| Background and Objective: Extravillous trophoblasts of normal placenta deeply invade the decidua, the inner one-third of the myometrium (interstitial invasion) and the maternal spiral arteries (endovascular invasion), leading to morphological and functional changes known as "vascular remodeling". Pregnancy-induced hypertension syndrome (PIH) is associated with abnormally shallow cytotrophoblast invasion. It's vascular remodeling in the spiral arteties is confined to the decidual portion. Placental bed's spiral arteries escape entirely from endovascular trophoblast invasion. This doesn't cause an increase in the luminal width of the spiral arteries, and results in a deficient blood and oxygen supply to the placenta. Insulin-like growth factor-Ⅱ (IGF-Ⅱ), transforming growth factor-β1 (TGF-β1), and their receptors are expressed in trophoblasts. The expession of IGF-Ⅱ and TGF-β1 may be altered in PIH placentas. Invasion activity of trophoblasts of PIH placentas may be regulated by IGF-Ⅱ and TGF-β1.The role of IGF-Ⅱ and TGF-β1 in the trophoblasts invasion in PIH were investigated in this study.Methods: Control group was consisted of thirty normal pregnancies. Study group was consisted of twenty-five women with PIH. The placental pathology of PIH was observed by HE staining. The cellular distribution of IGF-Ⅱ and TGF-β1 in placenta was determined by immunohistochemistry. The expression of IGF-ⅡmRNA and TGF-β1 mRNA in trophoblasts was detected by RT-PCR. The affection of IGF-Ⅱ and TGF-β1 in trophoblasts's invasion activity was measured by in vitro invasion assay.Results: 1. The histologic abnormalities of placentas from women with PIH are characterized by a villous tree exhibits prominent cytotrophoblast proliferating, basement membrane thickening, syncytiotrophoblast knotting increasing, syncytiotrophoblast budding, villus's fibrinoid necrosis increasing, fibrin depositing, more villus blood vessel, and most villus immature. 2. IGF-Ⅱand TGF-β1 distribution in PIH placenta was found in cytotrophoblast and syncytiotrophoblast, which was the same as that in normal placenta. The mean density of IGF-Ⅱ of PIH group was significantly lower than that of normal group(P<0.05). The more severe PIH was, the lower mean density of IGF-Ⅱ. The meandensity of TGF-β1 of PIH group was significantly higher than that of normal group(P<0.05). And it's increase was also related to the severity of PIH. 3. The expression of IGF-ⅡmRNA in trophoblasts isolated from severe PIH placenta was significantly decreased(P<0.05). The expression of TGF-β1mRNA in trophoblasts isolated from PIH placenta was higher than that of normal group(P<0.05). 4. In normal group, trophoblasts invasion was enhanced by IGF-Ⅱ and was inhibited by TGF-β1 in the invasion assay(P<0.05). In PIH, The invasive ability of cytotrophoblasts was dramatically decreased(P<0.05), and it couldn't be changed by adding IGF-Ⅱ or TGF-β1 into culture medium(P>0.05).Conclusion: 1. The histologic abnormalities of placentas from women with PIH is the adaptation response of villous trophoblast to ischemia and hypoxic conditions. 2. The expression of IGF-Ⅱand IGF-ⅡmRNA in trophoblasts from patients with PIH was significantly decreased, but that of TGF-β1 and TGF-β1 mRNA was significantly increased. IGF-Ⅱand TGF-β1 are related to shallow invasion of trophoblasts of PIH placenta. 3. The number of cytotrophoblasts on the bottom side of the filter from women with PIH was decreased, which illustrated that the invasive ability of cytotrophoblasts is dramatically decreased in PIH. 4. Invasion assay of trophoblasts isolated from normal placenta shows IGF-Ⅱ promote and TGF-β1 inhibit the invasion ability of trophoblasts. 5. Trophoblasts invasion in PIH group couldn't be affected by IGF-Ⅱand TGF-β1. The mechanisms of which need a further investigation. |
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