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#33667354   // To Up

An Outline of the Outset of Thrombopoiesis in Human Embryos At Last.

By single-cell transcriptome profiling of human yolk sacs and fetal livers, Wang et al. (2021) (in this issue of Cell Stem Cell) track two alternative routes for differentiation of megakaryocytes. The authors have shown that these megakaryocytes have hemostatic- and HSC-supporting functions, and that hESC-derived thrombospondin1-positive endothelial cells are capable of generating megakaryocytes in vitro.
Anna Rita Migliaccio, Ronald Hoffman

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#33530588   2021/01/26 To Up

Transcript Variants Have Distinct Roles in Ovarian Carcinoma and Differently Influence Platinum Sensitivity and Angiogenesis.

The prognosis of late-stage epithelial ovarian cancer (EOC) patients is affected by chemotherapy response and the malignant potential of the tumor cells. In earlier work, we identified hypermethylation of the gene () as a prognostic biomarker and contrary functions of transcript variants (TV1 and TV2) in A2780 and SKOV3 cells. The aim of the study was to further validate these results and to increase the knowledge about function in EOC. New overexpression models of high-grade serous ovarian cancer (HGSOC) were established and analyzed for phenotypic (IC determination, migration, proliferation and angiogenesis assay, DNA damage analysis) and transcriptomic consequences (NGS) of TV1 and TV2 overexpression. Platinum sensitivity was affected by a specific transcript variant depending on BRCA background. TV2 induced an increased sensitivity in BRCA1 cells (OVCAR3), whereas TV1 increased the sensitivity and induced a G2/M arrest under treatment in cells (A13-2-12). These different phenotypes relate to differences in DNA repair: homologous recombination deficient A13-2-12 cells show less γH2AX foci despite higher levels of Pt-DNA adducts. RNA-Seq analyses prove transcript variant and cell-line-specific effects. Pathway analyses revealed another clinically important function of RUNX3-regulation of angiogenesis. This was confirmed by thrombospondin1 analyses, HUVEC spheroid sprouting assays and proteomic profiling. Importantly, conditioned media (CM) from TV1 overexpressing A13-2-12 cells induced an increased HUVEC sprouting. Altogether, the presented data support the hypothesis of different functions of transcript variants related to the clinically relevant processes-platinum resistance and angiogenesis.
Karolin Heinze, Martin Hölzer, Martin Ungelenk, Melanie Gerth, Jürgen Thomale, Regine Heller, Claire R Morden, Kirk J McManus, Alexander S Mosig, Matthias Dürst, Ingo B Runnebaum, Norman Häfner

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#33484209   2021/02/12 To Up

TARBP2 promotes tumor angiogenesis and metastasis by destabilizing antiangiogenic factor mRNAs.

Tumor angiogenesis is a crucial step in the further growth and metastasis of solid tumors. However, its regulatory mechanism remains unclear. Here, we showed that TARBP2, an RNA-binding protein, played a role in promoting tumor-induced angiogenesis both in vitro and in vivo through degrading the mRNAs of antiangiogenic factors, including thrombospondin1/2 (THBS1/2), tissue inhibitor of metalloproteinases 1 (TIMP1), and serpin family F member 1 (SERPINF1), by targeting their 3'untranslated regions (3'UTRs). Overexpression of TARBP2 promotes tumor cell-induced angiogenesis, while its knockdown inhibits tumor angiogenesis. Clinical cohort analysis revealed that high expression level of TARBP2 was associated with poor survival of lung cancer and breast cancer patients. Mechanistically, TARBP2 physically interacts with the stem-loop structure located in the 3'UTR of antiangiogenic transcripts, leading to mRNA destabilization by the dsRNA-binding domains 1/2 (dsRBDs1/2). Notably, the expression level of TARBP2 in human tumor tissue is negatively correlated with the expression of antiangiogenic factors, including THBS1/2, and brain-specific angiogenesis inhibitor 1 (BAI1). Moreover, TARBP2 expression is strongly associated with tumor angiogenesis in a group of human lung cancer samples. Collectively, our results highlight that TARBP2 is a novel tumor angiogenesis regulator that could promote tumor angiogenesis by selectively downregulating antiangiogenic gene expression.
Meicen Zhou, Wenbao Lu, Bingwei Li, Xueting Liu, Ailing Li

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#33416154   2020/11/18 To Up

Exosomes derived from retinoblastoma cells enhance tumour deterioration by infiltrating the microenvironment.

The survival of young children (under 5 years of age) with malignant retinoblastoma remains poor, and clarification of the mechanism underlying tumour development is urgently needed. The present study aimed to reveal the role of exosomes (EXOs) from retinoblastoma cells in tumour development. The in vitro data indicated that EXOs derived from WERI‑Rb1 cells significantly inhibited the antitumour activity of macrophages and induced bone marrow mesenchymal stem cells to promote tumour growth via an increase in monocyte chemotactic protein 1 (also known as C‑C motif chemokine ligand 2) levels. In vivo data from a xenotransplantation model also showed that EXOs infiltrated the spleen, which induced a decrease in leukocytes and natural killer (NK) cells. Accordingly, the proportion of tumour‑associated macrophages was increased and the proportion of NK cells was decreased in tumours injected with EXOs compared with those injected with the control. EXOs were absorbed by Kupffer cells, and more metastases were observed in the liver. Thus, these results suggested that EXOs derived from retinoblastoma promoted tumour progression by infiltrating the microenvironment. Moreover, microRNAs (miRs), including miR‑92a, miR‑20a, miR‑129a and miR‑17, and C‑X‑C chemokine receptor type 4 and thrombospondin‑1 were detectable in EXOs, which might account for EXO‑mediated tumour deterioration.
Shuilian Chen, Xi Chen, Jin Qiu, Pei Chen, Xiaokun Han, Yihui Wu, Jiejie Zhuang, Meng Yang, Chuangran Wu, Nandan Wu, Ying Yang, Jian Ge, Keming Yu, Jing Zhuang

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#32824362   2020/08/16 To Up

Regulation of Female Folliculogenesis by Tsp1a in Nile Tilapia ().

TSP1 was reported to be involved in multiple biological processes including the activation of TGF-β signaling pathways and the regulation of angiogenesis during wound repair and tumor growth, while its role in ovarian folliculogenesis remains to be elucidated. In the present study, Tsp1a was found to be expressed in the oogonia and granulosa cells of phase I to phase IV follicles in the ovaries of Nile tilapia by immunofluorescence. homozygous mutants were generated by CRISPR/Cas9. Mutation of resulted in increased oogonia, reduced secondary growth follicles and delayed ovary development. Expression of the cell proliferation marker PCNA was significantly up-regulated in the oogonia of the mutant ovaries. Furthermore, transcriptomic analysis revealed that expressions of DNA replication related genes were significantly up-regulated, while cAMP and MAPK signaling pathway genes which inhibit cell proliferation and promote cell differentiation were significantly down-regulated. In addition, aromatase (Cyp19a1a) expression and serum 17β-estradiol (E2) concentration were significantly decreased in the mutants. These results indicated that lacking resulted in increased proliferation and inhibited differentiation of oogonia, which in turn, resulted in increased oogonia, reduced secondary growth follicles and decreased E2. Taken together, our results indicated that was essential for ovarian folliculogenesis in Nile tilapia.
Mimi Jie, He Ma, Li Zhou, Jiahong Wu, Minghui Li, Xingyong Liu, Deshou Wang

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#32792069   2020/06/29 To Up

α-Lipoic acid blocks the GMCSF induced protease/protease inhibitor spectrum associated with fetal membrane weakening in-vitro.

We use an in-vitro human fetal membrane (FM) explant-based model to study inflammation-induced FM weakening, a prerequisite for PPROM. In this system, GMCSF is a critical intermediate, both necessary and sufficient for TNFα and thrombin induced FM weakening. α-Lipoic-acid (LA) blocks TNFα and thrombin, as well as GMCSF-induced weakening. Recently, we reported LA concomitantly blocks GMCSF-induction of MMPs 2, 9 and 10 and inhibition of TIMPs 1-3. The aim of this study was to show that LA blocks GMCSF-induced increases in additional proteases and reductions in additional protease inhibitors.
R M Moore, R Katri, D Kumar, J M Mansour, B Mercer, J J Moore

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#32697967   2020/07/19 To Up

Thrombospondin1 as a potential therapeutic target for human nonalcoholic fatty liver disease.


Yongfeng Song, Ling Gao

1694 related Products with: Thrombospondin1 as a potential therapeutic target for human nonalcoholic fatty liver disease.

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#32323748   2020/02/20 To Up

Role of thrombospondin‑1 and thrombospondin‑2 in cardiovascular diseases (Review).

Thrombospondin (TSP)‑1 and TSP‑2 are matricellular proteins in the extracellular matrix (ECM), which serve a significant role in the pathological processes of various cardiovascular diseases (CVDs). The multiple effects of TSP‑1 and TSP‑2 are due to their ability to interact with various ligands, such as structural components of the ECM, cytokines, cellular receptors, growth factors, proteases and other stromal cell proteins. TSP‑1 and TSP‑2 regulate the structure and activity of the aforementioned ligands by interacting directly or indirectly with them, thereby regulating the activity of different types of cells in response to environmental stimuli. The pathological processes of numerous CVDs are associated with the degradation and remodeling of ECM components, and with cell migration, dysfunction and apoptosis, which may be regulated by TSP‑1 and TSP‑2 through different mechanisms. Therefore, investigating the role of TSP‑1 and TSP‑2 in different CVDs and the potential signaling pathways they are associated with may provide a new perspective on potential therapies for the treatment of CVDs. In the present review, the current understanding of the roles TSP‑1 and TSP‑2 serve in various CVDs were summarized. In addition, the interacting ligands and the potential pathways associated with these thrombospondins in CVDs are also discussed.
Kaijie Zhang, Miaomiao Li, Li Yin, Guosheng Fu, Zhenjie Liu

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#31965893   2020/01/22 To Up

Mouse skin-derived precursors alleviates ultraviolet B irradiation damage via early activation of TGF-β/Smad pathway by thrombospondin1.

Our previous research implied mouse skin-derived precursors (mSKPs) possessed the capacity of anti-ultraviolet B (UVB) irradiation damage, and the mechanisms might be associated with transforming growth factor-β (TGF-β) signaling pathway activation. In this study, we investigated and compared the response to UVB irradiation between mSKPs and dermal mesenchymal stem cells (dMSCs), and explored the underlying mechanisms. Irradiation damage such as decreased cell viability, cell senescence, and cell death was observed in both mSKPs and dMSCs at 24 h after UVB exposure. In mSKPs, change in cell morphology, viability, cell senescence and death at the following time points implied the recovery of UVB irradiation damage. Additionally, thrombospondin1 (TSP1) and TGF-β1 increased significantly in mSKPs' supernatant after UVB irradiation. The gene expression of TSP1, TGF-β1, metalloproteinase 1 (MMP1), and Collagen I elevated shortly after the UVB exposure. The protein expression of TSP1, TGF-β1, MMP1, Collagen I, smad2/3, and p-smad2/3 at multiple time points after the UVB exposure was consistent with the gene expression results. In dMSCs, no obvious recovery was noticed. Together, these results revealed that in mSKPs, one of the mechanisms to attenuate the UVB irradiation damage might be the early activation of TGF-β/Smad pathway by TSP1. Given that mSKPs could differentiate into fibroblast-like SKP-derived fibroblasts (SFBs) or with the presence of serum, mSKPs might serve as a therapeutic potential for fibroblasts supplement and UVB irradiation damage treatment. SKPs: skin-derived precursors; mSKPs: mouse SKPs; UVB: ultraviolet B; TGF-β/Smad: transforming growth factor-β/Smad; TSP1: thrombospondin 1; MMP 13: metalloproteinases 13; TβRII: TGF-β receptor II; SFBs: SKP-derived fibroblasts; KEGG: Kyoto encyclopedia of genes and genomes; DEGs: differentially expressed genes; dMSCs: dermal mesenchymal stem cells; LM: light microscope; CCK-8: cell counting kit 8; ELISA: Enzyme-linked immuno sorbent assay; qRT-PCR: quantitative real-time polymerase chain reaction; TSPs: thrombospondins; ECM: extracellular matrix; R-smads: receptor-regulated smads.
Yiming Li, Lidan Xiong, Jie Tang, Guonian Zhu, Ru Dai, Li Li

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#30897320   // To Up

Transcriptional Regulation of Thrombospondins and Its Functional Validation through CRISPR/Cas9 Mediated Gene Editing in Corpus Luteum of Water Buffalo (Bubalus Bubalis).

Thrombospondins (TSPs) are large multi-modular proteins, identified as natural angiogenesis inhibitors that exert their activity by binding to CD36 and CD47 receptors. The anti-angiogenic effect of TSPs in luteal regression of water buffalo has not been addressed. The present study characterized the expression pattern and localization of TSPs and their receptors in ovarian corpus luteum during different stages of development in buffalo. This study also elucidated the effect of exogenous Thrombospondin1 (TSP1) or the knocking out of the endogenous protein on luteal cell viability and function. Further, the in vitro transcriptional interaction of TSP1 with hormones, LH, PGF2α and angiogenic growth factors, VEGF and FGF2 were also evaluated.
Avishek Paul, Jaya Bharati, Meeti Punetha, Sai Kumar, Vidyalakshmi G Mallesh, Vikrant S Chouhan, Arvind Sonwane, Sadhan Bag, Sanjeev Kumar Bhure, Vijai Prakash Maurya, Gyanendra Singh, Kristin M Whitworth, Mihir Sarkar

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