Chemokine CCL2 enhances survival and invasiveness of endometrial stromal cells in an autocrine manner by activating Akt and MAPK/Erk1/2 signal pathway

Li, Ming‐Qing; Li, Huaping; Meng, Yuguang; Wang, Xiaoqiu; Zhu, Xiao‐Yong; Mei, Jie; Li, Da‐Jin

doi:10.1016/j.fertnstert.2011.12.049

Cited by 60 publications

(33 citation statements)

References 38 publications

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“…The implication of Akt, ERK1/2, and p38 in this C1P action is consistent with previous work by other groups showing that MCP-1 upregulated these kinases in different cell types, including rat aortic smooth muscle cells (55), proximal tubular cells (51), 3T3-L1 preadipocytes (56), vascular smooth muscle cells (12), and monocytes (33). Nonetheless, although MCP-1 release has been associated with activation of p38 in many instances (8,33,56; and our unpublished observations), other studies have indicated that this kinase is not involved in this process (31,35), and therefore the role of p38 in stimulation of MCP-1 secretion remains controversial.…”

Section: Discussionmentioning

confidence: 49%

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Ceramide 1-phosphate induces macrophage chemoattractant protein-1 release: involvement in ceramide 1-phosphate-stimulated cell migration

Arana

Ordoñez

Ouro

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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(C1P) is implicated in inflammatory responses and was recently shown to promote cell migration. However, the mechanisms involved in these actions are poorly described. Using J774A.1 macrophages, we have now discovered a new biological activity of C1P: stimulation of monocyte chemoattractant protein-1 (MCP-1) release. This novel effect of C1P was pertussis toxin (PTX) sensitive, suggesting the intervention of Gi protein-coupled receptors. Treatment of the macrophages with C1P caused activation of the phosphatidylinositol 3-kinase (PI3K)/Akt, mitogen-activated protein kinase kinase (MEK)/extracellularly regulated kinases (ERK), and p38 pathways. Inhibition of these kinases using selective inhibitors or specific siRNA blocked the stimulation of MCP-1 release by C1P. C1P stimulated nuclear factor-B activity, and blockade of this transcription factor also resulted in complete inhibition of MCP-1 release. Also, C1P stimulated MCP-1 release and cell migration in human THP-1 monocytes and 3T3-L1 preadipocytes. A key observation was that sequestration of MCP-1 with a neutralizing antibody or treatment with MCP-1 siRNA abolished C1P-stimulated cell migration. Also, inhibition of the pathways involved in C1P-stimulated MCP-1 release completely blocked the stimulation of cell migration by C1P. It can be concluded that C1P promotes MCP-1 release in different cell types and that this chemokine is a major mediator of C1P-stimulated cell migration. The PI3K/Akt, MEK/ ERK, and p38 pathways are important downstream effectors in this action.ceramide 1-phosphate; monocyte chemoattractant protein-1 release; macrophage migration; sphingosine 1-phosphate REGULATION OF CELL MIGRATION is a complex process involving hundreds of molecules. It is necessary for tissue homeostasis and is crucial for regulation of vital biological processes including embryogenesis, organogenesis, or regeneration (reviewed in Refs. 38, 48). Also, cell migration is fundamental to inflammatory responses (1, 49), but inadequate migratory signals may induce the migration of the wrong cell type to the wrong place, which may have severe effects in the organism. Some examples include autoimmune syndromes, angiogenesis, or the process of metastasis. Although cell migration is a subject of intense investigation, the mechanisms involved in controlling cell movements are incompletely understood. In this connection, growing evidence suggests that some sphingolipids are key metabolites for controlling chemotaxis (52). Our group recently reported that ceramide 1-phosphate (C1P), a sphingolipid metabolite that is present in serum or plasma (25), and which we found to regulate cell growth and survival (15,17,18,20,22), is a chemoattractant molecule for macrophages (23). This finding is particularly relevant when considering that macrophages play critical roles in chronic and acute inflammation and that these cells facilitate cancer cell migration (21, 46). In addition, Barth et al. (4) recently showed that ceramide kinase, the enzyme responsible for the phosphorylation of ce...

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Section: Discussionmentioning

confidence: 49%

“…However, inhibition of JNK did not alter macrophage migration. Of interest, and unlike PI3K/Akt and MEK/ERK, JNK was also not involved in upregulation of MCP-1 expression in endometrial stroma cells (35).…”

Section: Discussionmentioning

confidence: 89%

Ceramide 1-phosphate induces macrophage chemoattractant protein-1 release: involvement in ceramide 1-phosphate-stimulated cell migration

Arana

Ordoñez

Ouro

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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“…MCP-1, an 8 kDa secretory protein, is released from certain cells to exert a potent proinflammatory effect on its target cells by binding to the specific receptor CCR2 [7]. MCP-1/CCR2-mediated signaling drives the downstream phosphatidylinositol-3 kinase/Akt and MAPK pathways [8-10]. It is known that MCP-1 induces chemotaxis of macrophages and microglia, leading to pathological microgliosis and inflammatory activation in the lesions [11].…”

Section: Introductionmentioning

confidence: 99%

MCP-1/CCR2 signaling-mediated astrocytosis is accelerated in a transgenic mouse model of SOD1-mutated familial ALS

Kawaguchi-Niida

Yamamoto

Kato

et al. 2013

acta neuropathol commun

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BackgroundEmerging evidence suggests that innate immunity and increased oxidative stress contribute to pathomechanisms in amyotrophic lateral sclerosis (ALS). The aim of the present study was to verify the involvement of monocyte chemoattractant protein-1 (MCP-1) and its specific CC chemokine receptor 2 (CCR2) in the disease progression of ALS. We here demonstrate the expression state of MCP-1 and CCR2 in lumbar spinal cords of mice overexpressing a transgene for G93A mutant human superoxide dismutase 1 (SOD1) (ALS mice) as a mouse model of ALS as well as the involvement of MCP-1/CCR2-mediated signaling in behavior of cultured astrocytes derived from those mice.ResultsQuantitative polymerase chain reaction analysis revealed that MCP-1 and CCR2 mRNA levels were significantly higher in ALS mice than those in nontransgenic littermates (control mice) at the presymptomatic stage. Immunoblot analysis disclosed a significantly higher CCR2/β-actin optical density ratio in the postsymptomatic ALS mouse group than those in the age-matched control mouse group. Immunohistochemically, MCP-1 determinants were mainly localized in motor neurons, while CCR2 determinants were exclusively localized in reactive astrocytes. Primary cultures of astrocytes derived from ALS mice showed a significant increase in proliferation activity under recombinant murine MCP-1 stimuli as compared to those from control mice.ConclusionsOur results provide in vivo and in vitro evidence that MCP-1 stimulates astrocytes via CCR2 to induce astrocytosis in ALS with SOD1 gene mutation. Thus, it is likely that MCP-1/CCR2-mediated sigaling is involved in the disease progression of ALS.

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“…The activation of TIAR mechanisms results in the local production of estrogens, and may cause infiltration of the basal endometrium deep into the myometrial wall (Leyendecker et al 2009). Endometriotic cells have invasive potential and are capable of migrating by amoeboid contraction and expansion, which enables endometrial cells to penetrate into the myometrium after the en-dometrium-myometrium border breaks down (Ferenczy 1998, Li et al 2012.…”

Section: Trauma -Dependent Cause Of Adenomyosismentioning

confidence: 99%

“…Because E2 signaling promotes prolif-eration, the ability of E2 receptors to bind many ligands, including phytoestrogens and other endocrine disruptors, is a concern (Dusza et al 2006). In addition, the modification of P4 and E2 activity might promote changes in adenomyotic tissue, such as HOXA11 (Szczepańska et al 2012), chemokines (Li et al 2012), cytokines (Ulukus et al 2005) and lipoxins (Szczepańska et al 2012). In cows, the aspect of P4 resistance is considered in the postpartum period during bacterial infection (Lewis 2003).…”

Section: Hormonal Dependencymentioning

confidence: 99%

Is adenomyosis a problem in reproduction and fertility?

Korzekwa

Łupicka

Socha

et al. 2014

Polish Journal of Veterinary Sciences

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Adenomyosis is defined as the presence of glandular foci beside the endometrium of uterus: in the myometrium and/or perimetrium depending on the progress of the disorder. So far, adenomyosis has been diagnosed in women and rodents, and studies conducted on cows have been rare. In this review we: (1) summarize the knowledge regarding adenomyosis, (2) compare the symptoms and aetiopathology between women and cows, (3) describe angiogenic uterine processes related to adenomyosis development and (4) outline the influence of adenomyosis on proper fertility processes in cattle (conception and fertility rates).

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Chemokine CCL2 enhances survival and invasiveness of endometrial stromal cells in an autocrine manner by activating Akt and MAPK/Erk1/2 signal pathway

Cited by 60 publications

References 38 publications

Ceramide 1-phosphate induces macrophage chemoattractant protein-1 release: involvement in ceramide 1-phosphate-stimulated cell migration

Ceramide 1-phosphate induces macrophage chemoattractant protein-1 release: involvement in ceramide 1-phosphate-stimulated cell migration

MCP-1/CCR2 signaling-mediated astrocytosis is accelerated in a transgenic mouse model of SOD1-mutated familial ALS

Is adenomyosis a problem in reproduction and fertility?

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