Objective: To detect and compare the plasma level and expression of visfatin in placental tissue of missed abortion (MA) and induced abortion of unwanted normal pregnancy for exploring the possible role of visfatin in the pathogenesis of MA. Method: A total of 36 cases of MA (5-11 gestational weeks) and 20 cases of induced abortion of unwanted normal pregnancy (5-11 gestational weeks) were collected in the International Peace Maternal and Child Health Hospital affiliated to Shanghai Jiao Tong University between October, 2016 to April 2017. The double antibody enzyme-linked immunosorbent assay (ELISA) and immunohistochemical method (IHC) were used to detect visfatin level in plasma and expression of visfatin in placenta tissue. Result: By ELISA, the plasma level of visfatin in MA patients was (55.98±10.30) ng/mL and the plasma level of visfatin in induced abortion of unwanted normal pregnancy group was(70.19±11.70) ng/mL, the difference was statistically significant(P<0.001). By IHC, the expression of visfatin in placenta tissue was significantly lower in MA patients than in induced abortion of unwanted normal pregnancy group (P<0.001). Moreover, there was a significant correlation between the plasma level and placenta expression of visfatin (r=0.711, P<0.01). The degeneration rate of placental villus in MA group was higher than that in induced abortion of unwanted normal pregnancy group, and the low expression of visfatin was correlated with placental villus degeneration rate (r=-0684, P<0.001), and this correlation was more obvious than that between level of plasma visfatin and placental villus degeneration. Conclusions: The low expression of visfatin in plasma and placenta tissues may be involved in the pathogenesis of MA. Determining plasma visfatin level may be used as one of the indicators for monitoring the progress of pregnancy.
CAI Mei, WU Weibin, LIU Yuan, ZHANG Huijuan
. Low expression of visfatin and its correlation with vilius degeneration in patients with missed abortion[J]. Journal of Diagnostics Concepts & Practice, 2018
, 17(02)
: 170
-175
.
DOI: 10.16150/j.1671-2870.2018.02.010
[1] 乐杰. 妇产科学[M]. 7版. 北京: 人民卫生出版社,2008:56-58.
[2] 徐萍, 周赤艳, 钟少平. 孕早期母胎界面血管新生在稽留流产患者发病中作用[J]. 浙江临床医学,2016,18(6):1081-1083.
[3] Caniggia I, Winter J, Lye SJ, et al.Oxygen and placental development during the first trimester: implications for the pathophysiology of pre-eclampsia[J]. Placenta,2000,21(Suppl A):S25-S30.
[4] Broady AJ, Loichinger MH, Ahn HJ, et al.Protective proteins and telomere length in placentas from patients with pre-eclampsia in the last trimester of gestation[J]. Placenta,2017,50:44-52.
[5] 殷震惠. 稽留流产病因研究进展[J]. 现代诊断与治疗,2010,21(2):88-91.
[6] Baergen NR.人类胎盘病理学手册[M]. 美国: 天津科技翻译出版公司,2008:116-118.
[7] Grinschgl I, Mannweiler S, Holzapfel-Bauer M, et al.The role of morphology in combination with ploidy analysis in characterizing early gestational abortion[J]. Virchows Arch,2013,462(2):175-182.
[8] Fukuhara A, Matsuda M, Nishizawa M, et al.Visfatin: a protein secreted by visceral fat that mimics the effects of insulin[J]. Science,2005,307(5708):426-430.
[9] Demir R, Seval Y, Huppertz B.Vasculogenesis and angiogenesis in the early human placenta[J]. Acta Histochem,2007,109(4):257-265.
[10] Pavlová T, Novák J, Bienertová-Vašků J.The role of visfatin (PBEF/Nampt) in pregnancy complications[J]. J Reprod Immunol,2015,112:102-110.
[11] Porter B, Babbar S, Ye SQ, et al.The Role of Nicotinamide Phosphoribosyltransferase in Pregnancy: A Review[J]. Am J Perinatol,2016,33(14):1327-1336.
[12] Bae SK, Kim SR, Kim JG, et al.Hypoxic induction of human visfatin gene is directly mediated by hypoxia-inducible factor-1[J]. FEBS Lett,2006,580(17):4105-4113.
[13] Astern JM, Collier AC, Kendal-Wright CE.Pre-B cell colony enhancing factor (PBEF/NAMPT/Visfatin) and vascular endothelial growth factor (VEGF) cooperate to increase the permeability of the human placental amnion[J]. Placenta,2013,34(1):42-49.
[14] Cöl-Madendag I, Madendag Y, Altinkaya SÖ, et al.The role of VEGF and its receptors in the etiology of early pregnancy loss[J]. Gynecol Endocrinol,2014,30(2):153-156.
[15] Skrzypczak J, Wirstlein P, Mikołajczyk M, et al.TGF superfamily and MMP2, MMP9, TIMP1 genes expression in the endometrium of women with impaired reproduction[J]. Folia Histochem Cytobiol,2007,45(Suppl 1):S143-S148.
[16] Konac E, Alp E, Onen HI, et al.Endometrial mRNA expression of matrix metalloproteinases, their tissue inhibitors and cell adhesion molecules in unexplained infertility and implantation failure patients[J]. Reprod Biomed Online,2009,19(3):391-397.