Calcium/Calmodulin-Dependent Protein Kinase IV Limits Organ Damage in Hepatic Ischemia/reperfusion Injury Through Induction of Autophagy

Evankovich, John; Zhang, R.; Cardinal, Jon; Chen, J.; Huang, Hai; Beer‐Stolz, Donna; Rosengart, Matthew R.; Tsung, Allan

doi:10.1016/j.jss.2011.11.402

Cited by 14 publications

(17 citation statements)

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“…4). Two bands migrated to the appropriate molecular weight, which has been observed by us and others, and may be due to posttranslational modification, including phosphorylation and acetylation (23,25,26).…”

Section: Significancesupporting

confidence: 76%

Blue light reduces organ injury from ischemia and reperfusion

Yuan

Collage

Huang

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Evidence suggests that light and circadian rhythms profoundly influence the physiologic capacity with which an organism responds to stress. However, the ramifications of light spectrum on the course of critical illness remain to be determined. Here, we show that acute exposure to bright blue spectrum light reduces organ injury by comparison with bright red spectrum or ambient white fluorescent light in two murine models of sterile insult: warm liver ischemia/reperfusion (I/R) and unilateral renal I/R. Exposure to bright blue light before I/R reduced hepatocellular injury and necrosis and reduced acute kidney injury and necrosis. In both models, blue light reduced neutrophil influx, as evidenced by reduced myeloperoxidase (MPO) within each organ, and reduced the release of high-mobility group box 1 (HMGB1), a neutrophil chemotactant and key mediator in the pathogenesis of I/R injury. The protective mechanism appeared to involve an optic pathway and was mediated, in part, by a sympathetic (β3 adrenergic) pathway that functioned independent of significant alterations in melatonin or corticosterone concentrations to regulate neutrophil recruitment. These data suggest that modifying the spectrum of light may offer therapeutic utility in sterile forms of cellular injury.

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Section: Significancesupporting

confidence: 76%

Blue light reduces organ injury from ischemia and reperfusion

Yuan

Collage

Huang

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Thus, we postulate that the amplification of AMPK activity by DDT, and potentially other autocrine/paracrine effects, may occur via a calcium-dependent, energy-independent mechanism. The protective effect of the DDT/CD74/CaMKK2/AMPK pathway that we observed in the ischemic heart is of interest, in view of recent findings that CaMKK2 and downstream CaMKIV limit hepatic damage during ischemia-reperfusion (34). These protective actions of CaMKK2 are distinct from the effects of other Ca 2+ /calmodulin-dependent kinases during ischemia.…”

Section: Discussionmentioning

confidence: 62%

The vestigial enzyme D-dopachrome tautomerase protects the heart against ischemic injury

Qi¹,

Atsina²,

Qu³

et al. 2014

J. Clin. Invest.

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“…Mechanisms we initially characterized in Mfsw e r e observed to be equally relevant to the hepatocyte. Recent literature suggests a critical cytoprotective role for autophagy in both toxin-mediated and ischemia and reperfusion-induced injury in a variety of parenchymal cell types (6,7,71,72). Autophagic mechanisms directed at the removal of damaged mitochondria-or mitophagyare considered to be of particular importance in protecting against hepatocyte injury (73,74).…”

Section: Discussionmentioning

confidence: 99%

Calcium/calmodulin‐dependent protein kinase regulates the PINK1/Parkin and DJ‐1 pathways of mitophagy during sepsis

Zhang¹,

Yuan²,

Sun³

et al. 2017

FASEB j.

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During sepsis and shock states, mitochondrial dysfunction occurs. Consequently, adaptive mechanisms, such as fission, fusion, and mitophagy, are induced to eliminate damaged portions or entire dysfunctional mitochondria. The regulatory PINK1/Parkin and DJ-1 pathways are strongly induced by mitochondrial depolarization, although a direct link between loss of mitochondrial membrane potential (Δ) and mitophagy has not been identified. Mitochondria also buffer Ca, and their buffering capacity is dependent on Δ Here, we characterize a role for calcium/calmodulin-dependent protein kinase (CaMK) I in the regulation of these mechanisms. Loss of Δ with either pharmacologic depolarization or LPS leads to Ca-dependent mitochondrial recruitment and activation of CaMKI that precedes the colocalization of PINK1/Parkin and DJ-1. CaMKI is required and serves as both a PINK1 and Parkin kinase. The mechanisms operate in both immune and nonimmune cells and are induced in models of endotoxemia, sepsis, and hemorrhagic shock. These data support the idea that CaMKI links mitochondrial stress with the PINK1/Parkin and DJ-1 mechanisms of mitophagy.-Zhang, X., Yuan, D., Sun, Q., Xu, L., Lee, E., Lewis, A. J., Zuckerbraun, B. S., Rosengart, M. R. Calcium/calmodulin-dependent protein kinase regulates the PINK1/Parkin and DJ-1 pathways of mitophagy during sepsis.

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Calcium/Calmodulin-Dependent Protein Kinase IV Limits Organ Damage in Hepatic Ischemia/reperfusion Injury Through Induction of Autophagy

Abstract: activation, was significantly reduced in the REDD1 KO group compared to WT cells. Conclusions: These results demonstrate that REDD1 is a crucial mediator of inflammation and injury following liver I/R and implicate NF-kB as a downstream target through TLR4 signaling.

Cited by 14 publications

References 0 publications

Blue light reduces organ injury from ischemia and reperfusion

Blue light reduces organ injury from ischemia and reperfusion

The vestigial enzyme D-dopachrome tautomerase protects the heart against ischemic injury

Calcium/calmodulin‐dependent protein kinase regulates the PINK1/Parkin and DJ‐1 pathways of mitophagy during sepsis

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