TLR4 Activation Promotes the Secretion of IL-8 Which Enhances the Invasion and Proliferation of Endometrial Stromal Cells in an Autocrine Manner via the FAK Signal Pathway

Luo, Xuezhen; Zhou, Wen‐Jie; Yu, Tao; Wang, Xiaoqiu; Li, Da‐Jin

doi:10.1111/aji.12425

Cited by 17 publications

(7 citation statements)

References 46 publications

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“…Luo et al . 12 found that the expression of TLR4 in EU was higher than that in the normal endometrium, and was the highest in EC tissue. TLR4 activation stimulated IL-8 secretion, thus enhancing the invasion and proliferation of endometrial stromal cells through the FAK signal pathway, and these effects could be abolished by an anti-CXCL8 neutralizing antibody or by a FAK inhibitor.…”

Section: Discussionmentioning

confidence: 88%

“…Numerous studies have demonstrated that TLR-mediated activation of immune response may be associated with endometriosis and adenomyosis. It was reported that the expression of TLR4 in the ectopic endometrium of endometriosis was higher than that in the normal endometrium, and the levels of TLR2 and TLR9 mRNAs were higher in the peritoneal effusions of endometriosis than in the non-endometriosis group 12 , 13 .…”

Section: Introductionmentioning

confidence: 94%

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The Expression of Toll-like receptors in eutopic and ectopic endometrium and its implication in the inflammatory pathogenesis of adenomyosis

Jiang

Liu

Guo

et al. 2017

Sci Rep

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In this study, we investigated the expression profiles of Toll-like receptors(TLRs) in eutopic endometrium(EU) and ectopic endometrium(EC) and its implication in the inflammatory pathogenesis of adenomyosis. Thirty adenomyosis patients who underwent laparoscopy were recruited in this study. We tested the mRNA and protein expression of TLRs, and the mRNA expression of IL-6 and IL-8 in EU and EC of adenomyosis patients, and control endometrium without adenomyosis(CE). We found that the mRNA expression of IL-6 and IL-8 in EU was significantly higher than that in CE, and was the highest in EC (P < 0.01). The mRNA and protein expression of TLRs were higher in EU, with the expression of TLR1-6, 8 and 9 being significantly higher in EU than in CE, and were the highest in EC (except TLR6) (P < 0.05 or P < 0.01). Pearson correlation analysis showed that the expression of TLR1, 2, 4, 5 and 9 in EU and EC was positively correlated with that of IL-6 and IL-8 (P < 0.00139). This study suggested that adenomyosis was a state of inflammatory pathology. High expression of TLRs in EU and EC were positively correlated with IL-6 and IL-8, which may be involved in the inflammatory pathogenesis of adenomyosis.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 94%

The Expression of Toll-like receptors in eutopic and ectopic endometrium and its implication in the inflammatory pathogenesis of adenomyosis

Jiang

Liu

Guo

et al. 2017

Sci Rep

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“…A variety of molecules activate TLRs on the cell surface (69). TLR4 is best known to be targeted by LPS from bacteria, which leads to cytokine production (70). We therefore analyzed the effect of Fa27 on LPS-activated TLR4 signaling using a reporter cell line and indeed noticed an inhibitory effect of the peptide in the concentration range exerting MLLbcr protection.…”

Section: Discussionmentioning

confidence: 91%

A Fibrinogen Alpha Fragment Mitigates Chemotherapy-Induced MLL Rearrangements

et al. 2021

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Rearrangements in the Mixed Lineage Leukemia breakpoint cluster region (MLLbcr) are frequently involved in therapy-induced leukemia, a severe side effect of anti-cancer therapies. Previous work unraveled Endonuclease G as the critical nuclease causing initial breakage in the MLLbcr in response to different types of chemotherapeutic treatment. To identify peptides protecting against therapy-induced leukemia, we screened a hemofiltrate-derived peptide library by use of an enhanced green fluorescent protein (EGFP)-based chromosomal reporter of MLLbcr rearrangements. Chromatographic purification of one active fraction and subsequent mass spectrometry allowed to isolate a C-terminal 27-mer of fibrinogen α encompassing amino acids 603 to 629. The chemically synthesized peptide, termed Fα27, inhibited MLLbcr rearrangements in immortalized hematopoietic cells following treatment with the cytostatics etoposide or doxorubicin. We also provide evidence for protection of primary human hematopoietic stem and progenitor cells from therapy-induced MLLbcr breakage. Of note, fibrinogen has been described to activate toll-like receptor 4 (TLR4). Dissecting the Fα27 mode-of action revealed association of the peptide with TLR4 in an antagonistic fashion affecting downstream NFκB signaling and pro-inflammatory cytokine production. In conclusion, we identified a hemofiltrate-derived peptide inhibitor of the genome destabilizing events causing secondary leukemia in patients undergoing chemotherapy.

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“…A recent study by Luo et al showed enhanced Toll‐like receptor 4 (TLR4) expression the ectopic endometrium and stimulation of IL‐8 secretion by TLR4 ligands in ERK1/2 and p38 MAPK‐dependent manner in endometriotic stromal cells. Moreover, a previous report from our laboratory demonstrated the expression and regulation of T‐ERK1/2 and P‐ERK1/2 in endometrial stromal and glandular cells in women with or without endometriosis .…”

Section: Discussionmentioning

confidence: 99%

The extracellular signal‐regulated kinase 1/2 triggers angiogenesis in human ectopic endometrial implants by inducing angioblast differentiation and proliferation

Arlıer

Murk

Guzeloglu‐Kayisli

et al. 2017

American J Rep Immunol

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TLR4 Activation Promotes the Secretion of IL-8 Which Enhances the Invasion and Proliferation of Endometrial Stromal Cells in an Autocrine Manner via the FAK Signal Pathway

Cited by 17 publications

References 46 publications

The Expression of Toll-like receptors in eutopic and ectopic endometrium and its implication in the inflammatory pathogenesis of adenomyosis

The Expression of Toll-like receptors in eutopic and ectopic endometrium and its implication in the inflammatory pathogenesis of adenomyosis

A Fibrinogen Alpha Fragment Mitigates Chemotherapy-Induced MLL Rearrangements

The extracellular signal‐regulated kinase 1/2 triggers angiogenesis in human ectopic endometrial implants by inducing angioblast differentiation and proliferation

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