New markers in pelvic inflammatory disease

Yang, Shun Fa; Wu, Tzu Fan; Tsai, Hsiu Ting; Lin, Long Yau; Wang, Po Hui

doi:10.1016/j.cca.2014.02.004

Cited by 21 publications

(15 citation statements)

References 108 publications

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“…At least 20 different MMPs have been identified, and MMPs play major roles in various pathophysiological processes, including angiogenesis, arthritis, inflammation, skeletal growth and remodeling, photoaging, wound healing, and cancer . The gelatinases, namely MMP‐2 and MMP‐9, have been reported to play key roles in the degradation of the ECM and the promotion of tumor invasion and metastasis .…”

Section: Introductionmentioning

confidence: 99%

“…12,13 At least 20 different MMPs have been identified, and MMPs play major roles in various pathophysiological processes, including angiogenesis, arthritis, inflammation, skeletal growth and remodeling, photoaging, wound healing, and cancer. 11,[13][14][15] The gelatinases, namely MMP-2 and MMP-9, have been reported to play key roles in the degradation of the ECM and the promotion of tumor invasion and metastasis. [16][17][18] Despite advances in research and treatment over the past few years, no significant improvements have been made in the survival of patients with oral cancer, which is an ongoing challenge for the biomedical science community.…”

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confidence: 99%

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Geraniin inhibits oral cancer cell migration by suppressing matrix metalloproteinase‐2 activation through the FAK/Src and ERK pathways

Yeh

Hsieh

Yang

et al. 2019

Environmental Toxicology

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Geraniin has been reported to have numerous biological activities, including antiviral, antihypertensive, antihyperglycaemic, liver protective, antidiabetic, and apoptotic activities. However, the anti‐migration effects of geraniin on oral cancer remain elusive. In this study, we revealed the potential antitumor mechanisms of geraniin through the inhibition of the migration and invasion of human oral cancer cell lines SCC‐9 and SCC‐14. The results of gelatin zymography and Western blot assays revealed that geraniin significantly reduced the activity and expression of matrix metalloproteinase‐2 (MMP‐2) of oral cancer cells in a concentration‐dependent manner. Furthermore, geraniin potently suppressed the phosphorylation of focal adhesion kinase (FAK), Src, and extracellular signal‐regulated kinase (ERK)1/2 but did not affect the phosphorylation of p38 mitogen‐activated protein kinase (MAPK) and c‐Jun N‐terminal kinase 1/2. Moreover, blocking the MAPK/ERK1/2 pathway significantly enhanced the anti‐migration ability of geraniin in oral cancer cells. In conclusion, we demonstrated that geraniin inhibits the motility of SCC‐9 and SCC‐14 cells in vitro through a molecular mechanism that involves the attenuation of MMP‐2 expression and activity mediated by decreased FAK/Src and ERK1/2 pathways.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Geraniin inhibits oral cancer cell migration by suppressing matrix metalloproteinase‐2 activation through the FAK/Src and ERK pathways

Yeh

Hsieh

Yang

et al. 2019

Environmental Toxicology

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“…Our data showed that TLR3 deficiency in hOE cells significantly altered the Chlamydia -induced expression levels of biomarkers for chronic inflammation, persistence, and autoimmunity such as soluble CD163 (sCD163), Chitinase-3-like 1, Osteopontin (OPN), and Pentraxin-3 (58–60, 79–82). OPN was first identified in osteoclasts as an extracellular structural protein of bone and is known as an essential factor in bone remodeling (83).…”

Section: Discussionmentioning

confidence: 83%

“…Figures 10 and 11 show that TLR3 deficiency leads to significantly increased levels of osteopontin and pentraxin-3. The role of these proteins in Chlamydia infection is not clear; however, osteopontin is an inflammatory mediator often associated with autoimmune disease, chronic inflammatory disorders, and progression of tumor cells (58), while pentraxin-3 is a known biomarker for pelvic inflammatory disease (PID) and is also associated with autoimmune diseases (59, 60). Collectively, our findings indicate that TLR3 may have a functional role in regulating the expression of biomarkers symbolic of long-term or persistent disease states in the Chlamydia -infected hOE cells, which is a precondition that often correlates with the initiation of autoimmune responses and chronic sequelae (61–64).…”

Section: Resultsmentioning

confidence: 99%

TLR3 Deficiency Leads to Altered Immune Responses toChlamydia trachomatisInfection in Human Oviduct Epithelial Cells

Kumar

Gong

et al. 2019

Preprint

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Reproductive tract pathology caused by Chlamydia trachomatis infection is an important 24 global cause of human infertility. To better understand the mechanisms associated with 25 Chlamydia-induced genital tract pathogenesis in humans, we used CRISPR genome 26 editing to disrupt TLR3 function in the human oviduct epithelial (hOE) cell-line OE-27 E6/E7, in order to investigate the possible role(s) of TLR3 signaling in the immune 28 response to Chlamydia. Disruption of TLR3 function in these cells significantly 29 diminished the Chlamydia-induced synthesis of several inflammation biomarkers 30including IFN-β, IL-6, IL-6Ra, sIL-6Rβ (gp130), 31 TNFSF13B, MMP-1, MMP-2, and MMP-3. In contrast, the Chlamydia-induced synthesis 32 of CCL-5, IL-29 (IFNλ1) and IL-28A (IFNλ2) were significantly increased in the TLR3-33 deficient hOE cells when compared to their wild-type counterparts. Our results propose 34 a role for TLR3 signaling in limiting the genital tract fibrosis, scarring, and chronic 35 inflammation often associated with human chlamydial disease. Interestingly, we saw 36 that Chlamydia infection induced the production of biomarkers associated with 37 persistence, tumor metastasis, and autoimmunity such as soluble CD163 (sCD163), 38 chitinase-3-like protein 1, osteopontin, and pentraxin-3 in the hOE cells; however, their 39 expression levels were significantly dysregulated in the TLR3-deficient hOE cells. 40Finally, we demonstrate using the hOE cells that TLR3 deficiency resulted in an 41 increased amount of chlamydial LPS within the Chlamydia inclusion, which is 42 suggestive that TLR3 deficiency leads to enhanced chlamydial replication and possibly 43 increased genital tract pathogenesis during human infection. 44 45 3 KEYWORDS: Chlamydia trachomatis, TLR3, human oviduct epithelial cells. 46 Abbreviations: hOE, human OE-E6/E7 cells; TLR3 KO, TLR3 knockout cell line; poly 47 (I:C), Polyinosinic-polycytidylic acid sodium salt. 48 49 50 51 52 53 The bacterial pathogen Chlamydia trachomatis has caused 1,526,658 infections in the 54 United States in 2015 (an increase of 6% since 2014), and it is the most commonly 55 reported bacterial sexually transmitted disease (STD) in the United States (1). Genital 56 tract C. trachomatis infections are easily cured with antibiotics if properly diagnosed at 57 early stages of infection. However, because 75-90% of women infected with Chlamydia 58 are asymptomatic for clinical disease, opportunities for therapeutic interventions are 59 usually missed. The asymptomatic nature of the clinical symptoms is the major 60contributing factor to the continuing spread of the disease to uninfected partners, and 61 the more severe pathogenesis and sequelae that often lead to infertility in women. 62Further contributing to the growing rates of infectivity amongst the previously uninfected 63 populations are the statistics showing that up to 90% of men infected with Chlamydia 64 exhibit no symptoms (2, 3) and that an effective vaccine remains elusive (4). 65Chlamydia infections are also lead...

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“…Another bias might be a confounding bias for unknown variables not accounted for in our study. Third, the lack of sensitivity and specificity in the diagnosis of PID may affect the accuracy of the diagnosis [26], an issue which is unfortunately is well known regarding PID disease and PID studies. Moreover there is no standardized definition of recurrent PID, choosing 30 days was based on the standard readmission [10] rate and the PEACH trial [3], but as it was arbitrary it might be a source of information bias.…”

Section: Discussionmentioning

confidence: 99%