XCL1-XCR1 pathway promotes trophoblast invasion at maternal-fetal interface by inducing MMP-2/MMP-9 activity
XCL1-XCR1 pathway promotes trophoblast invasion at maternal-fetal interface by inducing MMP-2/MMP-9 activity
复制标题
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。
DOI：
10.1111/aji.12990
复制
发表时间：
2018
影响因子：
3.6
通讯作者：
Lin Yi
中科院分区：
文献类型：
--
作者：
Zhang Si Ming;Tian Fu Ju;Zeng Wei Hong;Ma Xiao Ling;Ren Jia Bin;Lin Yi
某些趋化因子及其受体可以促进或抑制人类早期妊娠胎盘滋养层细胞的迁移和侵袭。研究方法采用qRT-PCR方法检测人早孕期胎盘中趋化因子XCL 1及其受体XCR 1的表达模式，并通过创伤愈合和Transwell实验检测重组人XCL 1（rhXCL 1）对滋养层细胞功能的影响。结果XCR 1 mRNA在早孕蜕膜和绒毛组织中均有表达，且XCL 1和XCR 1 mRNA在早孕组织中的表达水平高于足月胎盘组织。RhXCL 1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（PI 3 K）/AKT激酶（AKT），丝裂原活化蛋白激酶（MEK），和JUN N末端激酶（JNK）信号通路。结论XCL 1-XCR 1趋化因子通路通过增加人孕早期胎盘中基质金属蛋白酶活性来促进滋养层侵袭。
ProblemCertain 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 studyThe 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.ResultsAbundantXCR1mRNA was expressed in the first‐trimester decidua and villi.XCL1andXCR1mRNA 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.ConclusionXCL1‐XCR1 chemokine pathway promotes trophoblast invasion by increasing matrix metalloproteinase activity in human first‐trimester placenta.