ABSTRACT
Background and Objectives@#Induced pluripotent stem cells (iPSCs) are usually generated by reprogramming differentiated cells through the introduction of specific transcription factors, but this is a difficult and inefficient process.Valproic acid (VPA) is a histone deacetylase inhibitor that significantly improves the efficiency of iPSC generation.But its role and mechanism are still unclear. @*Methods@#and Results: We transduced Bactrian camel fetal fibroblasts (BCFFs) with retroviruses carrying defined factors (OCT4, SOX2, KLF4, c-MYC and EGFP; OSKMG) in the presence of VPA. Cells were collected (Day 7) and analyzed using RNA-seq technology. Afterwards, different groups of cells and transcriptomics results were detected by PCR and qRT-PCR technology. The results showed that VPA promoted the expression of the endogenous gene c-Myc and inhibited cell proliferation; at the same time, it promoted the expression of VEGF and other genes related to angiogenesis. @*Conclusions@#When VPA is added to the culture medium, only the cells that have begun to reprogram can break the G2/M repression through the expression of the endogenous gene c-Myc, and use the nutrients and space in the culture dish to proliferate normally, which can achieve the purpose of directly improving the efficiency of reprogramming.Another new discovery for Bactrian camels, VPA significantly increased the expression of VEGFC and other genes, promoting the transformation of fibroblasts to endothelial cells (different from the mesenchymal-to-epithelial transition process of other species) to accelerate the early induction of Bactrian camels iPSc process. Overall, this study proved the new mechanism of VPA in enhancing the induction of pluripotency from the transcriptome level.
ABSTRACT
Background and Objectives@#Induced pluripotent stem cells (iPSCs) are usually generated by reprogramming differentiated cells through the introduction of specific transcription factors, but this is a difficult and inefficient process.Valproic acid (VPA) is a histone deacetylase inhibitor that significantly improves the efficiency of iPSC generation.But its role and mechanism are still unclear. @*Methods@#and Results: We transduced Bactrian camel fetal fibroblasts (BCFFs) with retroviruses carrying defined factors (OCT4, SOX2, KLF4, c-MYC and EGFP; OSKMG) in the presence of VPA. Cells were collected (Day 7) and analyzed using RNA-seq technology. Afterwards, different groups of cells and transcriptomics results were detected by PCR and qRT-PCR technology. The results showed that VPA promoted the expression of the endogenous gene c-Myc and inhibited cell proliferation; at the same time, it promoted the expression of VEGF and other genes related to angiogenesis. @*Conclusions@#When VPA is added to the culture medium, only the cells that have begun to reprogram can break the G2/M repression through the expression of the endogenous gene c-Myc, and use the nutrients and space in the culture dish to proliferate normally, which can achieve the purpose of directly improving the efficiency of reprogramming.Another new discovery for Bactrian camels, VPA significantly increased the expression of VEGFC and other genes, promoting the transformation of fibroblasts to endothelial cells (different from the mesenchymal-to-epithelial transition process of other species) to accelerate the early induction of Bactrian camels iPSc process. Overall, this study proved the new mechanism of VPA in enhancing the induction of pluripotency from the transcriptome level.
ABSTRACT
Objective To study the role of prostaglandin E1 in prevention of contrast-induced ne-phropathy (CIN)in elderly CHD patients undergoing PCI .Methods Three hundred elderly CHD patients who were going to undergo PCI in Tianjin Chest Hospital were divided into prostaglandin E1 treatment group (n=150) and conventional treatment group (n=150) .Patients in prostaglan-din E1 treatment group were treated with 20 μg prostaglandin E1 plus hydration therapy and those in conventional treatment group received simple hydration therapy .T heir serum levels of creatinine ,urea ,β2-microglobulin ,24 h proteinuria ,CRP ,IL-6 ,TNF-α,GPX ,SOD ,and creatinine clearance rate were measured before and 3 d after PCI .The incidence of CIN in two groups was analyzed .The hypotension events in prostaglandin E1 treatment group were recorded .Results The serum levels of CRP ,SOD ,GPX ,24 h proteinuria and the incidence of CIN were significantly lower while the creatinine clearance rate was significantly higher in prostaglandin E 1 treatment group than in conventional treatment group after PCI (P<0 .05) .The serum levels of CRP ,IL-6 , SOD ,GPX and 24 h proteinuria were significantly higher in two groups after PCI than before PCI (P<0 .05) .Conclusion Prostaglandin E1 can protect the renal function in CHD patients under-going PCI and play a certain role in preventing CIN .