Leco K J, Harvey M B, Hogan A, Copeland N G, Gilbert D J, Jenkins N A, Edwards D R, Schultz G A
Ontario Cancer Institute, Princess Margaret Hospital, Toronto, Canada.
Dev Genet. 1997;21(1):55-60. doi: 10.1002/(SICI)1520-6408(1997)21:1<55::AID-DVG6>3.0.CO;2-7.
The activity and expression of matrix metalloproteinase-9/gelatinase B (MMP-9), an enzyme implicated in the implantation process in mice, was investigated in normal and parthenogenetic blastocyst outgrowths. Conditioned media from parthenogenetic blastocysts after 4 days of culture had reduced levels of MMP-9 activity compared to conditioned medium from normal outgrowths. Levels of MMP-9 mRNA assayed by reverse transcription-polymerase chain reaction methods were also reduced in parthenogenetic blastocysts compared to normal outgrowths. Genetic mapping studies showed that Mmp9 maps to the distal end of chromosome 2 near the proximal boundary of a region affected by genomic imprinting. Both parental alleles of Mmp9, however, are expressed in 11.5-day embryos derived from interspecific crosses of Mus musculus and Mus spretus. Thus, loss of MMP-9 activity in parthenogenetic blastocysts does not appear to be due to imprinting but, rather, due to a defect of trophoblast giant cell proliferation and differentiation.
在正常和孤雌生殖囊胚体外生长中,研究了基质金属蛋白酶-9/明胶酶B(MMP-9)的活性和表达,该酶与小鼠着床过程有关。培养4天后,孤雌生殖囊胚的条件培养基中MMP-9活性水平低于正常体外生长的条件培养基。通过逆转录-聚合酶链反应方法检测,孤雌生殖囊胚中MMP-9 mRNA水平也低于正常体外生长。基因定位研究表明,Mmp9定位于2号染色体远端,靠近受基因组印记影响区域的近端边界。然而,Mmp9的两个亲本等位基因在小家鼠和西班牙小鼠种间杂交产生的11.5天胚胎中均有表达。因此,孤雌生殖囊胚中MMP-9活性的丧失似乎不是由于印记,而是由于滋养层巨细胞增殖和分化缺陷。