tosylphenylalanyl-chloromethyl-ketone and Endometriosis

tosylphenylalanyl-chloromethyl-ketone has been researched along with Endometriosis* in 4 studies

Other Studies

4 other study(ies) available for tosylphenylalanyl-chloromethyl-ketone and Endometriosis

ArticleYear
The cellular inhibitor of apoptosis protein-2 is a possible target of novel treatment for endometriosis.
    American journal of reproductive immunology (New York, N.Y. : 1989), 2014, Volume: 71, Issue:3

    How is the tumor necrosis factor (TNF) α-induced inhibitor of apoptosis (IAP) protein expression in endometriotic stromal cells (ESCs) involved in cell viability and signaling pathways?. Endometriotic stromal cells were isolated from ovarian chocolate cysts in 20 patients who underwent laparoscopic surgery. IAP protein expression and IκB phosphorylation were evaluated by Western blot analysis. Interleukin (IL)-8 protein expression and cell proliferation were assessed by ELISA.. Cellular IAP (cIAP)-2 protein expression in endometriotic tissue was higher than that of endometrium. TNFα markedly enhanced cIAP-2 protein expression in ESCs. Pretreatment with a nuclear factor (NF)-κB inhibitor attenuated TNFα-induced cIAP-2 expression. An antagonist of IAPs abrogated TNFα-induced cIAP-2 protein expression and showed a decrease in TNFα-induced IL-8 protein expression and BrdU incorporation in ESCs.. TNFα and its downstream NFκB pathway have proven to be critical regulators of highly expressed cIAP-2 in ESCs. cIAP-2 may be a novel therapeutic target for endometriosis.

    Topics: Cell Proliferation; Cells, Cultured; Endometriosis; Endometrium; Female; Gene Expression Regulation; Humans; I-kappa B Proteins; Inhibitor of Apoptosis Proteins; Interleukin-8; Molecular Targeted Therapy; NF-kappa B; Oligopeptides; Phosphorylation; Signal Transduction; Stromal Cells; Tosylphenylalanyl Chloromethyl Ketone; Tumor Necrosis Factor-alpha

2014
Thalidomide inhibits tumor necrosis factor-alpha-induced interleukin-8 expression in endometriotic stromal cells, possibly through suppression of nuclear factor-kappaB activation.
    The Journal of clinical endocrinology and metabolism, 2005, Volume: 90, Issue:5

    Endometriosis, a common disease among women of reproductive age, is characterized by the presence of endometrial-like tissue outside the uterus. TNF-alpha induces IL-8 production in endometriotic cells through nuclear factor-kappaB (NF-kappaB) activation. Thalidomide (Thal) inhibits inflammation by down-regulating the expression of proinflammatory cytokines in tumor cells and inflammatory cells. However, the mechanism of Thal action in human endometriotic stromal cells has not yet been elucidated.. We examined whether Thal abrogates TNF-alpha-induced up-regulation of IL-8 expression in endometriotic stromal cells.. Here, we show 1) that treatment of endometriotic stromal cells with TNF-alpha increased the expression of phosphorylated IkappaBalpha and degradation of total IkappaBalpha, which in turn activates NF-kappaB; 2) Thal significantly inhibits the TNF-alpha-induced expression of phosphorylated IkappaBalpha and degradation of IkappaBalpha; 3) TNF-alpha activation induced increased nuclear translocation of NF-kappaB, which was inhibited by pretreatment with either Thal or N-tosyl-L-phenylalanine chloromethyl ketone, an NF-kappaB inhibitor. Thal did not enhance the N-tosyl-L-phenylalanine chloromethyl ketone's action; and 4) Pretreatment with Thal reduced TNF-alpha-induced IL-8 protein production as well as mRNA expression.. The current study showed for the first time that Thal treatment attenuated the expression of IL-8 by reducing TNF-alpha-induced NF-kappaB activation.

    Topics: Active Transport, Cell Nucleus; Cells, Cultured; Endometriosis; Female; Humans; I-kappa B Proteins; Interleukin-8; NF-KappaB Inhibitor alpha; Stromal Cells; Thalidomide; Tosylphenylalanyl Chloromethyl Ketone; Tumor Necrosis Factor-alpha

2005
Lipopolysaccharide-promoted proliferation of endometriotic stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression.
    Fertility and sterility, 2004, Volume: 82 Suppl 3

    To evaluate the effect of lipopolysaccharide (LPS) on the expression of tumor necrosis factor alpha (TNFalpha) and interleukin-8 (IL-8) protein in endometriotic stromal cells (ESC) and their effect on the proliferation of ESC.. Prospective study.. Department of Obstetrics and Gynecology, Tottori University Hospital, Yonago, Japan.. Seventeen patients who underwent laparoscopic surgery.. Endometriotic stromal cells were obtained from chocolate cyst linings of the ovary.. We determined the effect of LPS on the production of TNFalpha and IL-8 and the effect of IL-8 antisense oligonucleotide and nuclear factor-kappaB (NF-kappaB) inhibitor on IL-8 production using ELISA. TNFalpha production was examined by immunocytochemical staining. We determined the effect of LPS and the effect of IL-8 antisense oligonucleotide and NF-kappaB inhibitor on LPS-promoted ESC proliferation.. LPS-stimulated ESC produced significant amounts of TNFalpha and IL-8 in a dose- and time-dependent fashion. Adding LPS promoted ESC proliferation. Anti-TNFalpha antibody and anti-IL-8 antibody inhibited the stimulatory effects of LPS. IL-8 antisense oligonucleotide and NF-kappaB inhibitor significantly decreased LPS-induced IL-8 protein production and LPS-induced ESC proliferation.. Pelvic inflammation may promote the progression of endometriosis.

    Topics: Cell Division; Dose-Response Relationship, Drug; Endometriosis; Female; Gene Expression; Humans; Immunohistochemistry; Interleukin-8; Lipopolysaccharides; Membrane Glycoproteins; NF-kappa B; Oligonucleotides, Antisense; Prospective Studies; Receptors, Cell Surface; Staining and Labeling; Stromal Cells; Toll-Like Receptors; Tosylphenylalanyl Chloromethyl Ketone; Tumor Necrosis Factor-alpha

2004
Tumor necrosis factor-alpha-induced interleukin-8 (IL-8) expression in endometriotic stromal cells, probably through nuclear factor-kappa B activation: gonadotropin-releasing hormone agonist treatment reduced IL-8 expression.
    The Journal of clinical endocrinology and metabolism, 2003, Volume: 88, Issue:2

    Endometriosis, a common disease among women of reproductive age, is characterized by the presence of endometrial-like tissue outside the uterus. We previously reported that TNFalpha promoted proliferation of endometriotic stromal cells by inducing IL-8 gene and protein expression. We hypothesize that TNFalpha may induce IL-8 production in endometriotic cells through nuclear factor-kappa B (NF-kappa B) activation. Western blot analyses and electrophoretic mobility shift assays revealed that incubation with TNF alpha induced the expression of phosphorylated inhibitor kappa B (p-I kappa B) and activation of NF-kappa B in endometriotic stromal cells. The NF-kappa B inhibitor, N-tosyl-L-phenylalanine chloromethyl ketone, reduced TNFalpha-induced IL-8 gene and protein expression. The medical treatment of endometriosis with GnRH agonist (GnRHa) has been shown to induce hypoestrogenemia and reduce the observable number of endometriotic implants. We compare the expression of IL-8 gene and protein in endometriotic stromal cells of patients treated with GnRHa and those of patients without treatment before laparoscopic cystectomy for endometrioma. The addition of TNFalpha (0.1 ng/ml) significantly increased protein and gene expression of IL-8 in the cells of patients without GnRHa treatment, but this expression was not observed in the cells of patients with GnRHa. The addition of estradiol (E2; 10(-7) M) enhanced the expression of IL-8. However, in the cells of patients who received GnRHa treatment, TNFalpha and E2 did not show any significant effect. In endometriotic stromal cells without GnRHa treatment, TNFalpha and E2 increased the expression of p-I kappa B. In contrast, TNFalpha and E2 had no significant effect on the expression of p-I kappa B in cells that received GnRHa treatment. These findings demonstrate that NF-kappa B activation is critical for TNFalpha-induced IL-8 expression in endometriotic stromal cells. The current study showed for the first time that GnRHa treatment attenuated the expression of IL-8 by reducing TNFalpha-induced NF-kappa B activation.

    Topics: Adult; Antineoplastic Agents; Cells, Cultured; Electrophoretic Mobility Shift Assay; Endometriosis; Estrogens; Female; Gene Expression; Gonadotropin-Releasing Hormone; Humans; I-kappa B Proteins; Interleukin-8; NF-kappa B; NF-KappaB Inhibitor alpha; Phosphorylation; Protein Synthesis Inhibitors; RNA, Messenger; Stromal Cells; Tosylphenylalanyl Chloromethyl Ketone; Tumor Necrosis Factor-alpha

2003
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