Abstract : Placenta is the main factor in the pathogenesis theory for the mechanism of preeclampsia. Development of laboratory modality related preeclampsia is needed in therapy and prevention improvement. The aim of this study is to investigate optimization of the isolation protocol of primary cells of trophoblast and development of an in vitro model of preeclampsia by measuring the level of sFLT-1 and PIGF. This is an in vitro laboratory experimental study. Placenta tissue was obtained from term pregnancy with caesarean delivery. Trophoblast cells was isolated from the placenta in several steps and identified by Cytokeratin 7 (CK-7) expression using immunocytochemical method. Subsequently, cells were inducted with serum preeclampsia. Both sFLT-1 and PIGF level were measured with ELISA. Expressed CK-7 in the cytoplasm confirmed the cells were trophoblast cells. After induction, sFLT-1 increased and PIGF decreased compared with control. Trophoblast cells express CK-7 protein in their cytoplasm. Isolated trophoblast cells stained brown in the cytoplasm confirmed that these cells expressing CK-7 protein. Increased expression of sFlt-1 level in cells induced with preeclampsia serum corresponds with other research that overexpression of sFlt-1 causes clinical manifestation that is similar with hypertension in mice. Meanwhile, sFlt-1 is capable to break PIGF causing a decrease of it. Our result shown in line that PIGF level in cells induced with preeclampsia serum decreased compared with control. This protocol shown to be applicable in isolation of trophoblast cells in placenta and can be used as a basis to develop in vitro model of preeclampsia