Thrombospondin-1 Is Produced by Retinal Glial Cells and Inhibits the Growth of Vascular Endothelial Cells

Yafai, Yousef; Eichler, Wolfdietrich; Iandiev, Ianors; Unterlauft, Jan-Darius; Jochmann, Claudia; Wiedemann, Peter; Bringmann, Andreas

doi:10.1159/000362371

Cited by 18 publications

(9 citation statements)

References 38 publications

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“…NR4A2, acting as a transcription factor, induced cell differentiation and maintained dopaminergic neurons 24 , 25 . THBS1 is an adhesive glycoprotein and affects cell adhesion and cell migration 26 , 27 . Activated Notch signaling attenuates HPV-induced cervical cell transformation while its inactivation promotes cell transformation and carcinogenesis 2 , 7 , 28 .…”

Section: Discussionmentioning

confidence: 99%

Notch Signaling Activation in Cervical Cancer Cells Induces Cell Growth Arrest with the Involvement of the Nuclear Receptor NR4A2

Sun¹,

Liu²,

Sun³

et al. 2016

J. Cancer

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Cervical cancer is a second leading cancer death in women world-wide, with most cases in less developed countries. Notch signaling is highly conserved with its involvement in many cancers. In the present study, we established stable cervical cell lines with Notch activation and inactivation and found that Notch activation played a suppressive role in cervical cancer cells. Meanwhile, the transient overexpression of the active intracellular domain of all four Notch receptors (ICN1, 2, 3, and 4) also induced the suppression of cervical cancer Hela cell growth. ICN1 also induced cell cycle arrest at phase G1. Notch1 signaling activation affected the expression of serial genes, especially the genes associated with cAMP signaling, with an increase of genes like THBS1, VCL, p63, c-Myc and SCG2, a decrease of genes like NR4A2, PCK2 and BCL-2. Particularly,The nuclear receptor NR4A2 was observed to induce cell proliferation via MTT assay and reduce cell apoptosis via FACS assay. Furthermore, NR4A2's activation could reverse ICN1-induced suppression of cell growth while erasing ICN1-induced increase of tumor suppressor p63. These findings support that Notch signaling mediates cervical cancer cell growth suppression with the involvement of nuclear receptor NR4A2. Notably, Notch/NR4A2/p63 signaling cascade possibly is a new signling pathway undisclosed.

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Section: Discussionmentioning

confidence: 99%

Notch Signaling Activation in Cervical Cancer Cells Induces Cell Growth Arrest with the Involvement of the Nuclear Receptor NR4A2

Sun¹,

Liu²,

Sun³

et al. 2016

J. Cancer

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“…MGCs and ECs cooperate in remodelling of the extracellular matrix by secreting MMPs and in retinal angiogenesis by the secretion of trophic factors (Jacobo & Kazlauskas, ; Lorenc, Jaldin‐Fincati, Luna, Chiabrando, & Sanchez, ). In addition, once the angiogenesis process has ended, MGCs secrete thrombospondin‐1 to arrest endothelial proliferation (Yafai et al., ).…”

Section: Mgcs In Healthmentioning

confidence: 99%

A journey into the retina: Müller glia commanding survival and death

Subirada

Paz

Ridano

et al. 2018

Eur J of Neuroscience

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Müller glial cells (MGCs) are known to participate actively in retinal development and to contribute to homoeostasis through many intracellular mechanisms. As there are no homologous cells in other neuronal tissues, it is certain that retinal health depends on MGCs. These macroglial cells are located at the centre of the columnar subunit and have a great ability to interact with neurons, astrocytes, microglia and endothelial cells in order to modulate different events. Several investigations have focused their attention on the role of MGCs in diabetic retinopathy, a progressive pathology where several insults coexist. As expected, data suggest that MGCs display different responses according to the severity of the stimulus, and therefore trigger distinct events throughout the course of the disease. Here, we describe physiological functions of MGCs and their participation in inflammation, gliosis, synthesis and secretion of trophic and antioxidant factors in the diabetic retina. We invite the reader to consider the protective/deleterious role of MGCs in the early and late stages of the disease. In the light of the results, we open up the discussion around and ask the question: Is it possible that the modulation of a single cell type could improve or even re-establish retinal function after an injury?

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“…Adenosine binds to G-protein-linked receptors which can be classified into the A 1 , A 2A , A 2B , and A 3 , 4 subtypes. It has been confirmed that all the four types of adenosine receptors exist in the retina [7][8][9]. Previous studies have demonstrated that A 2A receptor (A 2A R) promotes the release of glutamate and that A 2A R antagonists decrease its release.…”

Section: Introductionmentioning

confidence: 77%

A2AR Antagonists Upregulate Expression of GS and GLAST in Rat Hypoxia Model

Yan

Chen

et al. 2020

BioMed Research International

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Background. The aim of this study was to research the effects of glutamine synthetase (GS) and glutamate aspartate transporter (GLAST) in rat Müller cells and the effects of an adenosine A2AR antagonist (SCH 442416) on GS and GLAST in hypoxia both in vivo and in vitro. Methods. This study used RT-PCR and Western blotting to quantify the expressions of GS and GLAST under different hypoxic conditions as well as the expressions of GS and GLAST at different drug concentrations. A cell viability assay was used to assess drug toxicity. Results. mRNA and protein expression of GS and GLAST in hypoxia Group 24 h was significantly increased. mRNA and protein expressions of GS and GLAST both increased in Group 1 μM SCH 442416 compared with other groups. One micromolar SCH 442416 could upregulate GS and GLAST’s activity in hypoxia both in vivo and in vitro. Conclusions. Hypoxia activates GS and GLAST in rat retinal Müller cells in a short time in vitro. (2) A2AR antagonists upregulate the activity of GS and GLAST in hypoxia both in vivo and in vitro.

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Thrombospondin-1 Is Produced by Retinal Glial Cells and Inhibits the Growth of Vascular Endothelial Cells

Cited by 18 publications

References 38 publications

Notch Signaling Activation in Cervical Cancer Cells Induces Cell Growth Arrest with the Involvement of the Nuclear Receptor NR4A2

Notch Signaling Activation in Cervical Cancer Cells Induces Cell Growth Arrest with the Involvement of the Nuclear Receptor NR4A2

A journey into the retina: Müller glia commanding survival and death

A2AR Antagonists Upregulate Expression of GS and GLAST in Rat Hypoxia Model

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