Pre-eclampsia is associated with an increase in trophoblast glycogen content and glycogen synthase activity, similar to that found in hydatidiform moles.

Abstract

Pre-eclampsia is a placental disorder, but until now, biochemical details of dysfunction have been lacking. During an analysis ofthe oligosaccharide content ofsyncytiotrophoblast microvesicles purified from the placental chorionic villi of 10 primigravid women with proteinuric pre-eclampsia, we found an excess of glycogen breakdown products. Further investigation revealed a 10-fold increase in glycogen content (223±117 ,tg glycogen/ mg protein), when compared with controls matched for gestational age at delivery (23±18 ,ag glycogen/mg protein) (P < 0.01). This was confirmed by examination of electron micrographs of chorionic villous tissue stained for glycogen. The increase in glycogen content was associated with 16 times more glycogen synthase (1,323±1,013 relative to 83±96 pmol glucose/mg protein per min) (P < 0.001), and a threefold increase in glycogen phosphorylase activity (2,280±1,360 relative to 700±540 pmol glucose/ mg protein per min; P < 0.05).Similar changes in glycogen metabolism were found in trophoblast microvesicles derived from hydatidiform moles. Glycogen accumulation in villous syncytiotrophoblast may be a metabolic marker of immaturity of this cell which is unable to divide. The implications of these findings with regard to the pathogenesis of pre-eclampsia are discussed. (J. Clin. Invest.

Preeclampsia from a renal point of view: Insides into disease models, biomarkers and therapy

“…In the preeclamptic placenta trophoblasts do not develop normally and are unable to invade the myometrium effectively [25] . Specifically the placental tissue but not the foetus is involved in the development of preeclampsia, since preeclampsia also occurs in women with a hyaditiform mole [26][27][28][29] . Risk factors for preeclampsia include family history of preeclampsia, multiple gestation, nulliparity, obesity, older maternal age, molar pregnancies, diabetes mellitus, pre-existing hypertension, chronic renal disease and thrombotic vascular disease [30][31][32][33] .…”

“…Persistence of trophoblasts is associated with the development of preeclampsia in gestational trophoblastic disease [28,29] . Even though found only on the microscopic level, trophoblastic, tissue was found in patients with postpartum preeclampsia and suggests that it causes the disease.…”

Inhibition of TGF-β3 restores the invasive capability of extravillous trophoblasts in preeclamptic pregnancies

“…Progress has been made toward understanding the molecular basis of these observations. Villous trophoblasts from preeclamptic placentae have been found to exhibit an immature phenotype, ultrastructurally and biochemically, when compared with normal placentae (15,16). Specifically, EVT cells in the decidua of women whose pregnancies were complicated by preeclampsia exhibit a less invasive and more proliferative phenotype than normal (11).…”

Inositol Phosphoglycan P-Type in Preeclampsia

“…7 IPGs have been demonstrated to exert insulin-mimetic activity in both glucose and lipid metabolism mainly through the activation of pyruvate dehydrogenase phosphatase, glycogen synthase phosphatase, and glycerol-3-phosphate acyltransferase. 8,9 The elevated concentration of glycogen in terminal villi from preeclamptic placentas, because of an increased activity of glycogen synthase, 10 may be a consequence of the abnormal content of P-IPG in the placentas of preeclamptic patients.…”