Objective To comparatively study the features of two reprogramming systems of induced pluripotent stem cells (iPSCs)from human dental origin.Methods Two kinds of reprogramming system,i.e.STEMCCA lentivirus /feed layer and Sen-dai virus /matrigel were used to induce human stem cells from apical papilla(SCAP)into iPSCs,respectively.The induction efficien-cies,workload of generating iPSCs,aneuploidy karyotype ratio,complexities of eliminating exogenous transcription factors and spe-cific markers expression were compared between these two systems.Results The STEMCCA reprogramming system required to prepare the feeder cell MEF.The reprogramming efficiency was 0.1%.Transcription gene-free iPSCs cells were obtained by the Cre-loxp enzyme digestion technique at the later stage.Sendai virus reprogramming system was feeder-free and the preparation of matrigel was quite simple with unified standard.The reprogramming efficiency was 0.7%,which was much higher than that of STEMCCA system(P <0.05).The exogenous virus and transgenes could be gradually eliminated after several passages of natural subclone.Conclusion The Sendai virus/matrigle reprogramming system is much more applicable for the induction of iPSCs from dental origin than the STEMCCA system.

Non-exosomal non-coding RNAs (non-exo-ncRNAs) and exosomal ncRNAs (exo-ncRNAs) have been associated with the pathological development of myocardial infarction (MI). Accordingly, this analytical review provides an overview of current MI studies on the role of plasma non-exo/exo-ncRNAs. We summarize the features and crucial roles of ncRNAs and reveal their novel biological correlations via bioinformatics analysis. The following contributions are made: (1) we comprehensively describe the expression profile, competing endogenous RNA (ceRNA) network, and "pre-necrotic" biomarkers of non-exo/exo-ncRNAs for MI; (2) functional enrichment analysis indicates that the target genes of ncRNAs are enriched in the regulation of apoptotic signaling pathway and cellular response to chemical stress, etc.; (3) we propose an updated and comprehensive view on the mechanisms, pathophysiology, and biomarker roles of non-exo/exo-ncRNAs in MI, thereby providing a theoretical basis for the clinical management of MI.
Humans ; RNA, Untranslated/genetics* ; RNA ; Myocardial Infarction/genetics* ; Biomarkers ; Computational Biology ; MicroRNAs/genetics*