Immunohistochemical analysis of thoracic endometriosis

Haga, Takahiro; Kumasaka, Takashi; Kurihara, Masatoshi; Kataoka, Hideyuki; Miura, Myota

doi:10.1111/pin.12089

Cited by 23 publications

(14 citation statements)

References 19 publications

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“…The SMM is frequently found in peritoneal, [17][18][19][20] deep, 19,29,30 ovarian, 17,20,31,32 extragenital, 33,34 and pleuropulmonary endometriosis 35 as well as in adenomyosis. 36 The possibility of stromal cells differentiating into SMC, as happened in physiological SMM in the junctional zone of the uterus, 37,38 has been entertained 20,30 but nonetheless dismissed due to insufficient evidence.…”

Section: Discussionmentioning

confidence: 99%

Cellular Changes Consistent With Epithelial–Mesenchymal Transition and Fibroblast-to-Myofibroblast Transdifferentiation in the Progression of Experimental Endometriosis in Baboons

et al. 2016

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We have recently shown that platelets play important roles in development of endometriosis and proposed that endometriotic lesions are essentially wounds that undergo repeated tissue injury and repair (ReTIAR). Further investigation indicated that endometriotic lesions, stimulated by platelet-derived transforming growth factor β1 (TGF-β1), activate the TGF-β1/Smad3 signaling pathway and undergo epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast transdifferentiation (FMT), resulting in increased cellular contractility and collagen production and increased smooth muscle metaplasia (SMM), leading to fibrosis. Using serially dissected endometriotic tissue samples from baboons with induced endometriosis, we tested the hypothesis of progressive EMT, FMT, SMM, and fibrosis through TGF-β1/Smad activation using immunohistochemistry and immunoflurescence staining analyses. We found that platelets are aggregated in endometriotic lesions, and vimentin expression was increased in the epithelial compartment of the lesions as they progressively developed. We also found that the number of smooth muscle cells (SMCs) appeared to increase with time as lesions progressed and was concomitant with the increased vimentin-positive glandular epithelial cells in the lesions. As lesion development progressed, TGF-β1 and phosphorylated-Smad3 staining was elevated and the number of α-smooth muscle actin-positive myofibroblasts and highly differentiated SMCs increased in the stromal compartment, which correlated with the increasing extent of fibrosis. These results, taken together, provide support for the notion that ReTIAR occurs in the endometriotic lesions, resulting in EMT and FMT, leading to SMM and ultimately fibrosis as lesions progress. Consequently, our data also provide corroborative evidence that platelets drive the EMT and FMT in endometriotic lesions over time, promoting SMM and resulting ultimately in fibrosis in the endometriotic lesions. These findings cast a new light on the natural history of endometriosis which so far has been elusive.

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Section: Discussionmentioning

confidence: 99%

Cellular Changes Consistent With Epithelial–Mesenchymal Transition and Fibroblast-to-Myofibroblast Transdifferentiation in the Progression of Experimental Endometriosis in Baboons

et al. 2016

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“…72 The pathological diagnosis of TE can be challenging, because lesions are sometimes so small that glands may not be identified. 88 Positive histopathological confirmation has been reported to range from 57% to 87.5% 68,71,73,83,84,[89][90][91] . Furthermore, sometimes it is difficult to distinguish endometrial stroma and inflammatory cells by hematoxylin and eosin staining.…”

Section: Catamenial Pneumothorax and Endometriosisrelated Pneumothomentioning

confidence: 99%

Extra‐pelvic endometriosis: A review

Hirata

Koga

Osuga

2020

Reprod Medicine & Biology

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Endometriosis is defined as a condition in which endometrium-like tissues are present in organs other than the uterus. It has been reported that 5%-10% of women of reproductive age have endometriosis. 1-3 It is an estrogen-dependent inflammatory disease, which causes pelvic pain and infertility. Endometriosis usually involves the ovaries, ligaments, and peritoneal surfaces, and less commonly occurs in the intestine, bladder, abdominal wall, thoracic cavity, and other organs. The etiology of endometriosis has remained mostly unknown, despite much literature and some predominant theories. The most widely accepted theory for the pathogenesis of endometriosis is retrograde menstruation through the fallopian tubes into the pelvic cavity. 4 Once endometrial cells adhere to peritoneal surfaces, they can grow and invade onto peritoneal structures, under the influence

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“…We could not find any significant difference in the rates of visceral pleural endometriosis. This result is probably due to the difficulty of inspecting for thoracic endometriosis, because these endometriotic implants are very small, as we reported previously . When ectopic endometrial sites are found in the parietal or visceral pleura, the endometrial tissues may extend to both the parietal and visceral pleural surfaces.…”

Section: Discussionmentioning

confidence: 71%