Effects of 17β‐estradiol on the release of monocyte chemotactic protein‐1 and MAPK activity in monocytes stimulated with peritoneal fluid from endometriosis patients

Lee, Dong‐Hyung; Kim, Seung‐Chul; Joo, Jong‐Kil; Kim, Hwi-Gon; Na, Young-Jin; Kwak, Jong‐Young; Lee, Kyusup

doi:10.1111/j.1447-0756.2011.01734.x

Cited by 19 publications

(16 citation statements)

References 37 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 Nonetheless, although MCP-1 release has been associated with activation of p38 in many instances (8,33,56; and our unpublished observations), other studies have indicated that this kinase is not involved in this process (31,35), and therefore the role of p38 in stimulation of MCP-1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: Discussionsupporting

confidence: 79%

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: Discussionsupporting

confidence: 79%

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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“…While TGF‐β1 is well‐documented to induce EMT, the intracellular signaling responsible for this induction includes activation of ERK1/2, p38 MAPK, and JNK . Again, ERK1/2, p38 MAPK, and JNK have all been reported to be involved in endometriosis …”

Section: Mutations Of Cancer Driver Genes In Endometriosis and Their mentioning

confidence: 99%

“…261 Again, ERK1/2, p38 MAPK, and JNK have all been reported to be involved in endometriosis. [262][263][264][265][266][267] | 377…”

Section: Krasmentioning

confidence: 99%

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Guo

2018

Reprod Medicine & Biology

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BackgroundOne recent study reports cancer driver mutations in deep endometriosis, but its biological/clinical significance remains unclear. Since the natural history of endometriosis is essentially gradual progression toward fibrosis, it is thus hypothesized that the six driver genes reported to be mutated in endometriosis (the RP set) may play important roles in fibrogenesis but not necessarily malignant transformation.MethodsExtensive PubMed search to see whether RP and another set of driver genes not yet reported (NR) to be mutated in endometriosis have any roles in fibrogenesis. All studies reporting on the role of fibrogenesis of the genes in both RP and NR sets were retrieved and evaluated in this review.ResultsAll six RP genes were involved in various aspects of fibrogenesis as compared with only three NR genes. These nine genes can be anchored in networks linking with their upstream and downstream genes that are known to be aberrantly expressed in endometriosis, piecing together seemingly unrelated findings.ConclusionsGiven that somatic driver mutations can and do occur frequently in physiologically normal tissues, it is argued that these mutations in endometriosis are not necessarily synonymous with malignancy or premalignancy, but the result of enormous pressure for fibrogenesis.

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“…After treating monocytes with control peritoneal fluid (cPF) or endometriotic peritoneal fluid (ePF), the addition of E2 to the culture suppresses MCP1 release from cPF-treated monocytes. However, E2 does not suppress MCP1 release from ePF-treated monocytes (Lee et al 2012). E2 promotes a pro-inflammatory environment by increasing secretion of IL6 and TNF from peritoneal macrophages from women with endometriosis compared to control women.…”

Section: Pathogenesis and Progression Of Endometriosismentioning

confidence: 99%

Endometriosis: where are we and where are we going?

Greene¹,

Lang²,

Kendziorski³

et al. 2016

Reproduction

147

106

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Endometriosis currently affects ∼5.5 million reproductive-aged women in the U.S. with symptoms such as painful periods (dysmenorrhea), chronic pelvic pain, pain with intercourse (dyspareunia), and infertility. It is defined as the presence of endometrial tissue outside the uterine cavity and is found predominately attached to sites within the peritoneal cavity. Diagnosis for endometriosis is solely made through surgery as no consistent biomarkers for disease diagnosis exist. There is no cure for endometriosis and treatments only target symptoms and not the underlying mechanism(s) of disease. The nature of individual predisposing factors or inherent defects in the endometrium, immune system, and/or peritoneal cavity of women with endometriosis remains unclear. The literature over the last 5 years (2010-2015) has advanced our critical knowledge related to hormones, hormone receptors, immune dysregulation, hormonal treatments, and the transformation of endometriosis to ovarian cancer. In this review, we cover the aforementioned topics with the goal of providing the reader an overview and related references for further study to highlight the progress made in endometriosis research, while concluding with critical areas of endometriosis research that are urgently needed.

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Effects of 17β‐estradiol on the release of monocyte chemotactic protein‐1 and MAPK activity in monocytes stimulated with peritoneal fluid from endometriosis patients

Abstract: The ability of E2 to modulate MCP-1 production is impaired in ePF-treated monocytes, which may be related to regulation of MAPK activity. These findings suggest that the failure of E2 to suppress ePF-treated production of MCP-1 may be involved in the pathogenesis of endometriosis.

Cited by 19 publications

References 37 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

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Endometriosis: where are we and where are we going?

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