Effects of cigarette smoke on fertilization and embryo development in vivo

Huang, Junjiu; Okuka, Maja; McLean, Mark; Keefe, David L.; Liu, Lin

doi:10.1016/j.fertnstert.2008.07.1781

Cited by 61 publications

(51 citation statements)

References 48 publications

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“…It predicts that late proliferating oogonia, which give rise to late ovulating oocytes, have depleted telomere reserve from the multiple mitotic divisions that preceded their entry into meiosis (7,8). Over the decades before ovulation, the inescapable effects of ROS, exacerbated by lifestyle factors, including obesity and smoking, further erode telomeres in oocytes (75).…”

Section: Telomeres and Oocyte Competencymentioning

confidence: 99%

Oocyte competency is the key to embryo potential

Keefe¹,

Kumar²,

Kalmbach³

2015

Fertility and Sterility

171

118

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Section: Telomeres and Oocyte Competencymentioning

confidence: 99%

Oocyte competency is the key to embryo potential

Keefe¹,

Kumar²,

Kalmbach³

2015

Fertility and Sterility

171

118

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“…Oct4 is also transiently required for extraembryonic endoderm development from the ICM [9,10]. Oct4 promoter methylation is diminished in oocytes undergoing in vitro maturation [11] and Oct4 expression is decreased in embryos derived from smoke-exposed mouse females [12]. This suggests that environmental stimuli can change potency state and cause potency loss.…”

Section: Oct4 and Rex1mentioning

confidence: 99%

Development and Validation of a Rex1-RFP Potency Activity Reporter Assay That Quantifies Stress-Forced Potency Loss in Mouse Embryonic Stem Cells

Gomez‐Lopez

Drewlo

et al. 2016

Stem Cells and Development

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Assays for embryonic stem cells (ESCs) of the blastocyst are needed to quantify stress-induced decreases of potent subpopulations. High-throughput screens (HTSs) of stressed ESCs quantify embryonic stress, diminishing laboratory animal needs. Normal or stress-induced ESC differentiation is marked by Rex1 potency factor loss. Potency reporter ESC assays were developed, using low-stress techniques to create transgenic ESCs. Rex1 and Oct4 promoters drove RFP and green fluorescent protein (GFP) expression, respectively. Lentivirus infection and fluorescence-activated cell sorting selection of ESCs obviated the need for stressful electroporation and antibiotic selection, respectively. We showed using immunoblots, microscopic analysis, flow cytometry, and fluorescence microplate reader that the response to stress of potency-reporter ESCs is similar to parental ESCs assayed by biochemical means. Stress caused a dose-dependent decrease in bright Rex1-RFP + ESCs and increase in Rex1 dim ESCs. At highest stress, *20% of bright Rex1-RFP cells are lost coinciding with a 2.8-fold increase in Rex1-RFP dim cells that approach 20%. This conversion of bright to dim cells tested by flow cytometry is commensurate with about 60% loss in fluorescence measured by microplate reader. Dosedependent stress-induced Rex1-RFP and endogenous Rex1 protein decreases are similar. The data show that Rex1 reporter ESCs accurately report stress in a microplate reader-based HTS. The increasing dim Rex1 subpopulation size is balanced by the decreasing total ESC number during culture at multiple sorbitol doses. This is consistent with previous observations that stress forces potency decrease and differentiation increase to compensate for stress-induced diminished stem cell population growth.

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“…In addition, laboratory animals exposed to cigarette smoke have also exhibited reduced fecundity, as evidenced by reduced litter size and increased resorptions [Izzotti et al 2003;Khan et al 2008], poor embryo quality [Huang et al 2008], low fetal weight [Esposito et al 2008]), and fetal demise [Farkas et al 2006]. Early evidence connecting smoking during pregnancy with the risk of spontaneous miscarriage was controversial, with some groups reporting a positive association [Himmelberger et al 1978;Kline et al 1977] and others reporting no association [Harlap and Shiono 1980].…”

Section: Smoking and Spontaneous Abortionmentioning

confidence: 99%

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Detmar

Jurisicova

2010

Systems Biology in Reproductive Medicine

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Polycyclic aromatic hydrocarbons (PAHs) are released into the environment as a result of incomplete fossil fuel combustion from industrial furnaces, woodburning stoves, and automobile exhaust fumes; however, the primary source of human exposure to these compounds is cigarette smoke. Embryonic and fetal loss after treatment with high doses of PAHs have been well documented in animal studies; however, few studies have addressed the reproductive consequences of long-term, low-level exposure to these chemicals. We previously reported that low doses of PAHs administered to ICR mice over a period of 9 weeks prior to conception resulted in early embryonic resorptions, whereby treated dams lost approximately 50% of their litter. During the course of these studies, we observed greater numbers of infiltrating uterine natural killer (uNK) cells into the placenta of PAH-exposed conceptuses. While exposure to high levels of PAHs has been shown to be immunosuppressive, increasing evidence suggests that chronic, low-dose exposure to PAHs may stimulate immune cells. Thus, we hypothesized that low-dose, chronic PAH exposure in our mouse model is mediating embryonic resorption by hyperstimulating maternal immune cells. In this review of the literature, we outline the rationale of our argument and present preliminary data, focussing upon PAH-mediated alterations in uNK cell dynamics and how these changes may be linked to early embryonic resorptions.

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Effects of cigarette smoke on fertilization and embryo development in vivo

Cited by 61 publications

References 48 publications

Oocyte competency is the key to embryo potential

Oocyte competency is the key to embryo potential

Development and Validation of a Rex1-RFP Potency Activity Reporter Assay That Quantifies Stress-Forced Potency Loss in Mouse Embryonic Stem Cells

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

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