Modulation of gene expression in the preimplantation mouse embryo by TGF‐α and TGF‐β

Babalola, Gbolagade O.; Schultz, Richard M.

doi:10.1002/mrd.1080410203

Cited by 44 publications

(16 citation statements)

References 37 publications

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“…We also found transforming growth factor beta regulator 1 (TBRG1), a growth inhibitory protein induced in cells undergoing arrest in response to DNA damage and TGF-β1 [54], was more highly expressed in Pkd1flox/flox; Ksp-Cre mice than in matched wild type mice on the 1st day after birth in our proteomics study (data not shown). Further studies are needed to clarify the complex cross-talk between the cAMP-PKA and TGF-β-activated pathways in PKD.…”

Section: Discussionmentioning

confidence: 88%

The Effect of cAMP-PKA Activation on TGF-β1-Induced Profibrotic Signaling

Weng

Wang²,

Su³

et al. 2015

Cell Physiol Biochem

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Background: The cAMP-PKA signaling pathway and TGF-β1-dependent fibrosis pathways are of particular importance in ADPKD progression, but the cross-talk between these pathways remains unclear. Therefore, we used an MDCK-cell model and embryonic kidney-cyst model to study the regulatory role of cAMP-PKA signaling in the TGF-β1 induced fibrotic process. Method and Results: Pkd1^flox/flox; Ksp-Cre and Pkd1^+/+; Ksp-Cre mice were used as an in vivo model. Increased kidney volume, renal cysts formation and up-regulation of the fibrosis-related proteins TGF-β1, connective tissue growth factor (CTGF), and fibronectin (FN) can be observed in Pkd1^flox/flox; Ksp-Cre mice. In an embryonic kidneys-cyst model, TGF-β1, FN and collagen type I were highly expressed. Western blotting revealed the obviously up-regulation of TGF-β1, CTGF, FN and collagen type I expression following forskolin treatment in MDCK cells. Selective PKA inhibition with H89 may partially reversed the above effects. Pretreatment with the TGF-β RI kinase inhibitor VI SB431542 suppressed the increased expression of CTGF, FN and collagen type I caused by forskolin. Our data also indicate that forskolin inhibited TGF-β-induced ERK1/2 phosphorylation and FN up-regulation. ERK inhibition useing PD98059 significantly inhibited the expression of CTGF, FN and collagen type I caused by TGF-β1. Conclusions: The cAMP-PKA signaling pathway can directly promote the production of TGF-β1 and/or TGF-β1-dependent fibrogenetic molecules in MDCK cells and embryonic kidney cysts, but when TGF-β1 and its downstream pathways were highly expressed in MDCK cells, cAMP-PKA had a significantly negative effect on TGF-β1 induced p-ERK1/2 and FN expression.

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Section: Discussionmentioning

confidence: 88%

The Effect of cAMP-PKA Activation on TGF-β1-Induced Profibrotic Signaling

Weng

Wang²,

Su³

et al. 2015

Cell Physiol Biochem

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“…Recent studies have implicated a variety of putative growth factors including platelet-activating factor (PAF) [4], insulin-like growth factor I (IGF-I) [5,6], IGF-II [7], and epidermal growth factor/transforming growth factor ot [8,9]. Their mechanisms of action and their temporal pattern of action is poorly understood, while the very nature of autocrine mediators (produced by and acting on the same cell populations) make such studies difficult.…”

Section: Introductionmentioning

confidence: 98%

Autocrine Mediators are Required to act on the Embryo by the 2-Cell Stage to Promote Normal Development and Survival of Mouse Preimplantation Embryos in Vitro1

O’Neill

1998

Biology of Reproduction

101

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Autocrine mediators released by the early embryo are implicated in the support of embryo development. Their mechanisms and timing of action, however, are uncertain. This study shows that their action is necessary during the 2-cell stage of development, at which time they do not act as classical growth factors, having no impact on the rate of cell-cycle progression. Rather, they act as survival factors, protecting embryos from subsequent cell death. Culture of zygotes for the first 48 h after insemination (but not the first 24 h only) at a high concentration of 1 embryo/microl before transfer to a concentration of 1 embryo/100 microl significantly improved development compared with culture at the lower concentration for 120 h. By contrast, if the initial 48 h of culture was at 1 embryo/100 microl, subsequent culture at 1 embryo/microl caused no improvement. Platelet-activating factor (PAF) supplementation (0.186 microM) of media for the 48-h period after insemination (but not 24 h only) improved the development of embryos cultured at low embryo concentrations (1 embryo/10 microl) even when transferred to PAF-free media for the subsequent 72-h culture period. The ability of PAF to mimic the effects of higher embryo density implicates embryo-derived PAF as one of the autocrine mediators stimulating early embryo development. The cell death that occurred at low embryo concentration had a mixed phenotype: some cells had lost membrane integrity whereas others had intact membranes but punctate or fragmented chromatin. It is concluded that the action of autocrine diffusible factors, including PAF, are necessary during the 2-cell stage for subsequent survival and normal development of embryos to the blastocyst stage.

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“…During preimplantation development, many of these factors and their receptors are also expressed in the embryos. Addition of growth factors to the culture medium facilitates embryo development [5][6][7], suggesting that paracrine pathways exist between the oviduct and the preimplantation embryos.…”

Section: Introductionmentioning

confidence: 98%

Temporal Effect of Human Oviductal Cell and Its Derived Embryotrophic Factors on Mouse Embryo Development1

Cheung

Chan

et al. 2001

Biology of Reproduction

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Mouse embryos at different stages of development were cocultured with human oviduct cells or cultured in the presence of oviduct-derived embryotrophic factor-1, -2, and -3 (ETF-1, -2, and -3) for various amounts of time within the preimplantation period. Cocultures that included the period from 48 to 72 h post-hCG stimulated cell division and increased the cell numbers in the inner cell mass (ICM) of the exposed blastocyst. Exposure of embryos to oviductal cells from 96 to 120 h post-hCG increased the cell number in the trophectoderm (TE), blastocyst size, hatching rate, attachment, and in vitro spreading of the blastocyst. ETF-1 and ETF-2 affected embryos between 48 and 72 h post-hCG by increasing the number of cells in the ICM. In contrast, ETF-3 had a more profound effect on embryos that were exposed from 96 to 120 h post-hCG, where it mostly affected the development of TE cells, leading to higher hatching rate. Human oviductal cells improved mouse embryo development partly by the production of high molecular weight embryotrophic factors. These factors had differential effects on mouse embryo development.

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Modulation of gene expression in the preimplantation mouse embryo by TGF‐α and TGF‐β

Cited by 44 publications

References 37 publications

The Effect of cAMP-PKA Activation on TGF-β1-Induced Profibrotic Signaling

The Effect of cAMP-PKA Activation on TGF-β1-Induced Profibrotic Signaling

Autocrine Mediators are Required to act on the Embryo by the 2-Cell Stage to Promote Normal Development and Survival of Mouse Preimplantation Embryos in Vitro1

Temporal Effect of Human Oviductal Cell and Its Derived Embryotrophic Factors on Mouse Embryo Development1

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