OBJECTIVES: The aim of this study is to address the role of low-density lipoprotein (LDL) on mouse preimplantation embryos. METHODS: The temporal expression of low-density lipoprotein receptor (LDLR) and side-chain cleavage cytochrome P450 (P450scc) mRNAs in mouse oocytes and preimplantation embryos up to the hatched blastocyst stage were analyzed by RT-PCR and nested PCR techniques. Simultaneously, the expression of LDLR in the protein level was analyzed by fluorescent immunohistochemistory at oocyte, 4-cell embryo and blastocyst. Uptake of LDL was analyzed using the LDL labeled with the fluorescent probe DiO. RESULTS: LDLR mRNA was detected at oocyte, 8-cell, morula, blastocyst and hatched blastocyst stages. P450scc mRNA was detected at oocyte, 1-cell, 2-cell, 4-cell, blastocyst and hatched blastocyst stages. LDLR protein was detected in blastocyst. P450scc protein was detected in oocyte, 4-cell, and blastocyst. LDL-DiO was taken into embryo at blastocyst stage and this uptake was competitively suppressed by excess unlabeled LDL. CONCLUSIONS: It is suggested from the present study that LDLR may play an essential role in uptake of exogenous LDL into blastocyst stage and cholesterol derived from LDL may be the source of steroid hormone synthesis.
OBJECTIVES: The aim of this study is to address the role of low-density lipoprotein (LDL) on mouse preimplantation embryos. METHODS: The temporal expression of low-density lipoprotein receptor (LDLR) and side-chain cleavage cytochrome P450 (P450scc) mRNAs in mouse oocytes and preimplantation embryos up to the hatched blastocyst stage were analyzed by RT-PCR and nested PCR techniques. Simultaneously, the expression of LDLR in the protein level was analyzed by fluorescent immunohistochemistory at oocyte, 4-cell embryo and blastocyst. Uptake of LDL was analyzed using the LDL labeled with the fluorescent probe DiO. RESULTS:LDLR mRNA was detected at oocyte, 8-cell, morula, blastocyst and hatched blastocyst stages. P450scc mRNA was detected at oocyte, 1-cell, 2-cell, 4-cell, blastocyst and hatched blastocyst stages. LDLR protein was detected in blastocyst. P450scc protein was detected in oocyte, 4-cell, and blastocyst. LDL-DiO was taken into embryo at blastocyst stage and this uptake was competitively suppressed by excess unlabeled LDL. CONCLUSIONS: It is suggested from the present study that LDLR may play an essential role in uptake of exogenous LDL into blastocyst stage and cholesterol derived from LDL may be the source of steroid hormone synthesis.