activity. The SOD (2.44-fold) and CAT (2.19-fold) activities were significantly increased after overexpressing PvKelch-like-1. These results suggest that PvKelch-like-1 plays a vital role in shrimp innate immune defense by positively regulating the expression of antioxidant enzyme genes to respond to cadmium stress.

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“…The important role of DJ-1 as a potential mediator of HPC has been investigated in ours previous published experimental works, and studies have shown that DJ-1 is implicated in the cardioprotection of HPC against H/R-induced oxidative stress damage [6,8,25]. Interestingly, our recent studies have demonstrated that DJ-1-mediated cardioprotection is related to preserving mitochondrial complex I activity and subsequently inhibiting mitochondrial ROS generation [15].…”

Section: Discussionmentioning

confidence: 89%

“…A wealth of information has been collected on the molecular mechanisms involved in ischemic preconditioning, but many aspects of the signaling pathways and of the end effectors of the cardioprotection remain unknown [2,4,5]. An intriguing and unresolved aspect is the involvement of DJ-1 in the genesis of preconditioning [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanism Underlying Hypoxic Preconditioning-Promoted Mitochondrial Translocation of DJ-1 in Hypoxia/Reoxygenation H9c2 Cells

et al. 2019

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DJ-1 was recently reported to be involved in the cardioprotection of hypoxic preconditioning (HPC) against hypoxia/reoxygenation (H/R)-induced oxidative stress damage, by preserving mitochondrial complex I activity and, subsequently, inhibiting mitochondrial reactive oxygen species (ROS) generation. However, the molecular mechanism by which HPC enables mitochondrial translocation of DJ-1, which has no mitochondria-targeting sequence, to preserve mitochondrial complex I, is largely unknown. In this study, co-immunoprecipitation data showed that DJ-1 was associated with glucose-regulated protein 75 (Grp75), and this association was significantly enhanced after HPC. Immunofluorescence imaging and Western blot analysis showed that HPC substantially enhanced the translocation of DJ-1 from cytosol to mitochondria in H9c2 cells subjected to H/R, which was mimicked by DJ-1 overexpression induced by pFlag-DJ-1 transfection. Importantly, knockdown of Grp75 markedly reduced the mitochondrial translocation of DJ-1 induced by HPC and pFlag-DJ-1 transfection. Moreover, HPC promoted the association of DJ-1 with mitochondrial complex I subunits ND1 and NDUFA4, improved complex I activity, and inhibited mitochondria-derived ROS production and subsequent oxidative stress damage after H/R, which was also mimicked by pFlag-DJ-1 transfection. Intriguingly, these effects of HPC and pFlag-DJ-1 transfection were also prevented by Grp75 knockdown. In conclusion, these results indicated that HPC promotes the translocation of DJ-1 from cytosol to mitochondria in a Grp75-dependent manner and Grp75 is required for DJ-1-mediated protection of HPC on H/R-induced mitochondrial complex I defect and subsequent oxidative stress damage.

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Involvement of DJ-1 in ischemic preconditioning-induced delayed cardioprotection in vivo

Cited by 10 publications

References 33 publications

DJ‐1 plays an obligatory role in the cardioprotection of delayed hypoxic preconditioning against hypoxia/reoxygenation‐induced oxidative stress through maintaining mitochondrial complex I activity

DJ‐1 plays an obligatory role in the cardioprotection of delayed hypoxic preconditioning against hypoxia/reoxygenation‐induced oxidative stress through maintaining mitochondrial complex I activity

A Novel Kelch-Like-1 Is Involved in Antioxidant Response by Regulating Antioxidant Enzyme System in Penaeus vannamei

Molecular Mechanism Underlying Hypoxic Preconditioning-Promoted Mitochondrial Translocation of DJ-1 in Hypoxia/Reoxygenation H9c2 Cells

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