Reproductive biomedicine online · 2024
Chemokine ligand 2 may contribute to damage of fallopian tube epithelium in women with tubal endometriosis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Ji Sifan, Li Yamei, Liang Guiling, Zhang Huiyu, Yan Li, Zhao Xiaoya, Chen Luting, Zhang Jian
Аннотация
RESEARCH QUESTION: How does tubal endometriosis (TEM) impact the morphology and ultrastructure of tubal epithelium, and what are the underlying pathophysiological mechanisms of TEM?
DESIGN: Epithelial samples of fallopian tube were collected from patients with and without TEM (TEM group, n = 27; control group, n=28). Morphological characteristics, ultrastructure, percentage of ciliated cells and ciliary beat frequency (CBF) were assessed via haematoxylin and eosin staining, electron microscopy and high-speed camera. mRNA microarray analysis was conducted to identify differentially expressed genes (DEG) in tubal epithelium, which were further validated using quantitative polymerase chain reaction (qPCR), immunohistochemistry and Western blotting. The effects of recombinant chemokine ligand 2 (CCL2) protein on primary human fallopian tube epithelial cells (FTEC) were examined in vitro.
RESULTS: Patients with TEM exhibited abnormalities in the morphology and ultrastructure of tubal epithelium, with a significantly reduced percentage of ciliated cells (P < 0.0001) and CBF (P < 0.0001) compared with control patients. Among the 765 DEG identified in tubal epithelium, 512 genes were up-regulated and 253 genes were down-regulated in the TEM group. Validation using qPCR (P = 0.0288), immunohistochemistry and Western blotting (P = 0.0150) confirmed significant up-regulation of CCL2 expression in the TEM group. In-vitro experiments revealed that recombinant CCL2 protein significantly reduced CBF (100 ng/ml versus blank control: P < 0.0001), differentiation of ciliated cells (25 ng/ml versus blank control: P = 0.0206, 50 ng/ml versus blank control: P < 0.0001, 100 ng/ml versus blank control: P < 0.001) and ciliary length (P < 0.0001) in FTEC, suggesting a role for CCL2 in the development of the TEM-related pathological phenotype.
CONCLUSIONS: These findings indicate that CCL2 may contribute to the pathological phenotype associated with TEM, and could be a crucial signalling molecule in damage of tubal epithelium in patients with TEM.
DESIGN: Epithelial samples of fallopian tube were collected from patients with and without TEM (TEM group, n = 27; control group, n=28). Morphological characteristics, ultrastructure, percentage of ciliated cells and ciliary beat frequency (CBF) were assessed via haematoxylin and eosin staining, electron microscopy and high-speed camera. mRNA microarray analysis was conducted to identify differentially expressed genes (DEG) in tubal epithelium, which were further validated using quantitative polymerase chain reaction (qPCR), immunohistochemistry and Western blotting. The effects of recombinant chemokine ligand 2 (CCL2) protein on primary human fallopian tube epithelial cells (FTEC) were examined in vitro.
RESULTS: Patients with TEM exhibited abnormalities in the morphology and ultrastructure of tubal epithelium, with a significantly reduced percentage of ciliated cells (P < 0.0001) and CBF (P < 0.0001) compared with control patients. Among the 765 DEG identified in tubal epithelium, 512 genes were up-regulated and 253 genes were down-regulated in the TEM group. Validation using qPCR (P = 0.0288), immunohistochemistry and Western blotting (P = 0.0150) confirmed significant up-regulation of CCL2 expression in the TEM group. In-vitro experiments revealed that recombinant CCL2 protein significantly reduced CBF (100 ng/ml versus blank control: P < 0.0001), differentiation of ciliated cells (25 ng/ml versus blank control: P = 0.0206, 50 ng/ml versus blank control: P < 0.0001, 100 ng/ml versus blank control: P < 0.001) and ciliary length (P < 0.0001) in FTEC, suggesting a role for CCL2 in the development of the TEM-related pathological phenotype.
CONCLUSIONS: These findings indicate that CCL2 may contribute to the pathological phenotype associated with TEM, and could be a crucial signalling molecule in damage of tubal epithelium in patients with TEM.