Expression of interleukin-8 and monocyte chemotactic protein 1 in women with endometriosis

Ulukuş, Murat; Ulukuş, Emine Çağnur; Göker, Ege Nazan Tavmergen; Tavmergen, Erol; Zheng, Wenxin; Arıcı, Aydın

doi:10.1016/j.fertnstert.2007.12.067

Cited by 85 publications

(45 citation statements)

References 39 publications

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“…Our data indicate that cytokines such as GRO, MCP1, IL6, and IL8 could be upregulated in the endometrial cells in response to LCN2 and that these factors could induce cell migration. MCP1, IL8, and IL6 are important for endometriosis formation (Ulukus et al 2009, McKinnon et al 2012, so reducing the levels of these factors might inhibit endometriosis.…”

Section: Discussionmentioning

confidence: 99%

Lipocalin 2 induces the epithelial–mesenchymal transition in stressed endometrial epithelial cells: possible correlation with endometriosis development in a mouse model

Liao

Lee

et al. 2014

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Lipocalin 2 (LCN2) is an induced stressor that promotes the epithelial-mesenchymal transition (EMT). We previously demonstrated that the development of endometriosis in mice correlates with the secretion of LCN2 in the uterus. Here, we sought to clarify the relationship between LCN2 and EMT in endometrial epithelial cells and to determine whether LCN2 plays a role in endometriosis. Antibodies that functionally inhibit LCN2 slowed the growth of ectopic endometrial tissue in a mouse model of endometriosis, suggesting that LCN2 promotes the formation of endometriotic lesions. Using nutrient deprivation as a stressor, LCN2 expression was induced in cultured primary endometrial epithelial cells. As LCN2 levels increased, the cells transitioned from a round to a spindle-like morphology and dispersed. Immunochemical analyses revealed decreased levels of cytokeratin and increased levels of fibronectin in these endometrial cells, adhesive changes that correlate with induction of cell migration and invasion. Lcn2 knockdown also indicated that LCN2 promotes EMT and migration of endometrial epithelial cells. Our results suggest that stressful cellular microenvironments cause uterine tissues to secrete LCN2 and that this results in EMT of endometrial epithelial cells, which may correlate with the development of ectopic endometriosis. These findings shed light on the role of LCN2 in the pathology of endometrial disorders.

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Section: Discussionmentioning

confidence: 99%

Lipocalin 2 induces the epithelial–mesenchymal transition in stressed endometrial epithelial cells: possible correlation with endometriosis development in a mouse model

Liao

Lee

et al. 2014

Reproduction

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“…Although our finding with miR-200c regulation of KLF9 is the first of such validation, others reported VEGFA, FLT1, ETS1, SUZ12, PDGF, TGF-b2, and conexin43, as well as Notch pathway components, such as Jagged1 (JAG1) and mastermind-like [24][25][26][27][28][29][30]41 Because of the lack of adequate endometrial biopsies and endometrial cancer tissues, we could not determine the coexpression of VEGFA, FLT1, IKKb, and KLF9 in the same tissues; however, several studies reported their expression in human endometrium with altered or aberrant expression in endometriosis and endometrial cancer. [48][49][50][51][52][53][54][55][56][57][58] The biological significance of VEGFA and their receptors (FLT1 and VEGFR1), in various activities, including angiogenesis, is well established, including in normal endometrium throughout the menstrual cycle, dysfunctional uterine bleeding, and endometrial repair and endometrial cancer. 53,54,57 Additionally, IKKb by serving as a cofactor for activation of NFkb pathway plays a key role in regulating the expression of many proinflammatory mediators, including interleukin 8.…”

Section: Mir-200c Targets the Expression Of Zebs Vegfa Flt1 Ikkb mentioning

confidence: 99%

Endometrial miR-200c is Altered During Transformation into Cancerous States and Targets the Expression of ZEBs, VEGFA, FLT1, IKKβ, KLF9, and FBLN5

et al. 2012

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A number of microRNAs (miRNAs), including miR-200 family, are aberrantly expressed in endometriosis and endometrial cancer. Here we assessed the expression and functional aspects of miR-200c in endometrial tissues (N ¼ 52) from normal endometrial biopsies (N ¼ 15), endometrial tissues including those exposed to hormonal therapies (N ¼ 20), and grade I-III endometrial cancer (N ¼ 17). miR-200c expression was elevated in normal endometrial biopsies from mid-and late-luteal phase, and in endometrial tumors as compared to endometrial tissues from peri-and postmenopausal period (P < .05) and its pattern of temporal expression displayed an inverse relationship with the expression of ZEBs. The expression of E-cadherin (CDH1) varied, but expressed at low levels, specifically in endometrial tissues and endometrial tumors. The endometrial expression of ZEBs and CDH1 in patients who were exposed to Depo-Provera and gonadotropin-releasing hormone agonist GnRHa displayed a trend toward lower expression as compared to proliferative phase; however, treatment of Ishikawa cells with 17b-estradiol, progesterone, and medroxy progesterone acetate had modest effects on the expression of miR-200c and ZEBs without affecting CDH1 expression. Gain of function of miR-200c in Ishikawa cells repressed ZEBs, as well as VEGFA, FLT1, IKKb, and KLF9 expression at transcriptional and translational levels through direct interaction with their respective 3 0 untranslated regions and increased the rate of their proliferation. These results indicated that endometrial miR200c expression undergoes dynamic changes during transition from normal into cancerous states; possibly influenced by hormonal milieu and by targeting the expression of specific genes with key regulatory functions in cellular transformation, inflammation, and angiogenesis may influence these events during normal and disease progression.

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“…Em países industrializados, essa é uma das principais causas de hospitalização ginecológica 3 . Apesar de ser uma das doenças mais estudadas em ginecologia 4 , alguns aspectos continuam sendo alvo de pesquisa, destacando-se a busca pela sua etiopatogenia [5][6][7] . Muitos estudos têm sido realizados na tentativa de se identificar as alterações imunológicas, genéticas, ou mesmo as respostas a contaminantes ambientais que podem estar presentes em pacientes com endometriose.…”

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Fatores ambientais e endometriose: um ponto de vista

Bellelis¹,

Podgaec²,

Abrão³

2014

Rev. Bras. Ginecol. Obstet.

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Endometriose é uma afecção ginecológica comum, que atinge de 10 a 15% das mulheres no período reprodutivo e até metade das mulheres com dor pélvica crônica e/ou infertilidade 1,2 . Estima-se que o número de mulheres com endometriose seja de 7 milhões nos Estados Unidos da América e de mais de 70 milhões no mundo. Em países industrializados, essa é uma das principais causas de hospitalização ginecológica 3 . Apesar de ser uma das doenças mais estudadas em ginecologia 4 , alguns aspectos continuam sendo alvo de pesquisa, destacando-se a busca pela sua etiopatogenia [5][6][7] . Muitos estudos têm sido realizados na tentativa de se identificar as alterações imunológicas, genéticas, ou mesmo as respostas a contaminantes ambientais que podem estar presentes em pacientes com endometriose. Desta forma, seria possível chegar a uma explicação do porquê somente em algumas mulheres, as células endometriais que adentram a cavidade peritoneal, na menstruação retrograda, não são eliminadas.Na tentativa de se estabelecer um diagnóstico não invasivo e, desta forma, um tratamento mais precoce, cada vez mais estudos têm sido conduzidos para se avaliar possíveis fatores indutores/desencadeadores dessa doença. Desses possíveis fatores desencadeadores da endometriose, estão alguns fatores ambientais. É sabido que a poluição pode desencadear inúmeras doenças, principalmente, as respiratórias. No entanto, cada vez mais tem se observado que os referidos poluentes podem causar outras doenças, ou ainda, funcionarem como fatores concausais.Muitos desses poluentes ambientais são persistentes, com meias-vidas longas, podendo se acumular no meio ambiente e influenciar negativamente desde o processo gestacional até a vida adulta. Uma análise do Environmental Working Group 8 revelou a presença de 287 agentes químicos diferentes no cordão umbilical humano , e apesar de nem todas as crianças terem sido expostas a todos os poluentes detectados, nenhuma criança não foi exposta a nenhum poluente.Considerado o poluente ambiental mais tóxico ao homem, o tetrachlorodibenzo-p-dioxina (TCDD) 2,3,7,8 tem sido amplamente estudado 9 . Entretanto, certos bifenilos policlorados (PCBs) apresentam toxicidade biológica similar ao TCDD e, portanto, também podem agir comprometendo a função reprodutiva.Os PCBs foram amplamente utilizados em transformadores, capacitores e refrigerantes por décadas. Embora sua produção tenha sido proibida, os PCBs persistem no meio ambiente

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Expression of interleukin-8 and monocyte chemotactic protein 1 in women with endometriosis

Cited by 85 publications

References 39 publications

Lipocalin 2 induces the epithelial–mesenchymal transition in stressed endometrial epithelial cells: possible correlation with endometriosis development in a mouse model

Lipocalin 2 induces the epithelial–mesenchymal transition in stressed endometrial epithelial cells: possible correlation with endometriosis development in a mouse model

Endometrial miR-200c is Altered During Transformation into Cancerous States and Targets the Expression of ZEBs, VEGFA, FLT1, IKKβ, KLF9, and FBLN5

Fatores ambientais e endometriose: um ponto de vista

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