PMC:4277126 / 16099-17277 JSONTXT

{"project":"2_test","denotations":[{"id":"25552899-21764698-26094193","span":{"begin":48,"end":50},"obj":"21764698"},{"id":"25552899-21764698-26094194","span":{"begin":595,"end":597},"obj":"21764698"},{"id":"25552899-22025288-26094195","span":{"begin":1059,"end":1061},"obj":"22025288"}],"text":"Human umbilical vein endothelial cells\nLiu et al24 examined the effects of LBPs on angiotensin II-induced senescence of human umbilical vein endothelial cells (HUVECs) and the role of p53 and p16 in such effects. HUVECs were treated with 1×106 mM angiotensin II to induce cell senescence, which was identified using SA-β-gal staining. Flow cytometry was used for analyzing the cell cycle changes, and the cell viability was assessed. LBPs treatment of angiotensin II-exposed cells resulted in decreased β-gal-positive cells with a reduction in G0/G1 phase cells and an increase in S phase cells.24 It also increased the cell viability and significantly decreased the expression levels of p53 and p16 (both tumor suppressors and senescence regulators) in HUVECs. These results demonstrate that LBPs can delay angiotensin II-induced aging of HUVECs possibly by downregulating the expression of p53 and p16. The p16-mediated senescence acts through the retinoblastoma pathway inhibiting the action of the cyclin-dependent kinases leading to G1 cell cycle arrest.25 Retinoblastoma is maintained in a hypophosphorylated state resulting in the inhibition of transcription factor E2F1."}

{"project":"NEUROSES","denotations":[{"id":"T432","span":{"begin":493,"end":502},"obj":"PATO_0001997"},{"id":"T433","span":{"begin":653,"end":662},"obj":"PATO_0001997"},{"id":"T448","span":{"begin":176,"end":180},"obj":"CHEBI_50906"},{"id":"T449","span":{"begin":321,"end":324},"obj":"CHEBI_28260"},{"id":"T450","span":{"begin":505,"end":508},"obj":"CHEBI_28260"},{"id":"T451","span":{"begin":410,"end":419},"obj":"PATO_0000169"},{"id":"T452","span":{"begin":625,"end":634},"obj":"PATO_0000169"},{"id":"T453","span":{"begin":467,"end":474},"obj":"PATO_0001646"},{"id":"T454","span":{"begin":467,"end":474},"obj":"PATO_0002425"},{"id":"T455","span":{"begin":550,"end":555},"obj":"PATO_0000083"},{"id":"T456","span":{"begin":583,"end":588},"obj":"PATO_0000083"},{"id":"T457","span":{"begin":606,"end":615},"obj":"PATO_0000470"}],"text":"Human umbilical vein endothelial cells\nLiu et al24 examined the effects of LBPs on angiotensin II-induced senescence of human umbilical vein endothelial cells (HUVECs) and the role of p53 and p16 in such effects. HUVECs were treated with 1×106 mM angiotensin II to induce cell senescence, which was identified using SA-β-gal staining. Flow cytometry was used for analyzing the cell cycle changes, and the cell viability was assessed. LBPs treatment of angiotensin II-exposed cells resulted in decreased β-gal-positive cells with a reduction in G0/G1 phase cells and an increase in S phase cells.24 It also increased the cell viability and significantly decreased the expression levels of p53 and p16 (both tumor suppressors and senescence regulators) in HUVECs. These results demonstrate that LBPs can delay angiotensin II-induced aging of HUVECs possibly by downregulating the expression of p53 and p16. The p16-mediated senescence acts through the retinoblastoma pathway inhibiting the action of the cyclin-dependent kinases leading to G1 cell cycle arrest.25 Retinoblastoma is maintained in a hypophosphorylated state resulting in the inhibition of transcription factor E2F1."}