Role of interleukin-32 in the pathogenesis of endometriosis: in vitro, human and transgenic mouse data
| Autor: | Byung Moon Kang, Seung-Ho Heo, Kang-Hyun Kim, Chung-Hoon Kim, Mi-Young Lee, Hee Dong Chae, Young Sang Oh, Sung-Hoon Kim |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Adult Stromal cell Cell Survival medicine.medical_treatment Endometriosis Mice Transgenic Proinflammatory cytokine 03 medical and health sciences Endometrium Mice 0302 clinical medicine Cell Line Tumor medicine Animals Ascitic Fluid Humans Viability assay Cell Proliferation Inflammation 030219 obstetrics & reproductive medicine business.industry Interleukins Rehabilitation Obstetrics and Gynecology Interleukin medicine.disease Transplantation Interleukin 32 030104 developmental biology Cytokine Reproductive Medicine Cancer research Female Stromal Cells business |
| Zdroj: | Human reproduction (Oxford, England). 33(5) |
| ISSN: | 1460-2350 |
| Popis: | Study question Does interleukin-32 (IL-32) play a role in the pathogenesis of endometriosis? Summary answer IL-32 might be involved in the pathogenesis of endometriosis through increased viability, proliferation and invasion of endometrial cells. What is known already Endometriosis is characterized as a chronic inflammatory disease and several proinflammatory cytokines are suggested to be involved in its pathogenesis and pathophysiology. IL-32, recognized as a new proinflammatory cytokine and a strong inducer of other proinflammatory cytokines, has been shown to serve as a key modulator in several chronic inflammatory diseases. Study design, size, duration This study included comparison of IL-32 levels in the peritoneal fluids between women with and without endometriosis, in-vitro experiments using Ishikawa cells and endometrial stromal cells (ESCs), and experiments on IL-32 transgenic mice and wild-type mice with induced endometriosis. Participants/materials, setting, methods IL-32 levels in the peritoneal fluids were measured using enzyme-linked immunosorbent assays. Cell viability, expression of proliferating cell nuclear antigen (PCNA), and cellular invasiveness were analyzed following in-vitro treatment of Ishikawa cells and ESCs with recombinant IL-32 alpha (α) and gamma (γ). Ectopic endometriotic lesions were compared between IL-32 transgenic mice and wild-type mice after autologous endometrial transplantation with immunohistochemistry for Ki-67 antigen and PCNA. Main results and the role of chance The peritoneal fluid concentration of IL-32 was significantly higher in patients with advanced stage endometriosis compared with the controls. In-vitro treatment with IL-32 α and γ caused significant increases in cellular viability, PCNA expression, and invasiveness in Ishikawa cells and ESCs. The IL-32 transgenic mice had a significantly larger size of the ectopic endometrial lesions with higher expression of Ki-67 antigen and PCNA compared with wild-type mice. Large scale data N/A. Limitations, reasons for caution It is still unclear whether IL-32 is a main regulator, or one of several downstream proinflammatory cytokines, causing establishment and/or progression of endometriosis. Wider implications of the findings Further investigation on IL-32 signaling pathways may contribute to development a more effective treatment of endometriosis. Study funding/competing interest(s) This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant number: HI16C1682). None of the authors has anything to disclose. |
| Databáze: | OpenAIRE |
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