XCL1-XCR1 通路通过诱导 MMP-2/MMP-9 活性促进母胎界面滋养层侵袭。
XCL1-XCR1 pathway promotes trophoblast invasion at maternal-fetal interface by inducing MMP-2/MMP-9 activity.
机构信息
Department of Gynecology and Obstetrics, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Institute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao Tong University School of Medicine, The International Peace Maternity & Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
出版信息
Am J Reprod Immunol. 2018 Sep;80(3):e12990. doi: 10.1111/aji.12990. Epub 2018 Jun 1.
PROBLEM
Certain chemokines with their receptors can promote or inhibit trophoblast cell migration and invasion in human first-trimester placenta. Whether the lymphotactin (Lptn; XCL1)-XC chemokine receptor 1 (XCR1) chemokine pathway affects trophoblast cell migration and invasion in human first-trimester placenta remains unclear.
METHOD OF STUDY
The expression pattern of chemokine XCL1 and its receptor XCR1 was detected in human first-trimester by qRT-PCR, and the effect of recombinant human XCL1 (rhXCL1) on trophoblast cell function was tested by wound healing and Transwell assays. Matrix metalloproteinase (MMP) activity in trophoblast cells treated with rhXCL1 was assessed via qRT-PCR and gelatin zymography.
RESULTS
Abundant XCR1 mRNA was expressed in the first-trimester decidua and villi. XCL1 and XCR1 mRNA were expressed at a higher level in the first-trimester than in the term placenta. RhXCL1 promoted trophoblast cell migration and invasion by increasing MMP-9 and MMP-2 activity and that of the MMP-2/tissue inhibitor of metalloproteinases 2 (TIMP-2) complex via the phosphatidylinositol 3-kinase (PI3K)/AKT kinase (AKT), mitogen-activated protein kinase (MEK), and JUN N-terminal kinase (JNK) signaling pathways.
CONCLUSION
XCL1-XCR1 chemokine pathway promotes trophoblast invasion by increasing matrix metalloproteinase activity in human first-trimester placenta.
问题
某些趋化因子及其受体可以促进或抑制人早孕胎盘滋养层细胞的迁移和侵袭。淋巴毒素（Lptn；XCL1）-XC 趋化因子受体 1（XCR1）趋化因子通路是否影响人早孕胎盘滋养层细胞的迁移和侵袭尚不清楚。
研究方法
通过 qRT-PCR 检测人早孕组织中趋化因子 XCL1 及其受体 XCR1 的表达模式，通过划痕愈合和 Transwell 实验检测重组人 XCL1（rhXCL1）对滋养层细胞功能的影响。通过 qRT-PCR 和明胶酶谱法评估 rhXCL1 处理的滋养层细胞中基质金属蛋白酶（MMP）的活性。
结果
XCR1 mRNA 在早孕蜕膜和绒毛中大量表达。XCL1 和 XCR1 mRNA 在早孕时的表达水平高于足月胎盘。rhXCL1 通过增加 MMP-9 和 MMP-2 活性以及 MMP-2/金属蛋白酶组织抑制剂 2（TIMP-2）复合物的活性，通过磷脂酰肌醇 3-激酶（PI3K）/丝氨酸/苏氨酸激酶（AKT）激酶（AKT）、丝裂原活化蛋白激酶（MEK）和 JUN 氨基末端激酶（JNK）信号通路促进滋养层细胞的迁移和侵袭。
结论
XCL1-XCR1 趋化因子通路通过增加人早孕胎盘基质金属蛋白酶活性促进滋养层侵袭。
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