Tumour Necrosis Factor Α Binding to Human and Mouse Trophoblast

Ben-Yair, Edith; Less, Amir; Lev, Silvia; Ben‐Yehoshua, Liat Josefsberg; Tartakovsky, Boris

doi:10.1006/cyto.1997.0236

Cited by 22 publications

(19 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…FAX: 32 2 7645396; e-mail: dehertogh@obst. ucl.ac.be TE lineage [5]. These observations strongly suggest that the influence of TNF␣ on implanting embryos is predominantly inhibitory and that the ICM and TE lineages present cell-specific response patterns to the cytokine.…”

Section: Introductionmentioning

confidence: 89%

“…Tumor necrosis factor ␣ (TNF␣) is one of the cytokines whose role is extensively studied in the context of the interactions between the implanting embryo and the receptive uterus [2]. In rodents, TNF␣ synthesis has been detected in the uterus at the time of implantation [3], and the presence of TNF␣ receptors has been demonstrated in blastocysts [4], in trophectoderm (TE) cells [5], and in embryonic stem (ES) cells [6,7]. In vitro experiments have shown that TNF␣ decreases the rate of cell proliferation in the inner cell mass (ICM) lineage of blastocysts [8], the ability of ES cells to differentiate [7], and the expression level of receptors for other cytokines in the Accepted September 29, 1998.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Tumor Necrosis Factor α Decreases the Viability of Mouse Blastocysts In Vitro and In Vivo1

Wuu¹,

Pampfer²,

Becquet³

et al. 1999

Biology of Reproduction

View full text Add to dashboard Cite

Mouse blastocysts were exposed for 24 h to various concentrations of recombinant mouse tumor necrosis factor alpha (TNFalpha) and observed for their capacity to implant in vitro on a fibronectin-coated substrate or to develop in vivo after their transfer into surrogate females. Compared with findings in control blastocysts, exposure to TNFalpha resulted in a significant reduction in the average number of cells in the inner cell mass (ICM) lineage. This effect was associated with a significant increase in the frequency of cells identified as engaged in apoptosis by means of the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling technique. No difference was found in the incidence of nuclear fragmentation between control and TNFalpha-exposed blastocysts. When TNFalpha-pretreated blastocysts were allowed to implant in vitro, significantly fewer embryos were able to maintain a structured ICM cluster at the center of the trophectoderm outgrowth. Although no difference was found in the average surface area of the outgrowths, implants derived from TNFalpha-treated blastocysts contained significantly fewer nuclei than implants from control embryos. After transfer into recipient mice, TNFalpha-pretreated blastocysts implanted at about the same rate as control embryos, but a significantly higher rate of resorption was found among fetuses after exposure to the cytokine. In addition, the weight of the surviving fetuses was significantly lower than for control fetuses. These data indicate that the impact of TNFalpha on blastocysts is specifically aimed at the ICM lineage and that TNFalpha decreases the ability of embryos to differentiate into fetuses after implantation.

show abstract

Section: Introductionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor α Decreases the Viability of Mouse Blastocysts In Vitro and In Vivo1

Wuu¹,

Pampfer²,

Becquet³

et al. 1999

Biology of Reproduction

View full text Add to dashboard Cite

show abstract

“…Progesterone inhibits TNFa synthesis and secretion in endometrium (von Wolff et al 1999). TNFa appears to be inhibitory to the viability, growth and differentiation of preimplantation stage blastocysts (Hill et al 1987, Pampfer et al 1994a,b, Wuu et al 1999, Ben-yair et al 1997, Kurzawa et al 2001. However, human embryos secrete TNFa in vitro until morula stage, but not at blastocyst stage (Lachapelle et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Endometrial tumor necrosis factor α (TNFα) is a likely mediator of early luteal phase mifepristone-mediated negative effector action on the preimplantation embryo

Lalitkumar¹,

Sengupta²,

Ghosh³

2005

Reproduction

View full text Add to dashboard Cite

Cytokines and growth factors are important mediators of progesterone-regulated endometrial receptivity and embryo development. Early luteal phase administration of a potent antiprogestin-like mifepristone to the rhesus monkey results in endometrial desynchrony, loss of embryo viability and implantation failure. In the present study, administration of mifepristone (2 mg/kg body weight, s.c.) on day 2 after ovulation resulted in a significant increase (P < 0.01) in the level of tumor necrosis factor a (TNFa) in glandular and vascular compartments of endometrium, and in endometrial secretion and luminal fluid on day 6 after ovulation in the rhesus monkey. There was an associated lag in embryonic development, characterized by delayed mitochondrial maturity, poorly developed junctional complexes, a relative absence of intra-cytoplasmic filaments and a high degree of intra-cellular degenerative features. Exposure of TNFa (0, 0.5, 5, 50 ng/ml) to preimplantation stage mouse embryos in vitro showed a dose-dependent arrest in growth and development at both morula and blastocyst stages along with ultrastructural features of degeneration similar to those observed in embryos collected from early luteal phase mifepristone-treated monkeys. The de novo synthesized and released proteins in terms of trichloroacetic acid precipitable 35 S by morulae and blastocysts in vitro showed a marked depression following exposure to TNFa compared with control embryos. Based on the above observation and the fact that preimplantation stage embryos express receptors for TNFa, we suggest that increased levels of TNFa in endometrial and luminal compartments around the time of uterine receptivity following early luteal phase administration of mifepristone adversely affect the growth and viability of preimplantation stage embryos.Reproduction (2005) 129 323-335

show abstract

“…Recently, there have been several reports on apoptosis of human trophoblasts with its possible implication in the regulation of placental growth [2][3][4][5][6][7][8][9], and role of bcl-2 and its family in controlling the survival and death of cells [10][11][12]. The products of the bcl-2 gene, when elevated in cells either in vivo or in vitro, prevent the normal course of apoptotic cell death in a variety of cells induced by tropic factor deprivation or other stimuli without altering proliferation [13,14].…”

mentioning

confidence: 99%

Changes in Proliferative Potential, Apoptosis and Bcl-2 Protein Expression in Cytotrophoblasts and Syncytiotrophoblast in Human Placenta over the Course of Pregnancy.

et al. 2000

View full text Add to dashboard Cite

Abstract.In order to evaluate placental trophoblast proliferation and apoptosis during pregnancy, we investigated proliferating cell nuclear antigen (PCNA) expression, apoptosis and Bcl-2 protein expression in the human placenta using avidin/biotin immunoperoxidase method to examine PCNA and Bcl-2 protein expression, and TUNEL method to assess apoptosis. The appearance of apoptotic cells in very early term placental trophoblasts was also examined by transmission electron microscopy.PCNA was immunolocalized in the nuclei of cytotrophoblasts (C-cells). Determination of the mean percentage of PCNA-positive nuclei of C-cells revealed that PCNA expression in C-cells was highest in very early term (4th to 5th wk) placentas and significantly decreased with the advance of pregnancy. Bcl-2 protein was immunolocalized in the cytoplasm of syncytiotrophoblast (S-cell), being least abundant in very early term placentas, less abundant in early term and midterm placentas, and most abundant in term placentas.On the basis of TUNEL method, apoptosis was apparent in the nuclei of both C-cells and S-cell. The apoptosis positive rate of C-cell nuclei was highest in very early term 4th to 5th wk placentas, and significantly decreased in early term 7th to 9th wk and midterm placentas, but somewhat increased in term placentas compared to that in midterm placentas. On the other hand, apoptosis positive rate of S-cell nuclei was remarkably higher only in very early term 4th to 5th wk placentas compared to that in early term, midterm and term placentas.Transmission electron microscopy revealed the appearance of apoptotic nucleus in very early term placental trophoblasts.These results demonstrate for the first time that apoptosis in the human normal placenta predominates in both C-cells and S-cell in very early term 4th to 5th wk pregnancy and drastically diminished after 7th wk of pregnancy.An apparent increase in apoptosis in C-cells in term placentas compared to that in midterm placentas may reflect aging of the placenta or parturitionassociated biological change. The abundant expression of Bcl-2 protein in S-cell in term placentas may be responsible for the diminished occurrence of apoptosis in S-cell in term placentas.

show abstract

Tumour Necrosis Factor Α Binding to Human and Mouse Trophoblast

Cited by 22 publications

References 0 publications

Tumor Necrosis Factor α Decreases the Viability of Mouse Blastocysts In Vitro and In Vivo1

Tumor Necrosis Factor α Decreases the Viability of Mouse Blastocysts In Vitro and In Vivo1

Endometrial tumor necrosis factor α (TNFα) is a likely mediator of early luteal phase mifepristone-mediated negative effector action on the preimplantation embryo

Changes in Proliferative Potential, Apoptosis and Bcl-2 Protein Expression in Cytotrophoblasts and Syncytiotrophoblast in Human Placenta over the Course of Pregnancy.

Contact Info

Product

Resources

About