Elevated immunoreactivity to tissue factor and its association with dysmenorrhea severity and the amount of menses in adenomyosis

Liu, Xishi; Nie, Jichan; Guo, Sun‐Wei

doi:10.1093/humrep/deq311

Cited by 57 publications

(56 citation statements)

References 64 publications

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“…The endometrial expression and activation of F3 has been reported to increase endometrial cell proliferation and IL6 and IL8 secretion (34). In addition, increased expression of IL8 and F3 has been associated with heavy menses and abnormal uterine bleeding in progestin-onlycontraceptives users (47)(48)(49). Considering the F3-induced activation of prothrombin to thrombin is a key step in coagulation cascades (50) and regulated by proinflammatory mediators such as IL8, miR-93/106b regulation of either F3 and/or IL8 may have a profound biological and clinical significance, specifically in women with symptomatic leiomyomas experiencing abnormal bleeding.…”

Section: Discussionmentioning

confidence: 99%

miR-93/106b and Their Host Gene, MCM7, Are Differentially Expressed in Leiomyomas and Functionally Target F3 and IL-8

Chuang

Panda

et al. 2012

Molecular Endocrinology

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miR-93/106b and their host gene minichromosome maintenance complex component 7 (MCM7) reside at chr7q22, a region frequently rearranged in leiomyomas. We explored the expression of miR-93/106b in leiomyoma and paired myometrium (n = 63) from untreated and patients exposed to hormonal therapies (GnRH agonist, Depo-Provera, and oral contraceptives) from African-Americans and Caucasians and their regulatory functions in isolated paired (n = 15) leiomyoma and myometrial smooth muscle cells and the leiomyosarcoma cell line. At tissue level leiomyomas expressed significantly lower levels of miR-93 and elevated MCM7 as compared with myometrium with limited racial influence or hormonal exposure on their expression. Assessing the regulatory function of miR-93/106b through doxycycline-inducible lentiviral transduction in a microarray analysis, tissue factor (F3) and IL8 were identified as their possible targets. At the tissue level, leiomyomas expressed a significantly lower level of F3 and an elevated IL-8 level, which exhibited an inverse relationship with miR-93 but with limited racial or hormonal influences. The gain of function of miR-93/106b in leiomyoma smooth muscle cells, myometrial smooth muscle cells, and the leiomyosarcoma cell line dose dependently repressed F3 and IL8 through direct interactions with their respective 3'-untranslated region and indirectly through F3 repression inhibited IL8, CTGF, and PAI-1 expression, confirmed by using small interfering RNA silencing or factor Vlla (FVIIa) activation of F3, as well as reducing the rate of proliferation, while increasing caspase-3/7 activity. We concluded that differential expression of miR-93/106b and their direct and/or indirect regulatory functions on F3, IL8, CTGF, and PAI-1 expression, with key roles in inflammation and tissue turnover may be of significance in the outcome of leiomyoma growth and associated symptoms.

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Section: Discussionmentioning

confidence: 99%

miR-93/106b and Their Host Gene, MCM7, Are Differentially Expressed in Leiomyomas and Functionally Target F3 and IL-8

Chuang

Panda

et al. 2012

Molecular Endocrinology

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“…The patients recruited to this study were reported previously [21,22]. Briefly, 50 women with histologically confirmed adenomyosis (excluding endometriosis) seen at the Shanghai Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China, were recruited for this study.…”

Section: Methodsmentioning

confidence: 99%

“…The protocol for immunohistochemistry analysis, including the quantification method, used for this study was identical to the one in our previous studies [21,22]. Briefly, serial 4-µm sections were obtained from each block, with the first resultant slide being stained for HE to confirm pathologic diagnosis, and the subsequent slides stained for HDAC1–3.…”

Section: Methodsmentioning

confidence: 99%

“…Immunoreactive staining was characterized quantitatively by digital image analysis using the Image Pro-Plus 6.0 (Media Cybernetics, Inc., Bethesda, Md., USA), as reported in [26] and identical to what we have published previously [21,22] without prior knowledge of any of the clinicopathological information. Briefly, images were obtained with a microscope (Olympus BX51; Olympus, Tokyo, Japan) fitted with a digital camera (Olympus DP70; Olympus).…”

Section: Methodsmentioning

confidence: 99%

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Elevated Immunoreactivity against Class I Histone Deacetylases in Adenomyosis

Liu

Nie

Guo

2012

Gynecol Obstet Invest

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Background/Aims: Adenomyosis is a common condition with a poorly understood pathogenesis. Recent data suggest that it may be an epigenetic disease. This study investigated the expression and localization of class I histone deacetylases (HDACs) in women with and without adenomyosis. Methods: The ectopic and homologous eutopic endometrium of 50 women with adenomyosis and the endometrium of 18 age- and menstrual phase-matched women without adenomyosis were used for immunohistochemical analysis. Tissue sections were immunostained with HDAC1, -2, and -3. Microscopic evaluation to assess the presence and localization of HDAC1–3 throughout the menstrual cycle in both eutopic endometrial and endometriotic tissues of women with adenomyosis was performed and compared with the normal endometrium. Results: We found that, compared with the normal endometrium, immunoreactivity against HDAC1 and HDAC3 was higher in both the eutopic and the ectopic endometrium. Increased HDAC2 in the eutopic endometrium was found to be associated with the severity of dysmenorrhea. Conclusion: Given the potential wide-ranging effect of histone deacetylation on gene expression, these findings suggest that HDACs may be involved in adenomyosis. They also suggest the possibility that HDAC2 may be involved in dysmenorrhea and its severity and that HDACs may be potential therapeutic targets in adenomyosis.

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“…It has been a challenge for the effective treatment of adenomyosis. Clinically, hysterectomy was usually used for the treatment of severe adenomyosis; however, this would lead to loss of fertility and severe trauma in patients suffering from this operation [6,7]. Alternative therapeutic strategies include gonadotrophinreleasing hormone (GnRH) agonists and some other therapeutic options; nevertheless, these therapeutic administrations possess generally specific shortages, such as short duration and frequent relapse [7,8].…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA inhibits the proliferation, migration and invasion of ectopic endometrial stromal cells of adenomyosis via 14-3-3ζ downregulation

Wan

Zou

Wan

et al. 2015

Arch Gynecol Obstet

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Elevated immunoreactivity to tissue factor and its association with dysmenorrhea severity and the amount of menses in adenomyosis

Abstract: These results suggest that TF is involved in adenomyosis-associated heavy menstrual bleeding and dysmenorrhea and thus may be a potential therapeutic target in treating symptomatic adenomyosis and perhaps also chronic pelvic pain in women with adenomyosis.

Cited by 57 publications

References 64 publications

miR-93/106b and Their Host Gene, MCM7, Are Differentially Expressed in Leiomyomas and Functionally Target F3 and IL-8

miR-93/106b and Their Host Gene, MCM7, Are Differentially Expressed in Leiomyomas and Functionally Target F3 and IL-8

Elevated Immunoreactivity against Class I Histone Deacetylases in Adenomyosis

Tanshinone IIA inhibits the proliferation, migration and invasion of ectopic endometrial stromal cells of adenomyosis via 14-3-3ζ downregulation

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