Difference between revisions of "Pantner 2021 Sci Rep"
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|title=Pantner Y, Polavarapu R, Chin LS, Li L, Shimizu Y, Calvert JW (2021) DJ-1 attenuates the glycation of mitochondrial complex I and complex III in the post-ischemic heart. Sci Rep 11:19408. | |title=Pantner Y, Polavarapu R, Chin LS, Li L, Shimizu Y, Calvert JW (2021) DJ-1 attenuates the glycation of mitochondrial complex I and complex III in the post-ischemic heart. Sci Rep 11:19408. | ||
|info=[https://pubmed.ncbi.nlm.nih.gov/34593886 PMID: 34593886 Open Access] | |info=[https://pubmed.ncbi.nlm.nih.gov/34593886 PMID: 34593886 Open Access] | ||
|authors=Pantner | |authors=Pantner Yvanna, Polavarapu Rohini, Chin Lih-Shen, Li Lian, Shimizu Yuuki, Calvert John W | ||
|year=2021 | |year=2021 | ||
|journal=Sci Rep | |journal=Sci Rep | ||
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{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Genetic knockout;overexpression | ||
| | |organism=Mouse | ||
|tissues=Heart | |||
|preparations=Isolated mitochondria | |||
|additional=2021-10 | |additional=2021-10 | ||
}} | }} |
Latest revision as of 13:49, 5 October 2021
Pantner Y, Polavarapu R, Chin LS, Li L, Shimizu Y, Calvert JW (2021) DJ-1 attenuates the glycation of mitochondrial complex I and complex III in the post-ischemic heart. Sci Rep 11:19408. |
Pantner Yvanna, Polavarapu Rohini, Chin Lih-Shen, Li Lian, Shimizu Yuuki, Calvert John W (2021) Sci Rep
Abstract: DJ-1 is a ubiquitously expressed protein that protects cells from stress through its conversion into an active protease. Recent work found that the active form of DJ-1 was induced in the ischemic heart as an endogenous mechanism to attenuate glycative stress-the non-enzymatic glycosylation of proteins. However, specific proteins protected from glycative stress by DJ-1 are not known. Given that mitochondrial electron transport proteins have a propensity for being targets of glycative stress, we investigated if DJ-1 regulates the glycation of Complex I and Complex III after myocardial ischemia-reperfusion (I/R) injury. Initial studies found that DJ-1 localized to the mitochondria and increased its interaction with Complex I and Complex III 3 days after the onset of myocardial I/R injury. Next, we investigated the role DJ-1 plays in modulating glycative stress in the mitochondria. Analysis revealed that compared to wild-type control mice, mitochondria from DJ-1 deficient (DJ-1 KO) hearts showed increased levels of glycative stress following I/R. Additionally, Complex I and Complex III glycation were found to be at higher levels in DJ-1 KO hearts. This corresponded with reduced complex activities, as well as reduced mitochondrial oxygen consumption ant ATP synthesis in the presence of pyruvate and malate. To further determine if DJ-1 influenced the glycation of the complexes, an adenoviral approach was used to over-express the active form of DJ-1(AAV9-DJ1ΞC). Under I/R conditions, the glycation of Complex I and Complex III were attenuated in hearts treated with AAV9-DJ1ΞC. This was accompanied by improvements in complex activities, oxygen consumption, and ATP production. Together, this data suggests that cardiac DJ-1 maintains Complex I and Complex III efficiency and mitochondrial function during the recovery from I/R injury. In elucidating a specific mechanism for DJ-1's role in the post-ischemic heart, these data break new ground for potential therapeutic strategies using DJ-1 as a target.
β’ Bioblast editor: Plangger M
Labels: MiParea: Respiration, Genetic knockout;overexpression
Organism: Mouse
Tissue;cell: Heart
Preparation: Isolated mitochondria
2021-10