CXC Chemokine Ligand 2 Induced by Receptor Activator of NF-κB Ligand Enhances Osteoclastogenesis

Ha, Jung Min; Choi, Hyo Sun; Lee, Youngkyun; Kwon, Hee Jung; Song, Yeong Wook; Kim, Hong Hee

doi:10.4049/jimmunol.0902444

Cited by 82 publications

(70 citation statements)

References 23 publications

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“…Leukemia inhibitory factor regulates the commitment of CSCs to the endothelial cell lineage, contributing to revascularization in the process of tissue remodeling and/or regeneration (59). The CXCL family chemokines play important roles in promoting stem cell migration and homing through JNK and NFB signaling pathways (60,61). Among them, EGF, BMP3, and the FGF family cytokines are essential for stem cell survival and proliferation (62,63).…”

Section: Discussionmentioning

confidence: 99%

The Heme Oxygenase 1 Inducer (CoPP) Protects Human Cardiac Stem Cells against Apoptosis through Activation of the Extracellular Signal-regulated Kinase (ERK)/NRF2 Signaling Pathway and Cytokine Release

Cai¹,

Teng²,

et al. 2012

Journal of Biological Chemistry

109

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Background: Nothing is known regarding the anti-apoptotic effect of HO-1 on hCSCs. Results: HO-1 expression induced by CoPP enhances hCSC survival through activation of the ERK/NRF2 signaling pathway and cytokine release. Conclusion: CoPP is a cytoprotective agent that could improve the efficacy of CSC-based therapies for heart disease. Significance: Strategies to enhance donor cell survival would have enormous therapeutic implications for patients with ischemic heart disease.

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Section: Discussionmentioning

confidence: 99%

The Heme Oxygenase 1 Inducer (CoPP) Protects Human Cardiac Stem Cells against Apoptosis through Activation of the Extracellular Signal-regulated Kinase (ERK)/NRF2 Signaling Pathway and Cytokine Release

Cai¹,

Teng²,

et al. 2012

Journal of Biological Chemistry

109

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“…Among the other secreted signaling molecules showing drastic differences in expression was the gene encoding the chemokine Cxcl2 (32-fold upregulated in susceptible mice). This chemokine plays a major role as a neutrophil attractant and has been implicated in certain inflammatory diseases (14). It would be of interest to investigate if this molecule might have a role in the progression of ECM, especially given its elevated expression.…”

Section: Resultsmentioning

confidence: 99%

Molecular Correlates of Experimental Cerebral Malaria Detectable in Whole Blood

et al. 2011

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Cerebral malaria (CM) is a primary cause of deaths caused by Plasmodium falciparum in young children in sub-Saharan Africa. Laboratory tests based on early detection of host biomarkers in patient blood would help in the prognosis and differential diagnosis of CM. Using the Plasmodium berghei ANKA murine model of experimental cerebral malaria (ECM), we have identified over 300 putative diagnostic biomarkers of ECM in the circulation by comparing the whole-blood transcriptional profiles of resistant mice (BALB/c) to those of two susceptible strains (C57BL/6 and CBA/CaJ). Our results suggest that the transcriptional profile of whole blood captures the molecular and immunological events associated with the pathogenesis of disease. We find that during ECM, erythropoiesis is dysfunctional, thrombocytopenia is evident, and glycosylation of cell surface components may be modified. Furthermore, analysis of immunity-related genes suggests that slightly distinct mechanisms of immunopathogenesis may operate in susceptible C57BL/6 and CBA/CaJ mice. Furthermore, our data set has allowed us to create a molecular signature of ECM composed of a subset of circulatory markers. Complement component C1q, ␤-chain, nonspecific cytotoxic cell receptor protein 1, prostate stem cell antigen, DnaJC, member 15, glutathione S-transferase omega-1, and thymidine kinase 1 were overexpressed in blood during the symptomatic phase of ECM, as measured by quantitative real-time PCR analysis. These studies provide the first host transcriptome database that is uniquely altered during the pathogenesis of ECM in blood. A subset of these mediators of ECM warrant validation in P. falciparum-infected young African children as diagnostic markers of CM.

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“…groβ could activate the sphingomyelin pathway or Jnk1 and induced apoptosis in proliferating cells (21)(22). groβ also induce the activation of mek/erk signal pathway and promote cell proliferation (15,20,21,23). However, little is known about the relationship between groβ and chemotherapeutic agent-induced apoptosis.…”

Section: Groβ and Its Downstream Effector Egr1 Regulate Cisplatin-indmentioning

confidence: 99%

“…our result showed that inhibition of expression of groβ by rnA interference could decrease cisplatin-induced apoptosis in WHco1 cells. groβ was reported to activate many signal pathways, such as Jnk (21,22) and mek/erk signal pathway (15,20,21,23). many of these pathways were correlated to cisplatin-induced apoptosis.…”

mentioning

confidence: 99%

GROβ and its downstream effector EGR1 regulate cisplatin-induced apoptosis in WHCO1 cells

Dong

Zhang²,

Hendricks³

et al. 2011

Oncol Rep

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Abstract. cisplatin is one of the most widely used chemotherapeutic agents employed for treatment of a wide variety of solid tumors, including human esophageal squamous cell carcinoma (escc). However, a major limitation of cisplatinbased chemotherapy of escc is the rather low-effective rate. Understanding the molecular events of limited efficacy of cisplatin-based chemotherapy of escc could lead to strategies resulting in improved therapeutic benefits. the cXc chemokine family has been reported to be related to inflammatory reaction, injure recovery, cell proliferation, apoptosis and even to be involved in the regulation of chemotherapeutic agent-induced apoptosis. cXcl2 chemokine, also known as groβ (growth-related gene product β), belongs to the cXc chemokine group. the known functions of groβ are related to attracting neutrophils to sites of inflammation, modulation of the neurotransmitter release, cell proliferation and apoptosis. However, little is known about the relationship between groβ and chemotherapeutic agent-induced apoptosis. this study was designed to provide insights into the possible role of groβ in the regulation of cisplatin-induced apoptosis in esccs. We report here that inhibition of expression of groβ can decrease cisplatin-induced apoptosis in WHco1 cells. egr1 is a downstream factor regulated by groβ. silencing expression of egr1 can also decrease cisplatin-induced apoptosis in WHco1 cells. the activation of caspase 9 was delayed in cells in which groβ and egr1 were knocked down after cisplatin treatment. All these results indicate that groβ and its downstream factor egr1 are involved in regulating cisplatininduced apoptosis in WHco1 cells, and during this process the intrinsic apoptotic pathway is activated. It may be useful to examine the expression levels of groβ and egr1 in escc patients to select those likely to respond well to cisplatin.

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CXC Chemokine Ligand 2 Induced by Receptor Activator of NF-κB Ligand Enhances Osteoclastogenesis

Cited by 82 publications

References 23 publications

The Heme Oxygenase 1 Inducer (CoPP) Protects Human Cardiac Stem Cells against Apoptosis through Activation of the Extracellular Signal-regulated Kinase (ERK)/NRF2 Signaling Pathway and Cytokine Release

The Heme Oxygenase 1 Inducer (CoPP) Protects Human Cardiac Stem Cells against Apoptosis through Activation of the Extracellular Signal-regulated Kinase (ERK)/NRF2 Signaling Pathway and Cytokine Release

Molecular Correlates of Experimental Cerebral Malaria Detectable in Whole Blood

GROβ and its downstream effector EGR1 regulate cisplatin-induced apoptosis in WHCO1 cells

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