Blood: miR-125a-5p regulates the formation of platelet precursors by actin binding protein L-Plastin.

There is a genetic variation in platelet counting between individuals !----, which better understands its regulatory genetic factors or the process of resolving platelet generationMicroRNAs (miRs) are involved in regulating normal conditions and gene expression in a variety of diseases, miRs lack a low count of macronuclear cells (MKs) and platelets, but the role of miRs in normal human MK and platelet production is unclearthrough genome-wide miR spectral analysis, Bhatlekar and others observed a strong correlation between human bone marrow MK, platelets, and differentiated umbilical cord blood sources of MK cultures, and it was made clear that MK's miR-125a-5p was associated with the number of platelets in humans, but not with white blood cells or hemoglobin levelsover expression and knock-down tests showed that in vitro, miR-125a-5p positive control of the formation of the human MK platelet precursor (PP)inhibition of miR-125a-5p in the body can reduce platelet count in miceanalysis of transcription groups of MK and platelets found that LCP1 was the target of miR-125a-5pLCP1 encodes the actin binding protein, L-plastin, which has not been studied in MK beforeresearchers found that miR-125a-5p directly targets and reduces the expression of MK L-plastinexpression and knock-down tests showed that L-plastin promotes MK precursor cell migration, but is negatively correlated with human platelet count, and L-plastin inhibits MK PP formationthis study, miR-125a-5p is closely related to platelet counting, and for the first time it has been demonstrated that the actin binding protein L-plastin is the regulatory factor of human MK PP formationmiR-125a-5p and L-plastin may be targets for increasing in vitro platelet production and treating diseases associated with platelet defects.