Neutralization of chemokine CXCL14 (BRAK) expression reduces CCl4 induced liver injury and steatosis in mice

Li, Jingjing; Gao, Jin; Yan, Dejun; Yuan, Yunsheng; Sah, Sunita; Satyal, Uttam; Liu, Man; Wang, Han; Yu, Yan

doi:10.1016/j.ejphar.2011.09.174

Cited by 25 publications

(23 citation statements)

References 24 publications

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“…Furthermore, inhibition of CXCL14 was shown to reduce hepatic damage and mortality in a murine hepatotoxicity model. However, hepatic immune cell infiltration was not investigated 31. Interestingly, Wehr et al showed that inhibition of CXCL16 reduced macrophage infiltration in an inflammatory model of NASH 32.…”

Section: Discussionmentioning

confidence: 99%

Adipose tissue macrophages induce hepatic neutrophil recruitment and macrophage accumulation in mice

Bijnen

Josefs

Cuijpers

et al. 2017

Gut

105

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Section: Discussionmentioning

confidence: 99%

Adipose tissue macrophages induce hepatic neutrophil recruitment and macrophage accumulation in mice

Bijnen

Josefs

Cuijpers

et al. 2017

Gut

105

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“…CXCL14-deficient mice are viable and fertile with no obvious immune defects,39 however they appear to be protected in obesity-induced insulin resistance models 40 41. In preclinical hepatic fibrosis models, CXCL14 expression is elevated in response to carbon tetrachloride-induced liver injury,42 43 bile duct ligation43 and schistosome infection;44 multiple hepatic fibrosis models are Hh dependent 45. Elevated CXCL14 expression has been reported in association with multiple tumour types, and it has been reported as an autocrine growth factor for fibroblasts and as being involved in prostate tumour growth 46 47.…”

Section: Discussionmentioning

confidence: 99%

CXCL14 is a candidate biomarker for Hedgehog signalling in idiopathic pulmonary fibrosis

Jia¹,

Chandriani²,

Abbas³

et al. 2017

Thorax

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“…In rats, CXCL14 expression was increased in the liver injury phase and returned to normal after [2] liver regeneration, suggesting its involvement in the liver injury or regeneration regulation [5,9] . Inhibition of HO-1 has been shown to protect against tissue injury in livers exposed to CCl4 [11,39] . Animals pretreated with hemin and then exposed to CCl4 showed a reduced leukocyte infiltration.…”

Section: Mechanisms Of Action Of Hmox-1 In the Livermentioning

confidence: 99%

“…During maturation, dendritic cells (DCs) inhabit a variety of microenvironments that contain different levels of chemokines and chemokine receptors. Immature DCs express CCR1, CCR2, CCR5 and CXCR1, while mature DCs express high levels of CCR7, CCL22, CCL5, CCL2 and CXCL10 [39] . In CoPPIX-treated mice, CCR7 was observed to be markedly down-regulated in liver DCs [49] .…”

Section: Mechanisms Of Action Of Hmox-1 In the Livermentioning

confidence: 99%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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The activation of heme oxygenase-1 (HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and rejection. In addition, the products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis C and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the CO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of REVIEW 541October 27, 2013|Volume 5|Issue 10| WJH|www.wjgnet.com low concentrations of exogenous CO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload (with signs of a chronic hepatitis) and iron deficiency anemia (with paradoxical increased levels of ferritin). Hypoxia induces HO-1 expression in multiple rodent, bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types (endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and CO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury.

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Neutralization of chemokine CXCL14 (BRAK) expression reduces CCl4 induced liver injury and steatosis in mice

Cited by 25 publications

References 24 publications

Adipose tissue macrophages induce hepatic neutrophil recruitment and macrophage accumulation in mice

Adipose tissue macrophages induce hepatic neutrophil recruitment and macrophage accumulation in mice

CXCL14 is a candidate biomarker for Hedgehog signalling in idiopathic pulmonary fibrosis

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

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