Objective To investigate the expression and correlation of soluble FMS-like tyrosine kinase-1 （sFlt-1） and placental growth factor （PlGF） in placenta of patients with preeclampsia. Methods The maternal placenta during delivery and clinical data of 10 patients with preeclampsia （study group） and 12 normal pregnant women （control group） were collected and retrieved, who gave birth in our hospital from August 2021 to December 2022. The expression of sFlt-1 and PlGF in placental tissue was detected by Western blotting （WB）. Results Compared with the control group, there was no significant difference in the age and body mass index of pregnant women in the study group （P>0.05）. Urine protein was negative in the control group and positive in the study group. The gestational age and neonatal weight in the study group were significantly lower than those in the control group （P<0.01）. Systolic blood pressure and diastolic blood pressure in the study group were significantly higher than those in the control group （P<0.01）. WB detection showed that compared with the control group, the expression level of sFlt-1 in placental tissue of the study group was significantly higher than that of the control group （Z=–3.962, P<0.01）. The expression level of PlGF in the study group was significantly lower than that in the control group （Z=–3.957, P<0.01）. Conclusion The increase of anti-vascular factor sFlt-1 expression and the decrease of pro-angiogenic factor PlGF in placental tissue of preeclampsia patients abnormally regulate vasomotor contraction and relaxation and participate in the occurrence, development, and target organ damage of preeclampsia.
ZHOU Wenli
,
WANG Caili
,
KANG Wei
,
FENG Caixia
. Expression and correlation of sFlt-1 and PlGF in placenta of patients with preeclampsia[J]. Surgical Research and New Technique, 2024
, 13(2)
: 96
-100
.
DOI: 10.3969/j.issn.2095-378X.2024.02.003
[1] Liona CP, Laura AM, Stefan V, et al.A literature review and best practice advice for second and third trimester risk stratification, monitoring, and management of pre-eclampsia: Compiled by the Pregnancy and Non-Communicable Diseases Committee of FIGO the International Federation of Gynecology and Obstetrics[J]. Int J Gynaecol Obstet, 2021, 154(Suppl 1): 3-31.
[2] Offer E, Roberto R, Eunjung J, et al.Preeclampsia and eclampsia: the conceptual evolution of a syndrome[J]. Am J Obstet Gynecol, 2022, 226(2S): S786-S803.
[3] Rana S, Burke SD, Karumanchi SA.Imbalances in circulating angiogenic factors in the pathophysiology of preeclampsia and related disorders[J]. Am J Obstet Gynecol, 2022, 226(2S):S1019-S1034.
[4] Yu W, Gao W, Rong D, et al.Molecular determinants of microvascular dysfunction in hypertensive pregnancy and preeclampsia[J]. Microcirculation, 2018, 19: e12508.
[5] Jürgen P, Sigrid V, Jennet B, et al.Regulation of placental extravillous trophoblasts by the maternal uterine environment[J]. Front Immunol, 2018: 9: 2597.
[6] Bhavisha AB, Frank TS, Heather AD, et al.Preeclampsia: linking placental ischemia with maternal endothelial and vascular dysfunction[J]. Compr Physiol, 2020, 11(1): 1315-1349.
[7] Ahmad S, Ahmed A.Elevated placental soluble vascular endothelial growth factor receptor-1 inhibits angiogenesis in preeclampsia[J]. Circ Res, 2004, 95(9): 884-891.
[8] Maynard SE, Min JY, Merchan J, et al.Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia[J]. J Clin Invest, 2003, 111(5): 649-658.
[9] Dania AS, Raouf AK.Bioactive factors in uteroplacental and systemic circulation link placental ischemia to generalized vascular dysfunction in hypertensive pregnancy and preeclampsia[J]. Biochem Pharmacol, 2015, 95(4): 211-226.
[10] Chau K, Hennessy A, Makris A.Placental growth factor and pre-eclampsia[J]. J Hum Hypertens, 2017, 31(12): 782-786.
[11] Levine RJ, Maynard SE, Qian C, et al.Circulating angiogenic factors and the risk of preeclampsia[J]. N Engl J Med, 2004,350(7): 672-683.
