Monocyte chemoattractant protein 1 (MCP-1) expression occurs in toxic rat liver injury and human liver disease

Czaja, Mark J.; Geerts, Albert; Xu, Jun; Schmiedeberg, Phyllis; Ju, Yue

doi:10.1002/jlb.55.1.120

Cited by 117 publications

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“…Moreover, Foxf1 ϩ/Ϫ liver exhibited a delayed increase in MCP-1 expression after CCl 4 injury, confirming defective activation of stellate cells and a potential delay in recruitment of inflammatory cells. 37,38 In summary, Foxf1 ϩ/Ϫ mice displayed abnormal liver repair, diminished activation of hepatic stellate cells, and increased pericentral hepatic apoptosis following CCl 4 injury. This inhibition of stellate cell activation was associated with diminished induction of expression of type I collagen, Notch-2 protein, and IP-10 mRNA and delayed induction of MCP-1 levels.…”

Section: Discussionmentioning

confidence: 92%

Foxf1 +/− mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury

et al. 2003

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Previous studies have shown that haploinsufficiency of the splanchnic and septum transversum mesoderm Forkhead Box (Fox) f1 transcriptional factor caused defects in lung and gallbladder development and that Foxf1 heterozygous (؉/؊) mice exhibited defective lung repair in response to injury. In this study, we show that Foxf1 is expressed in hepatic stellate cells in developing and adult liver, suggesting that a subset of stellate cells originates from septum transversum mesenchyme during mouse embryonic development. Because liver regeneration requires a transient differentiation of stellate cells into myofibroblasts, which secrete type I collagen into the extracellular matrix, we examined Foxf1 ؉/؊ liver repair following carbon tetrachloride injury, a known model for stellate cell activation. We found that regenerating Foxf1 ؉/؊ liver exhibited defective stellate cell activation following CCl 4 liver injury, which was associated with diminished induction of type I collagen, ␣-smooth muscle actin, and Notch-2 protein and resulted in severe hepatic apoptosis despite normal cellular proliferation rates. Furthermore, regenerating Foxf1 ؉/؊ livers exhibited decreased levels of interferon-inducible protein 10 (IP-10), delayed induction of monocyte chemoattractant protein 1 (MCP-1) levels, and aberrantly elevated expression of transforming growth factor ␤1. T he Forkhead Box (Fox) family of transcription factors shares homology in the winged helix DNA binding domain, 1 and its members play important roles in cellular proliferation, differentiation, and metabolic homeostasis. [2][3][4][5][6] Haploinsufficiency of the Foxf1 gene (previously known as HFH-8 or Freac-1) in heterozygous (ϩ/Ϫ) mice causes perinatal lethality from pulmonary hemorrhage and severe defects in alveolarization, vascularization, and fusion of lung lobes. 7-9 Lung hemorrhage was observed in one half of newborn Foxf1 ϩ/Ϫ mice that had an 80% reduction in pulmonary Foxf1 levels (low Foxf1 ϩ/Ϫ) and reduced expression of genes involved in lung morphogenesis. 7 Interestingly, expression of these lung developmental genes was unchanged in 40% of the newborn Foxf1 ϩ/Ϫ mice that had near wildtype (WT) pulmonary levels of Foxf1 messenger RNA (mRNA) (high Foxf1 ϩ/Ϫ mice) without pulmonary hemorrhage, but they exhibited diminished alveolar septation. 7 Moreover, the high Foxf1 ϩ/Ϫ mice had normal life spans and adult lung morphology, suggesting that these mice compensated for the alveolar septation defect but exhibited defective lung repair in response to injury. 10 Liver development initiates at 9 days postcoitum (dpc) of mouse embryogenesis, when the cardiac mesenchyme induces the hepatic primordium to emerge from the foregut endoderm that invades the septum transversum mesenchyme. 6 Previous expression studies have shown

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Section: Discussionmentioning

confidence: 92%

Foxf1 +/− mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury

et al. 2003

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“…MCP-1 expression is elevated in patients with chronic viral hepatitis and in experimental liver injury models. 8,9 In cultured HSC, proinflammatory cytokines including TNF-␣, IL-1␣, and IFN-␥ potently stimulate MCP-1 expression. 8,12 Activated HSCs promote hepatic inflammation by production of potent neutrophil chemoattractants such as cytokine-induced neutrophil chemoattractant, the rat homolog to human IL-8.…”

Section: Discussionmentioning

confidence: 99%

“…5,7 Hepatic stellate cells (HSCs) mediate fibrosis and inflammation in the injured liver. HSCs regulate leukocyte trafficking and activation through secretion of chemokines such as monocyte chemotactic protein-1 (MCP-1) 8,9 and IL-8. 10 HSCs express CD40, which activates nuclear factor B (NF-B) and c-Jun N-terminal kinase (JNK) and up-regulates chemokine secretion.…”

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confidence: 99%

Toll-Like receptor 4 mediates inflammatory signaling by bacterial lipopolysaccharide in human hepatic stellate cells

et al. 2003

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“…Monocyte migration into the liver is facilitated by the production of CCL2, which is released in the first 1-4 h after the onset of CCl 4 -induced liver injury [21,29,30]. IL-1α can promote CCL2, as well as CCL3, CCL4, CCL5, CXCL2 productions [31,32]. However, the role of IL-1α in regulating myeloid cell migration during acute liver injury has not been clearly demonstrated.…”

Section: Introductionmentioning

confidence: 99%

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice

et al. 2015

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Interleukin-1α is mainly expressed on the cell membrane, but can also be secreted during inflammation. The roles of secreted and membrane IL-1α in acute liver inflammation are still not known. Here, we examined the functions of secreted and membrane IL-1α in a mouse model of carbon tetrachloride-induced acute liver injury. We show that secreted IL-1α aggravates liver damage and membrane IL-1α slightly protects mice from liver injury. Further studies showed that secreted IL-1α promotes T-cell activation. It also increased the expansion of CD11b + Gr1 + myeloid cells, which may serve as a negative regulator of acute liver inflammation. Moreover, secreted IL-1α induced IL-6 production from hepatocytes. IL-6 neutralization reduced the proliferation of CD11b + Gr1 + myeloid cells in vivo. CCL2 and CXCL5 expression was increased by secreted IL-1α in vitro and in vivo. Antagonists of the chemokine receptors for CCL2 and CXCL5 significantly reduced the migration of CD11b + Gr1 + myeloid cells. These results demonstrate that secreted and membrane IL-1α play different roles in acute liver injury. Secreted IL-1α could promote Tcell activation and the recruitment and expansion of CD11b + Gr1 + myeloid cells through induction of CCL2, CXCL5, and IL-6. The controlled release of IL-1α could be a critical regulator during acute liver inflammation.Keywords: Acute liver injury r CD11b + Gr1 + myeloid cells r Membrane IL-1α r Secreted IL-1α r T-cell activation Additional supporting information may be found in the online version of this article at the publisher's web-site Correspondence: Dr. Haiyan Liu e-mail: hliu@suda.edu.cn IntroductionThe liver plays a central role in metabolic homeostasis [1]. Liver injury is mainly caused by various insults such as drug, chemical agents, viral hepatitis (hepatitis B or C viruses), alcohol, and C 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu Eur. J. Immunol. 2015. 45: 2084-2098 Molecular immunology 2085 autoimmune attack of hepatocytes [2]. Liver damage by proinflammatory cytokines induced by these causes is a relevant mechanism for liver cell death [3]. Acute liver injury remains one of the most challenging problems in liver diseases, and new therapeutic options for treatment of acute liver injury are urgently needed [4]. Carbon tetrachloride (CCl 4 ) is widely used as a chemical inducer of acute or chronic liver injury in rodents depending on the dosage and administration frequency [5]. ROS and oxidative stress are then generated and inflammatory cells are recruited, which leads to hepatocyte degeneration and necrosis [6,7]. Parenchymal cells could regenerate that involves a complex regulated response after CCl 4 -induced acute liver injury [8]. Therefore, anti-oxidative and anti-inflammatory therapies are thought to be the effective ways to prevent and attenuate CCl 4 -induced liver damage. IL-1 is a pleiotropic cytokine and affects inflammatory immune responses. The IL-1 family includes two important agonistic proteins, IL-1α and IL-1β, which play an important role in ...

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Monocyte chemoattractant protein 1 (MCP-1) expression occurs in toxic rat liver injury and human liver disease

Cited by 117 publications

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Foxf1 +/− mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury

Foxf1 +/− mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury

Toll-Like receptor 4 mediates inflammatory signaling by bacterial lipopolysaccharide in human hepatic stellate cells

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice

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Monocyte chemoattractant protein 1 (MCP-1) expression occurs in toxic rat liver injury and human liver disease

Cited by 117 publications

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Foxf1 +/− mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury

Foxf1 +/− mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury

Toll-Like receptor 4 mediates inflammatory signaling by bacterial lipopolysaccharide in human hepatic stellate cells

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b+Gr1+ cells in carbon tetrachloride‐induced liver injury in mice

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Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice