CD14-dependent regulation of Grp78 in the liver and lungs of mice after burn injury

Cho, Ki-Ho; Thomas, Rita; Greenhalgh, David G.

doi:10.1016/s0014-4800(03)00071-6

Cited by 3 publications

(4 citation statements)

References 22 publications

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“…Although CD14 has been recognized as an important inflammation mediator in burn-associated pathological responses in multiple organs including the liver (11,13,14), lung (14), skin (43), and adrenal gland (12), its role in myocardium and myocardial mitochondrial function has not been elucidated. A recent study from our laboratory suggests that burn injury significantly elevated CD14 expression in the heart tissue and in cardiomyocytes (5).…”

Section: Discussionmentioning

confidence: 99%

“…However, most studies to date have focused on the effects of total intracellular ROS. We hypothesize that burn injury produces functional defects of myocardial mitochondria and causes overproduction of mitochondrial ROS (mtROS), leading to a cascade of molecular events that generate cardiac contractile dysfunction.CD14, a member of the toll-like receptor 4 (TLR4) signalosome, is involved in the regulation of postburn pathogenic responses in distant organs such as the liver (11,13,14), lung (14), skin (43), and adrenal gland (12). Consistently, recent clinical research has correlated genetic variations within the TLR4 gene with the risk of post-trauma organ failure (4, 41).…”

mentioning

confidence: 99%

“…CD14, a member of the toll-like receptor 4 (TLR4) signalosome, is involved in the regulation of postburn pathogenic responses in distant organs such as the liver (11,13,14), lung (14), skin (43), and adrenal gland (12). Consistently, recent clinical research has correlated genetic variations within the TLR4 gene with the risk of post-trauma organ failure (4, 41).…”

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confidence: 99%

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Burn serum causes a CD14-dependent mitochondrial damage in primary cardiomyocytes

Zang

Maass

Wigginton

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Studies from animal models suggest that myocardial mitochondrial damage contributes to cardiac dysfunction after burn injury. In this report, we used an ex vivo model of primary cardiomyocyte culture to investigate the mechanisms of burn-induced mitochondrial impairment. Briefly, blood serum was collected from Sprague-Dawley (SD) rats subjected to 40% total body surface area burn and added (10% vol/vol) to primary cardiomyocytes prepared from SD rats. The effect of the burn serum on mitochondrial function and membrane integrity in the myocytes was analyzed. Exposure of myocytes to burn serum doubled the mitochondrial membrane damage measured by two independent assays. This treatment also significantly elevated mitochondrial oxidative stress, indicated by a more than 30% increase in lipid oxidation. Downregulation of mitochondrial antioxidant defense was also evident since the activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were reduced by about 30% and 50%, respectively. Burn serum also induced deficiency of mitochondrial metabolism, indicated by a 30% decrease in the activity of cytochrome c oxidase. These mitochondrial dysfunctions appear to be generated by oxidative stress because burn serum induced a significant increase of mitochondrial oxygen species (mtROS) in cardiomyocytes, and pretreatment of cardiomyocytes with the antioxidant N-acetyl-cysteine prevented the mitochondrial damages induced by burn serum. Remarkably, the increase in mtROS was abolished by an antibody-mediated blockade of CD14. Furthermore, burn injury-induced mitochondrial damage in cardiomyocytes was prevented in CD14 knockout mice. Taken together, these data suggested that burn injury produces CD14-dependent mitochondrial damage via oxidative stress in myocardium.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Burn serum causes a CD14-dependent mitochondrial damage in primary cardiomyocytes

Zang

Maass

Wigginton

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…on April 30, 2019. by guest www.bloodjournal.org From mRNA levels of GRP78 27 and the spliced form of XBP-1, 28 both of which are known to be up-regulated in response to UPR. We have shown that WT and ␣ 4 -R/A GFFKR cells expressed comparable levels of GRP78 and the spliced XBP-1 ( Figure 2D).…”

Section: Generation Of Knockin Mice In Which the Membrane-proximal Samentioning

confidence: 99%

Genetic perturbation of the putative cytoplasmic membrane-proximal salt bridge aberrantly activates α4 integrins

Imai

Park

Peer

et al. 2008

Blood

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CD14 Involvement in Third-degree Skin Burn-induced Myocardial Injury via the MAPK Signaling Pathway

Zhu

Zou

Gao

et al. 2021

Cell Biochem Biophys

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CD14-dependent regulation of Grp78 in the liver and lungs of mice after burn injury

Cited by 3 publications

References 22 publications

Burn serum causes a CD14-dependent mitochondrial damage in primary cardiomyocytes

Burn serum causes a CD14-dependent mitochondrial damage in primary cardiomyocytes

Genetic perturbation of the putative cytoplasmic membrane-proximal salt bridge aberrantly activates α4 integrins

CD14 Involvement in Third-degree Skin Burn-induced Myocardial Injury via the MAPK Signaling Pathway

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