| Summary: | 碩士 === 馬偕醫學院 === 生物醫學研究所 === 107 === Abstract
Placental immunity is a mystery and the underlying mechanisms in the regulation of immune response to avoid spontaneous abortion and has the immunity at the same time are curious. Slit proteins were initially identified in the developing central nervous system of Drosophila as axonal repellents and Slit–Robo signaling functions have been demonstrated in a variety of developmental organs and systems, such as kidney development, chemo-attractants of vascular endothelial cells, leukocytes, cancer cell migration and placental angiogenesis. It is also related to the immune re-sponse and has been demonstrated to be detected in placentas. The aim of this study is to investigate whether human Slit2 protein could regulate the migration and proin-flammatory signal pathways of macrophage. Conditional medium of human placenta mesenchymal stromal cells (hPMSCs) was taken used to demonstrate the presence of Slit2 protein. We also used recombinant human Slit2 protein, lipopolysaccharide (LPS) and mouse macrophage (RAW 264.7) to study the inflammatory reaction. From our results, we found that Slit2 protein was detected in the conditioned medium of hPMSCs and Robo4 receptor was detected with the highest amount in mouse macrophages. After treatment with LPS on the macrophages, the migration of mac-rophage was inhibited by Slit2 protein.
Our study on the NFκB and MAPK p38 signaling pathways also revealed that the activation of NFκB and MAPK p38 signals were decreased by the co-treatment of Slit2 protein. In conclusion, Slit2 may play an important role in the regulation of in-flammation in the placenta (hPMSCs) and Slit-Robo signaling is in macrophages. Slit2 protein exerted inhibitory effect on the migration of LPS-stimulated macro-phage with the downregulation of NFB and MAPK p38 pathways. Future studies are worth
for demonstrating the function in other cell types in the immune system, such as T cells or B cells.
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