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Interleukin-1ß induces cyclooxygenase-2 expression and promotes the invasive ability of human mesenchymal stem cells derived from ovarian endometrioma
Oleh:
Kao, An-Pei
;
Wang, Kai-Hung
;
Long, Cheng-Yu
;
Chai, Chee-Yin
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 96 no. 03 (Sep. 2011)
,
page 678-684.
Topik:
Cell invasion
;
cyclooxygenase-2
;
endometriosis
;
interleukin-1ß
;
mesenchymal stem cells
Ketersediaan
Perpustakaan FK
Nomor Panggil:
F02.K.2011.01
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
Objective To elucidate the role of interleukin-1ß (IL-1ß) on cyclooxygenase-2 (COX-2) expression and invasion of endometrioma-derived ectopic endometrial mesenchymal stem cells (EN-MSCs) and to develop an organoid method to study the invasive ability of endometrial cells. Design Gene expression and cell functions. Setting Kaohsiung Medical University, Kaohsiung, Taiwan. Patient(s) Human eutopic and endometrioma-derived ectopic EN-MSCs were isolated from different endometrium biopsy samples after surgery for treatment of endometriosis. Intervention(s) Chemical treatment of cell culture. Main Outcome Measure(s) Comparative analysis of genomewide messenger RNA (mRNA) expression, cell migration, and invasion abilities in cell culture and organoid culture. Result(s) Gene expression profiles revealed that the expression of IL-1ß and COX-2 were statistically significantly higher in ectopic EN-MSCs compared with eutopic EN-MSCs. These enhanced expressions coincided with a greater ability for cell migration and invasion in ectopic EN-MSCs and were found to be distinctly regulated by IL-1ß which up-regulates COX-2 expression. Furthermore, IL-1ß treatment of ectopic EN-MSCs in organoids was found to induce tentacle-like structures that mimicked cell invasion. Conclusion(s) These results indicate that COX-2 and IL-1ß regulate the invasion ability of ectopic EN-MSCs. The information may be useful for developing a new therapeutic strategy for endometriosis. The ex vivo invasion model will be useful for characterization of EN-MSCs.
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