RESUMEN
The chemical and physical structure of cationic liposomes pays an important effect on their gene transfection efficiency. Investigation on the structure-function relationship of cationic liposomes will guide the design of novel cationic liposomes with high transfection efficiency and biosafety. In this paper, two novel series of lipids based on the backbone of pentaerythritol and trimethylolpropane were discovered, and their gene transfection efficiencies were assayed in vitro. The four lipids 8c, 9c, 14b, and 15b, exhibited much better transfection efficiency in the HEK293 cell lines compared with Lipo2000, lipid 9c also showed good transfection efficiency in the SW480 cell lines. And the structure-efficiency relationship revealed that a hydroxyethyl polar head group boosted transfer potency in trimethylolpropane-type lipids, but reduced in pentaerythritol-type lipids.
Asunto(s)
Lípidos , Liposomas , Cationes/química , ADN/química , Células HEK293 , Humanos , Lípidos/química , Lípidos/farmacología , Liposomas/química , Glicoles de Propileno , TransfecciónRESUMEN
Sporadic outbreaks of Seneca Valley virus (SVV) have been detected in recent years causing huge economic losses to the pig industry. SVV infection can lead to redness and fever of the mouth, nose or hoof wall, ulcerative injury and inflammation in pigs. Although long non-coding RNAs (lncRNAs) have been shown to play an important role in antiviral and inflammatory regulation, how lncRNAs regulate and induce SVV infection inflammation remains unclear. Here, we found the differential expression of 1332 lncRNAs and 3299 mRNAs in SVV-infected ST cells using RNA-seq. Functional annotation analysis revealed that regulated transcripts are mainly involved in signaling pathways related to host immunity and inflammatory responses. We identified lnc-MSTRG.18940.1 as an important immune regulator in SVV infection. Lnc-MSTRG.18940.1 silencing specifically inhibited SVV replication and the production of inflammatory factors TNF-α, IL-1, IL-6, and IL-8. Our findings aid to a better understanding of host responses to SVV infection and provide new directions for understanding the potential association between lncRNAs and SVV pathogenesis.