Concordant in situ and in vitro data show that maternal cigarette smoking negatively regulates placental cytotrophoblast passage through the cell cycle☆

Genbačev, Olga; McMaster, Michael; Lazic, Jelena; Nedeljkovic, Slavin; Cvetković, Dragoš; Joslin, Rebecca J.; Fisher, Susan J.

doi:10.1016/s0890-6238(00)00107-6

Cited by 59 publications

(34 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…By immunohistochemistry staining for cytokeratin and sFRP1, sFRP1 appeared to be localized to invasive extravillous trophoblasts (Figure 1, D-G). In addition, consistent with previously published studies (17,18), placentas from smoking mothers showed evidence of significantly decreased proliferative activity, as shown by Ki67 staining in cytotrophoblasts (Supplemental Figure 1, C and D). Taken together with prior gene-targeting experiments that suggest a role for WNT signaling in murine placental development (19)(20)(21), the present data support the concept that elevated placental expression of sFRP1 may lead to abnormalities in placentation.…”

Section: Resultssupporting

confidence: 91%

Excess placental secreted frizzled-related protein 1 in maternal smokers impairs fetal growth

Wang¹,

Zsengellér²,

Hecht³

et al. 2015

Journal of Clinical Investigation

View full text Add to dashboard Cite

show abstract

Section: Resultssupporting

confidence: 91%

Excess placental secreted frizzled-related protein 1 in maternal smokers impairs fetal growth

Wang¹,

Zsengellér²,

Hecht³

et al. 2015

Journal of Clinical Investigation

View full text Add to dashboard Cite

show abstract

“…A reduced number of Ki-67-positive cytotrophoblasts means that fewer cells are in the S-phase causing a premature depletion of cytotrophoblast stem cell population [10]. We can thus conclude that the cytotrophoblast population in placentas of smoking mothers is reduced.…”

Section: Discussionmentioning

confidence: 73%

“…Few studies on maternal smoking and placental apoptosis have been conducted [3,10,17]. Some controversy exists as to the effect of smoking on apoptosis [3,9, 10, 17,18 -20].…”

Section: Introductionmentioning

confidence: 99%

Maternal Smoking, Intrauterine Growth Restriction, and Placental Apoptosis

et al. 2004

View full text Add to dashboard Cite

Pregnant women who smoke are at greater risk of delivering a growth-restricted infant than nonsmoking mothers. We wanted to see if apoptosis could be involved in the mechanisms behind smoke-induced growth restriction, and our aim was to compare apoptosis in the placenta of smoking mothers giving birth to growth-restricted infants and nonsmoking mothers with infants of appropriate weight. The project was conducted at the Magee-Womens Hospital and Magee-Womens Research Institute, University of Pittsburgh, PA. Histological sections from 20 placentas were selected from smoking mothers who had given birth to small-forgestational-age infants (birth weight Յ 2 SD). The controls were gestational-age matched nonsmoking mothers with infants having appropriate-for-gestationalage weight. The TUNEL method was used to demonstrate DNA fragmentation in nuclei, and a monoclonal antibody M30, specific for a neo-epitope on cytokeratin 18, was used to identify apoptotic epithelial cells. The positive nuclei (TUNEL) and positive cells (M30-positive cytoplasm) were counted blindly both in villous tissue and in decidual/basal plate tissue. M30-positive cells in villous tissues were significantly increased in placentas from smoking mothers compared to nonsmoking mothers. When evaluated by the TUNEL method, the difference between the two groups of women was not significant. Our study shows that apoptosis was increased in the placentas of smoking mothers with growth-restricted infants. The difference between the two groups was mainly in the syncytiotrophoblast layer and in connection with perivillous fibrin deposition. Cigarette smoke with reduction in blood flow has previously been shown to increase apoptosis, and it is possible that this could be one of the mechanisms playing a role in the growth restriction.

show abstract

“…The actual influences are determined by the individual compounds and the dose to which the endometrium is exposed. Human placental trophoblastic cell lines exposed to compounds within cigarette smoke have been reported to lead to altered expression of epidermal growth factor (387), matrix metalloproteases (121), alterations of hCG secretion (40), L-selectin expression (383), in addition to increased apoptosis, altered cellular architecture, and reduced cytotrophoblast invasion (80,122). Cigarette smoking women are exposed to high levels of cadmium and lead, and these metals have been found within the endometrium of cigarette smokers, correlating with the number of cigarettes smoked and the duration of smoking (289).…”

Section: Implantationmentioning

confidence: 99%

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

Hart

2016

Physiological Reviews

175

119

View full text Add to dashboard Cite

Across the Western World there is an increasing trend to postpone childbearing. Consequently, the negative influence of age on oocyte quality may lead to a difficulty in conceiving for many couples. Furthermore, lifestyle factors may exacerbate a couple's difficulty in conceiving due mainly to the metabolic influence of obesity; however, the negative impacts of low peripheral body fat, excessive exercise, the increasing prevalence of sexually transmitted diseases, and smoking all have significant negative effects on fertility. Other factors that impede conception are the perceived increasing prevalence of the polycystic ovary syndrome, which is further exacerbated by obesity, and the presence of uterine fibroids and endometriosis (a progressive pelvic inflammatory disorder) which are more prevalent in older women. A tendency for an earlier sexual debut and to have more sexual partners has led to an increase in sexually transmitted diseases. In addition, there are several genetic influences that may limit the number of oocytes within the ovary; consequently, by postponing attempts at childbearing, a limitation of oocyte number may become evident, whereas in previous generations with earlier conception this potentially reduced reproductive life span did not manifest in infertility. Environmental influences on reproduction are under increasing scrutiny. Although firm evidence is lacking however, dioxin exposure may be linked to endometriosis, phthalate exposure may influence ovarian reserve, and bisphenol A may interfere with oocyte development and maturation. However, chemotherapy or radiotherapy is recognized to lead to ovarian damage and predispose the woman to ovarian failure.

show abstract

Concordant in situ and in vitro data show that maternal cigarette smoking negatively regulates placental cytotrophoblast passage through the cell cycle☆

Cited by 59 publications

References 34 publications

Excess placental secreted frizzled-related protein 1 in maternal smokers impairs fetal growth

Excess placental secreted frizzled-related protein 1 in maternal smokers impairs fetal growth

Maternal Smoking, Intrauterine Growth Restriction, and Placental Apoptosis

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

Contact Info

Product

Resources

About