Placental lactogen (PL) is a peptide hormone secreted throughout pregnancy by both animal and human specialized endocrine cells. PL plays an important role in the regulation of insulin secretion in pancreatic β-cells, stimulating their proliferation and promoting the expression of anti-apoptotic proteins. Cases of pregnancy affected by metabolic conditions, including obesity and diabetes, are related to alterations in the PL secretion pattern. Whereas obesity is most often associated with lower PL serum concentrations, diabetes results in increased PL blood levels. Disruptions in PL secretion are thought to be associated with an increased prevalence of gestational complications, such as placental dysfunction, diabetic retinopathy, and abnormalities in fetal growth. PL is believed to be positively correlated with birth weight. The impaired regulation of PL secretion could contribute to an increased incidence of both growth retardation and fetal macrosomia. Moreover, the dysregulation of PL production during the intrauterine period could affect the metabolic status in adulthood. PL concentration measurement could be useful in the prediction of fetal macrosomia in women with normal oral glucose tolerance test (OGTT) results or in evaluating the risk of fetal growth restriction, but its application in standard clinical practice seems to be limited in the era of ultrasonography.

The placenta is a part of feto-maternal unit that develops from the maternal decidua basalis and fetal-derived trophoblast cells. The regulation of its early development is extremely intricate, albeit the elusive trophoblast stem cells (TSCs) are thought to give rise to the fetal part of the placenta. TSCs may be isolated in both animal and human models. In detail, TSCs can be efficiently obtained from the early conceptus tissues – blastocysts or early placental tissue. The isolation of murine TSCs pave the way for analyses of human trophoblast cell lineages. Both human and animal stem cells retain similar characteristic properties – the ability for unrestricted self-renewal and differentiation into all trophoblast cell lines. Nevertheless, there are some essential differences across the various species which are especially pronounced when pertaining to their distinct optimal cell culture requirements. Moreover, there are several crucial discrepancies in the stemness marker gene transcription profiles between human and murine TSCs models. In vitro TSC models can be adapted to the elucidation of the pathophysiology of various reproductive complications. For instance, their properties may illustrate the conditions observed during the implantation or simulate the state of abnormal placentation. Observations gained from the experimental studies could potentially explain the cause of some cases of infertility, preeclampsia, and fetal growth abnormalities. Running title : Update on the trophoblast stem cells