scholarly journals The role of SOCS3 in modulating leukaemia inhibitory factor signalling during murine placental development

2008 ◽  
Vol 77 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Kristy Boyle ◽  
Lorraine Robb
2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Naguib Salleh ◽  
Nelli Giribabu

Leukaemia inhibitory factor (LIF) plays an indispensible role in embryo implantation. Aberrant LIF production is linked to implantation failure. LIF regulates multiple processes prior to and during implantation such as uterine transformation into a receptive state, decidualization, blastocyst growth and development, embryo-endometrial interaction, trophoblast invasion, and immune modulation. Due to its critical role, LIF has been a target for a nonhormonal contraception. In this review, we summarize up-to-date information on the role of LIF in implantation and its role in contraception.


Reproduction ◽  
2005 ◽  
Vol 130 (2) ◽  
pp. 131-145 ◽  
Author(s):  
Susan J Kimber

Leukaemia inhibitory factor (LIF) is one of the most important cytokines in the reproductive tract. Without expression of LIF in the uterus, implantation of a blastocyst cannot begin. Yet, 13 years after publication of the phenotype of the LIF knockout mouse we are only just beginning to understand how LIF functions in the uterus. This review addresses our knowledge of the role of LIF in regulating implantation through its influence on the luminal epithelium and stromal decidualization, but also its influence on reproductive tract cells such as leukocytes and glandular epithelium, during the pre-implantation phase of pregnancy.


1999 ◽  
Vol 160 (2) ◽  
pp. 181-190 ◽  
Author(s):  
D Vogiagis ◽  
LA Salamonsen

Leukaemia inhibitory factor (LIF) is a pleiotrophic cytokine required for blastocyst implantation in mice. Uterine expression of LIF and that of its receptors has been demonstrated in a number of mammalian species indicating that LIF may have widespread importance in the establishment of pregnancy. The variations in the reaction of the uterus in preparation for and during implantation are considerable between species and understanding the differences and similarities assists in the interpretation of how this cytokine functions. Recent studies suggest that reduced endometrial LIF contributes to human infertility. Studies also demonstrate a potential role in placentation and fetal development. Thus, LIF has become an important cytokine warranting further investigation in the human. It is anticipated that when the mechanisms underlying normal embryonic and endometrial development are elucidated, fertility and infertility will be more precisely understood and hence able to be effectively controlled.


Author(s):  
Susan J Kimber ◽  
Ali A Fouladi-Nashta ◽  
Lisa Mohamet ◽  
Carolyn Jp Jones ◽  
Gemma Schofield

2010 ◽  
Vol 34 (8) ◽  
pp. 791-797 ◽  
Author(s):  
Jie Xu ◽  
Feng Wang ◽  
Zhouping Tang ◽  
Yanqiang Zhan ◽  
Jinping Zhang ◽  
...  

2011 ◽  
Vol 23 (5) ◽  
pp. 714 ◽  
Author(s):  
Golla Jaya Prakash ◽  
Pankaj Suman ◽  
Diana M. Morales Prieto ◽  
Udo R. Markert ◽  
Satish K. Gupta

Leukaemia inhibitory factor (LIF) is one of the cytokines that is indispensable for embryo implantation. The aim of the present study was to investigate the role of activation of extracellular signal-regulated kinase (ERK) 1/2 in LIF-mediated proliferation of HTR-8/SVneo cells. Stimulation of HTR-8/SVneo cells with LIF (50 ng mL–1) resulted in an increase in cell proliferation (P < 0.05) via increased transition of cells to the G2/M phase of cell cycle. Stimulation with LIF resulted in the activation of both signal transducer and activator of transcription (STAT) 3 Tyr705 and ERK1/2, but inhibition of ERK1/2 signalling by pretreatment of cells with U0126 (10 µM) for 2 h resulted in abrogation of LIF-mediated increases in G2/M transition, with a significant decrease (P < 0.05) in absolute cell numbers compared with control. Although STAT3 silencing had no effect on LIF-dependent proliferation of HTR-8/SVneo cells, it did result in an increase in cell apoptosis, which increased further upon inhibition of ERK1/2 activation irrespective of LIF stimulation. Stimulation of cells with LIF increased the Bcl-2/Bax ratio, whereas ERK1/2 inhibition decreased the Bcl-2/Bax ratio, even after LIF stimulation. Hence, it can be inferred that ERK1/2 activation is essential for LIF-mediated increases in proliferation and that both STAT3 and ERK1/2 activation are important for the survival of HTR-8/SVneo cells.


1998 ◽  
Vol 13 (suppl 3) ◽  
pp. 237-243 ◽  
Author(s):  
S.K. Smith ◽  
D.S. Charnock-Jones ◽  
A.M. Sharkey

2021 ◽  
Vol 22 (4) ◽  
pp. 1823
Author(s):  
Tullia Todros ◽  
Luana Paulesu ◽  
Simona Cardaropoli ◽  
Alessandro Rolfo ◽  
Bianca Masturzo ◽  
...  

Proinflammatory cytokines are produced in pregnancy in response to the invading pathogens and/or nonmicrobial causes such as damage-associated molecules and embryonic semi-allogenic antigens. While inflammation is essential for a successful pregnancy, an excessive inflammatory response is implicated in several pathologies including pre-eclampsia (PE). This review focuses on the proinflammatory cytokine macrophage migration inhibitory factor (MIF), a critical regulator of the innate immune response and a major player of processes allowing normal placental development. PE is a severe pregnancy-related syndrome characterized by exaggerated inflammatory response and generalized endothelial damage. In some cases, usually of early onset, it originates from a maldevelopment of the placenta, and is associated with intrauterine growth restriction (IUGR) (placental PE). In other cases, usually of late onset, pre-pregnancy maternal diseases represent risk factors for the development of the disease (maternal PE). Available data suggest that low MIF production in early pregnancy could contribute to the abnormal placentation. The resulting placental hypoxia in later pregnancy could produce high release of MIF in maternal serum typical of placental PE. More studies are needed to understand the role of MIF, if any, in maternal PE.


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