Blastocyst implantation depends on maternal expression of leukaemia inhibitory factor

Stewart, Colin L.; Kašpar, Petr; Brunet, Lisa J.; Bhatt, Harshida; Gadi, Inder K.; Köntgen, Frank; Abbondanzo, Susan J.

doi:10.1038/359076a0

Cited by 1,907 publications

(1,250 citation statements)

References 24 publications

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“…Several key maternal factors that may contribute to maximal 53" uterine receptivity have been identified: ultrastructural components such as pinopodes 54" (Psychoyos & Nikas, 1994); steroids or cytokines and growth factors (Pollard et al, 55" 1991;Stewart et al, 1992;Fukuda et al, 1995, Zhu et al, 1998Hoffman et al, 1998).…”

Section: "mentioning

confidence: 99%

Oviductal and endometrial mRNA expression of implantation candidate biomarkers during early pregnancy in rabbit

Saeed¹,

Saenz-de-Juano

Marco‐Jiménez

et al. 2013

Zygote

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SummaryPrenatal losses are a complex problem. Pregnancy requires orchestrated communication between the embryo and the uterus that includes secretions from the embryo to signal pregnancy recognition and secretion and remodelling from the uterine epithelium. Most of these losses are characterized by asynchronization between embryo and uterus. To better understand possible causes, an analysis was conducted of gene expression of a set of transcripts related to maternal recognition and establishment of rabbit pregnancy (uteroglobin, SCGB1A1; integrin α1, ITGA1; interferon-γ, IFNG; vascular endothelial growth factor, VEGF) in oviduct and uterine tissue at 16, 72 or 144 h post-ovulation and insemination. In the oviduct tissue, a significant decrease in the level of SCGB1A1 mRNA expression was observed from 144 h post-ovulation. In the case of ITGA1, the transcript abundance was initially lower, but mRNA expression increased significantly at 72 and 144 h post-ovulation. For IFNG, a huge decrease was observed from 16 to 72 h post-ovulation. Finally, no significant differences were observed in the VEGF transcript. For the endometrium, the results showed a significant decline in the level of SCGB1A1 mRNA expression from 16 to 144 h post-ovulation induction. The highest levels of ITGA1 transcript were detected at 144 h, followed by the 16 h group and lower at 72 h post-ovulation. For IFNG there were no significant differences among post-ovulation induction times. Finally, it was possible to observe that VEGF mRNA abundance was present at low levels at 16 h post-ovulation and remained low at 72 h, but increased at 144 h. The functional significance of these observations may provide new insights into the maternal role in prenatal losses.

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Section: "mentioning

confidence: 99%

Oviductal and endometrial mRNA expression of implantation candidate biomarkers during early pregnancy in rabbit

Saeed¹,

Saenz-de-Juano

Marco‐Jiménez

et al. 2013

Zygote

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“…Mice with a targeted deletion of the LIF gene were generously provided by Dr. Colin L. Stewart (NCI Frederick, Maryland) and maintained on a CD1 background (Stewart et al, 1992). CD1 wild-type (wt) mice were used as controls.…”

Section: Animalsmentioning

confidence: 99%

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

Cohen

Fields

2008

Neuron Glia Biol.

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Activity-dependent signaling between neurons and astrocytes contributes to experience-dependent plasticity and development of the nervous system. However, mechanisms responsible for neuronglial interactions and the releasable factors that underlie these processes are not well understood. The pro-inflammatory cytokine, leukemia-inhibitory factor (LIF), is transiently expressed postnatally by glial cells in the hippocampus and rapidly up-regulated by enhanced neural activity following seizures. To test the hypothesis that spontaneous neural activity regulates glial development in hippocampus via LIF signaling, we blocked spontaneous activity with the sodium channel blocker tetrodotoxin (TTX) in mixed hippocampal cell cultures in combination with blockers of LIF and purinergic signaling. TTX decreased the number of GFAP-expressing astrocytes in hippocampal cell culture. Furthermore, blocking purinergic signaling by P2Y receptors contributed to reduced numbers of astrocytes. Blocking activity or purinergic signaling in the presence of function-blocking antibodies to LIF did not further decrease the number of astrocytes. Moreover, hippocampal cell cultures prepared from LIF −/− mice had reduced numbers of astrocytes and activity-dependent neuron-glial signaling promoting differentiation of astrocytes was absent. The results show that endogenous LIF is required for normal development of hippocampal astrocytes, and this process is regulated by spontaneous neural impulse activity through the release of ATP.

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“…Argiris Efstratiadis (Columbia University, New York, NY) and Colin L. Stewart (National Cancer Institute, Frederick, MD) (Stewart et al, 1992;Liu et al, 1993) and were crossed to generate Lif/Igf-I double mutant mice and maintained on a hybrid genetic background as previously described (Pichel et al, 2003). Mice maintained at the Servicio de Experimentación Animal (USAL) were handled in accordance with the European Communities Council Directive (86/ 609/EEC) and procedures approved by the Ethics Committee of the CSIC.…”

Section: Embryos and Histologymentioning

confidence: 99%

Alterations in alveolar epithelium differentiation and vasculogenesis in lungs of LIF/IGF‐I double deficient embryos

Moreno-Barriuso¹,

López-Malpartida²,

Pablo³

et al. 2006

Developmental Dynamics

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Previous studies on double deficient mice for leukemia inhibitory factor (LIF) and insulin-like growth factor I (IGF-I) reported that they died of respiratory failure, with abnormal lung histology and altered expression of pulmonary markers. Here we analyzed prenatal Lif/Igf-I double mutant mouse embryos to characterize LIF and IGF-I cooperative roles in distal lung epithelium and vascular maturation. Lungs of IGF-I-deficient embryos displayed a higher proportion of type II pneumocytes, less differentiated type I pneumocytes, and failure in alveolar capillary remodeling compared to wild type and LIF-deficient mice. Lif/Igf-I double knockout lungs showed aggravated pulmonary hypoplasia, lower airway volume, increased proliferation, and elevated levels of ERK1/2 activation. In addition, their alveoli were collapsed and lined by type II cells. The differentiation of type I cells barely occurred and capillaries remained in the abundant mesenchyme. These results indicate that LIF collaborates with IGF-I in lung alveolar epithelium and vascular maturation.

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Blastocyst implantation depends on maternal expression of leukaemia inhibitory factor

Cited by 1,907 publications

References 24 publications

Oviductal and endometrial mRNA expression of implantation candidate biomarkers during early pregnancy in rabbit

Oviductal and endometrial mRNA expression of implantation candidate biomarkers during early pregnancy in rabbit

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

Alterations in alveolar epithelium differentiation and vasculogenesis in lungs of LIF/IGF‐I double deficient embryos

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