| http://purl.uniprot.org/citations/29398368 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29398368 | http://www.w3.org/2000/01/rdf-schema#comment | "The treatment of atherosclerosis (AS), a severe condition associated with the pathogenesis of cardiovascular diseases (CVDs), is still not satisfactory worldwide. In this study, we aim to investigate whether protein sprout homologue 1 (SPRY1), a upstream mediator of MAPK signal pathway, is the target of miR-29b in vascular endothelium during the development of AS. ApoE-/- mice model was established, and an inverse correlation was noticed between level of miR-29b and SPRY1 expression in the aortic tissues. Meanwhile, the tumor necrosis factor-α (TNF-α), reactive oxygen species (ROS) expression and NADPH oxidase activity were up-regulated in atherosclerotic tissues. In vitro experiments were carried out to investigate the roles of miR-29b in regulating the expression of SPRY1 in cultured human umbilical vein endothelial cells (HUVECs). We found that miR-29b mimic and antagomir could modulate the expression of SPRY1 protein in cultured HUVECs. However, the expression of SPRY1 mRNA showed no statistical difference when treating with miR-29b mimic or antagomir. These indicated that the modulation of SPRY1 induced by miR-29b was at the posttranslational level. Dural luciferase reporter assay was conducted to detect the potential interaction between miR-29b and the 3'UTR of SPRY1, which indicated that SPRY1 was a target of miR-29b. Besides, miR-29b antagomir induced decrease of TNF-α, ROS production and NADPH oxidase activity and down-regulated the expression of p-ERK and p-p38 in the presence of oxLDL. In conclusion, inhibition of miR-29b could attenuate AS by inhibiting the SPRY1/MAPK signaling pathway and inflammation in aorta. In future, treatment options based on miR-29b may be applicable for the treatment of AS."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.vph.2018.01.006"xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/author | "Lu Z."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/author | "Wang F."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/author | "Wang X."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/author | "Zhu H.Q."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/author | "Yu P."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/author | "Tang S.T."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/name | "Vascul Pharmacol"xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/pages | "29-36"xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/title | "Inhibition of miR-29b suppresses MAPK signaling pathway through targeting SPRY1 in atherosclerosis."xsd:string |
| http://purl.uniprot.org/citations/29398368 | http://purl.uniprot.org/core/volume | "102"xsd:string |
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