Giraldez et al. observed that injection of miR-430 rescues the early morphogenesis defects in dicer mutants. So the high expression of miR-430 family here may be the organism’s strategy to rescue the impairment or to balance the disorders of miRNAs and their target system caused by MCRR. It has been demonstrated that miR-125b is an important negative regulator of p53 and p53-induced apoptosis during development as well as in stress response. The aberrant expression of these typical miRNAs in the present study indicates that MC-RR has significant influence on these important regulation factors and certainly on most cellular process during development of embryos. We also for the first time detected the decreased number of complete ISVs in embryos after MC-RR exposure. MiR-31 and miR-126, two miRNAs that have been KRX-0401 proved to contribute to vascular development were significantly altered in the present study. Pedrioli et al. observed that over-expression of miR-31 reduce venous sprouting of zebrafish embryo. MiR-126 regulates vascular endothelial growth factor -dependent PI3 kinase and MAP kinase signaling by directly targeting PI3KR2 and SPRED1, two negative regulators of the VEGF signaling pathway, respectively, knockdown of miR-126 in zebrafish results in loss of vascular integrity and hemorrhage during embryonic development. Thus, in the present study, the upregulation of miR-31 and downregulation of miR-126 may be related to the vascular defects of embryos caused by MC-RR exposure. Furthermore, to verify this hypothesis, we performed a rescue experiment for testing whether the deficit in ISV formation is related to the altered expression of miR-126 induced by MC-RR. We coinjected miR-126 duplex with MC-RR into the embryos and found that miR-126 overexpression could only slightly rescue the ISV phenotype. As we known, miRNAs that have been identified in zebrafish is very limited and the function of most miRNAs still remains unknown. It is possible that except miR-126 and miR-31 there are other known or unknown miRNAs contributing to the formation of ISVs. All miRNAs are required but not sufficient individually to precisely regulate the ISVs formation. In addition, other factors besides miRNAs might have contributed together to the defects of ISV formation post MC-RR exposure. So this is an intriguing question and further researches will be done in our future work. Although mRNAs are the direct targets of miRNA, it is of great importance to further consider the alteration of the final product of gene regulation – protein.