Thymic stromal lymphopoietin promotes the proliferation of human trophoblasts via phosphorylated STAT3-mediated c-Myc upregulation

Pu, Huahua; Duan, Jie; Wang, Y.; Fan, Daming; Li, D.-J.; Jin, Liping

doi:10.1016/j.placenta.2012.01.015

Cited by 17 publications

(12 citation statements)

References 15 publications

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“…Bovine MYC was uniformly expressed in all the iBT cells lines, whereas the exogenous hMYC , which was integrated into all of the iBT cell lines, was not. The expression of endogenous bovine MYC in the cell lines is consistent with the demonstrated maintenance of Myc expression in mouse trophectoderm stem cells (Erlebacher, Price, & Glimcher, ); MYC overexpression inducing trophectoderm differentiation from human ESCs (Sumi, Tsuneyoshi, Nakatsuji, & Suemori, ); high expression of MYC in proliferative human cytotrophoblast tissue (Rydnert, Pfeifer‐Ohlsson, Goustin, & Ohlsson, ); MYC up‐regulation in the cytokine‐induced proliferation of human cytotrophoblast cells (Pu et al, ); MYC up‐regulation in the trophectoderm of bovine blastocysts treated with epidermal growth factor (Tetens, Kliem, Tscheudschilsuren, Navarrete Santos, & Fischer, ); and ectopic MYC expression increasing the efficiency of mouse induced trophectoderm stem cell derivation from embryonic fibroblasts (Benchetrit et al, ).…”

Section: Discussionsupporting

confidence: 72%

Bovine trophectoderm cells induced from bovine fibroblasts with induced pluripotent stem cell reprogramming factors

et al. 2017

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Thirteen independent induced bovine trophectroderm (iBT) cell lines were established by reprogramming bovine fetal liver-derived fibroblasts after viral-vector transduction with either six or eight factors, including POU5F1 (OCT4), KLF4, SOX2, MYC, NANOG, LIN28, SV40 large T antigen, and hTERT. Light- and electron-microscopy analysis showed that the iBT cells had epithelial cell morphology typical of bovine trophectoderm cells. Reverse-transcription-PCR assays indicated that all of the cell lines expressed interferon-tau (IFNT) at passages 1 or 2. At later passages (≥ passage 8), however, immunoblot and antiviral activity assays revealed that more than half of the iBT cell lines had stopped expressing IFNT. Messenger RNAs specific to trophectoderm differentiation and function were found in the iBT cell lines, and 2-dimensional-gel analysis for cellular proteins showed an expression pattern similar to that of trophectoderm cell lines derived from bovine blastocysts. Integration of some of the human reprogramming factors, including POU5F1, KLF4, SOX2, MYC, NANOG, and LIN28, were detected by PCR, but their transcription was mostly absent in the iBT cell lines. Gene expression assessment of endogenous bovine reprogramming factor orthologs revealed endogenous bLIN28 and bMYC transcripts in all; bSOX2 and bNANOG in none; and bKLF4 and bPOU5F1 in less than half of the iBT cell lines. These results demonstrate that bovine trophectoderm can be induced via reprogramming factor expression from bovine liver-derived fibroblasts, although other fibroblast populations-e.g., derived from fetal thigh tissue-may produce similar results, albeit at lower frequencies.

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Section: Discussionsupporting

confidence: 72%

Bovine trophectoderm cells induced from bovine fibroblasts with induced pluripotent stem cell reprogramming factors

et al. 2017

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“…Studies in mice show that the embryonic-lethal phenotype seen in c-MYC-null animals can be largely corrected if the expression of this gene is maintained selectively in trophoblast (26,27). In humans, the rapid decline in MYC expression as primary term cytotrophoblast cells exit the cell cycle (28), together with the observation that JEG-3 choriocarcinoma cells have significantly reduced levels of proliferation in its absence, initially suggested a role in trophoblast regulation (29). Direct evidence is presented here; overexpression of miR-377 and let-7a reduced expression of both ERK and MYC and attenuated proliferation.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Regulation of Mitogenic Signaling Networks in the Human Placenta

Farrokhnia

Aplin

Westwood

et al. 2014

Journal of Biological Chemistry

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Placental cell growth depends on an adaptable combination of an endogenous developmental program and the exogenous influence of maternal growth factors, both of which may be influenced by microRNA (miR)-dependent effects on gene expression. We have previously shown that global miR suppression in placenta accelerates proliferation and enhances levels of growth factor signaling mediators in cytotrophoblast. This study aimed to identify miRs involved in regulating placental growth. An initial array revealed 58 miR species whose expression differs between first trimester, when cytotrophoblast proliferation is rapid, and term, by which time proliferation has slowed. In silico analysis defined potential growth-regulatory miRs; among these, hsa-miR-145, hsa-miR-377, and hsa-let-7a were predicted to target known placental growth genes and were higher at term than in the first trimester, so they were selected for further analysis. Overexpression of miR-377 and let-7a, but not miR-145, in first trimester placental explants significantly reduced basal cytotrophoblast proliferation and expression of ERK and MYC. PCR arrays, in silico analysis, Western blotting, and 3′-UTR luciferase reporter assays revealed targets of miR-145 within the insulin-like growth factor axis. Analysis of proliferation in placental explants overexpressing miR-145 demonstrated its role as a mediator of insulin-like growth factor-induced trophoblast proliferation. These findings identify miR-377 and let-7a in regulation of endogenous cell growth and miR-145 in the placental response to maternal stimulation and will aid the development of therapeutic strategies for problem pregnancies.

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“…One final link that has been made between TSLP and immune tolerance is in maternal-fetal tolerance during pregnancy(Li & Guo, 2009). TSLP was produced and secreted by first semester trophoblasts, and tissue from normal pregnancies demonstrated a TH2 bias and higher levels of TSLP expression than samples from miscarriages (Guo et al, 2010; Pu et al, 2012; Wu, Guo, Jin, Liang, & Li, 2010). Thus, while TSLP expression and a TH2 bias may lead to disease progression in cancer, TSLP may contribute to tolerance at the maternal-fetal interface.…”

Section: Tslp-associated Diseasesmentioning

confidence: 95%

The Biology of Thymic Stromal Lymphopoietin (TSLP)

Ziegler¹,

Roan

Bell

et al. 2013

Advances in Pharmacology

258

207

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Originally shown to promote the growth and activation of B cells, thymic stromal lymphopoietin (TSLP) is now known to have wide-ranging impacts on both hematopoietic and non-hematopoietic cell lineages, including dendritic cells (DCs), basophils, eosinophils, mast cells, CD4+, CD8+ and natural killer (NK) T cells, B cells and epithelial cells. While TSLP's role in the promotion of TH2 responses has been extensively studied in the context of lung- and skin-specific allergic disorders, it is becoming increasingly clear that TSLP may impact multiple disease states within multiple organ systems, including the blockade of TH1/TH17 responses and the promotion of cancer and autoimmunity. This review will highlight recent advances in the understanding of TSLP signal transduction, as well as the role of TSLP in allergy, autoimmunity and cancer. Importantly, these insights into TSLP's multifaceted roles could potentially allow for novel therapeutic manipulations of these disorders.

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Thymic stromal lymphopoietin promotes the proliferation of human trophoblasts via phosphorylated STAT3-mediated c-Myc upregulation

Cited by 17 publications

References 15 publications

Bovine trophectoderm cells induced from bovine fibroblasts with induced pluripotent stem cell reprogramming factors

Bovine trophectoderm cells induced from bovine fibroblasts with induced pluripotent stem cell reprogramming factors

MicroRNA Regulation of Mitogenic Signaling Networks in the Human Placenta

The Biology of Thymic Stromal Lymphopoietin (TSLP)

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