Increased expression of p21-activated kinase 4 in adenomyosis and its regulation of matrix metalloproteinase-2 and -9 in endometrial cells

Yi, Kyong Wook; Kim, Sung Hoon; Ihm, Hyo Jin; Oh, Yumi; Chae, Hee Dong; Kang, Byung Moon

doi:10.1016/j.fertnstert.2014.12.124

Cited by 24 publications

(18 citation statements)

References 46 publications

(75 reference statements)

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“…Cell invasion is a vital hallmark of tumor formation and progression. Indeed, upregulation of several MMPs has also been linked to the pathogenesis of adenomyosis (39,40). Weigel et al (41) demonstrated obvious differences in the expression pattern of MMP2 and MMP9 in different stages of endometriosis and suggested that these markers may be used to evaluate the aggressiveness and invasiveness of endometriotic lesions.…”

Section: Discussionmentioning

confidence: 99%

Berberine inhibits the LPS‑induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

et al. 2017

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Abstract.A previous study by our group has demonstrated that lipopolysaccharide (LPS) induces adenomyosis through stimulating inflammatory cell proliferation and invasive growth of stromal cells via Toll-like receptor 4 (TLR4) signaling. The present study aimed to investigate the effects of berberine (BBR) on LPS-induced ectopic endometrial stromal cells (EESCs) isolated from patients with adenomyosis. The viability of EESCs treated with LPS or LPS plus BBR was detected by a cell counting kit-8 assay, and the cell cycle distribution and apoptosis were evaluated by flow cytometry. The effect of BBR on the expression of key molecules of inflammatory proliferation and invasive growth of LPS-induced EESCs was also evaluated. BBR significantly inhibited the LPS-induced proliferation of EESCs in a dose-and time-dependent manner. BBR induced cell cycle arrest in G0/G1 phase and enhanced apoptosis of LPS-induced EESCs. Furthermore, BBR inhibited the expression of interleukin (IL)-6, IL-8, transforming growth factor-β, epithelial growth factor, vascular endothelial growth factor and matrix metalloproteinase 2 in LPS-induced EESCs. To the best of our knowledge, the present study was the first to demonstrate that BBR has a protective effect on ameliorating the LPS-induced progression of adenomyosis. This result may provide a novel therapeutic strategy for the clinical treatment of the disease.

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Section: Discussionmentioning

confidence: 99%

Berberine inhibits the LPS‑induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

et al. 2017

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“…We suggested that blunting of progesterone-induced down-regulation of Pak1 might lead to establishment of adenomyosis as well as endometriosis, based on our previous findings showing that Pak1 is down-regulated by progesterone along with its decreased expression in endometriosis [ 22 ]. In a recent study, we also showed an increased expression of Pak4 in adenomyosis and demonstrated that the Pak4 expression is NF-κB–dependent and that Pak4 can activate MMP (matrix metalloproteinase)-2 and -9 in endometrial cells, which eventually leads to the infiltration of endometrial cells into myometrial layer [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Increased expression of nuclear factor kappa-B p65 subunit in adenomyosis

et al. 2016

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ObjectiveNuclear factor kappa-B (NF-κB) is a critical proinflammatory regulator that has been suggested to play a pivotal role in the pathogenesis and pathophysiology of endometriosis. In the present study, we aimed to evaluate whether the expression of NF-κB p65 subunit is increased in the eutopic endometrium and/or in the adenomyosis nodule of women with adenomyosis.MethodsThirty-three women with histologically confirmed adenomyosis after laparoscopic or transabdominal hysterectomy were recruited. Women with carcinoma in situ of uterine cervix without evidence of adenomyosis or endometriosis (n=32) served as controls. Formalin-fixed, paraffin-embedded archival tissues were sectioned and immunostained utilizing a monoclonal anti-human NF-κB p65 subunit antibody, and the immunoreactivity of NF-κB p65 subunit was compared between women with and without adenomyosis.ResultsThe immunoreactivities of both the nuclear and the cytoplasmic NF-κB p65 subunit were significantly increased in the stromal cells in the eutopic endometrium as well as in the adenomyosis nodule of women with adenomyosis compared with controls, respectively. The nuclear expression of NF-κB p65 subunit was significantly higher in the glandular cells in the eutopic endometrium as well as the adenomyosis nodule of women with adenomyosis compared with controls, respectively.ConclusionThe expression of NF-κB p65 is increased in the eutopic endometrium and adenomyosis nodule of women with adenomyosis, which strongly suggest that NF-κB plays a critical role in the pathogenesis and/or pathophysiology of adenomyosis.

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“…Activation of PAK1, a serine/threonine kinase, triggers several downstream signaling pathways including MMPs, which mediate spinal cord edema and disruption of the BSCB integrity after SCI [12][13][14][15][16][17][18]. Because PAK1 is an important upstream regulator of a variety of MMPs, inhibition of PAK1 by IPA-3 may exert neuroprotection via inhibition of certain types of MMPs.…”

Section: Discussionmentioning

confidence: 99%

“…12 Moreover, PAK family proteins are reported to be upstream regulators of matrix metalloproteinase (MMPs). [13][14][15][16][17][18][19] Therefore, PAK1 may be an important culprit in the SCI, because NF-KB, P38 MAPK , caspase-1, and MMPs are blamed for tissue edema and BSCB disruption after SCI. Because spinal cord edema and BSCB disruption were predominantly responsible for the development of secondary injury after SCI, 3 administration of PAK1 inhibitor IPA-3 may be a promising agent for reducing the secondary injury after SCI.…”

mentioning

confidence: 99%

Inhibition of p21-Activated Kinase 1 by IPA-3 Promotes Locomotor Recovery After Spinal Cord Injury in Mice

Zhang²,

Zhang³

et al. 2016

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Increased expression of p21-activated kinase 4 in adenomyosis and its regulation of matrix metalloproteinase-2 and -9 in endometrial cells

Cited by 24 publications

References 46 publications

Berberine inhibits the LPS‑induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

Berberine inhibits the LPS‑induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

Increased expression of nuclear factor kappa-B p65 subunit in adenomyosis

Inhibition of p21-Activated Kinase 1 by IPA-3 Promotes Locomotor Recovery After Spinal Cord Injury in Mice

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