scholarly journals Unexpected In Vivo Interaction Between Growth Hormone, the Suppressor of Cytokine Signaling SOCS2, and Intestinal Polyposis

2006 ◽  
Vol 5 (5) ◽  
pp. 466-466
Keyword(s):  
Growth Hormone ◽  
Cytokine Signaling ◽  
Intestinal Polyposis ◽  
Suppressor Of Cytokine Signaling

scholarly journals Interference with NTSR1 Expression Exerts an Anti-Invasion Effect via the Jun/miR-494/SOCS6 Axis of Glioblastoma Cells

2018 ◽  
Vol 49 (6) ◽  
pp. 2382-2395 ◽  
Author(s):  
Qing Ou-yang ◽  
Xuzhi He ◽  
Anqi Yang ◽  
Bing Li ◽  
Minhui Xu
Keyword(s):  
Western Blotting ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cytokine Signaling ◽  
Glioblastoma Cells ◽  
Suppressor Of Cytokine Signaling ◽  
Underlying Mechanisms ◽  
Neurotensin Receptor 1

Background/Aims: Glioblastoma is the most common and aggressive brain tumor and carries a poor prognosis. Previously, we found that neurotensin receptor 1 (NTSR1) contributes to glioma progression, but the underlying mechanisms of NTSR1 in glioblastoma invasion remain to be clarified. The aim of this study was to investigate the molecular mechanisms of NTSR1 in glioblastoma invasion. Methods: Cell migration and invasion were evaluated using wound-healing and transwell assays. Cell proliferation was detected using CCK-8. The expression of NTSR1, Jun, and suppressor of cytokine signaling 6 (SOCS6) was detected using western blotting. The expression of miR-494 was detected by Quantitative real-time PCR. Chromatin immunoprecipitation assay was performed to examine the interaction between Jun and miR-494 promoter. Dual-luciferase reporter assay and western blotting were performed to identify the direct regulation of SOCS6 by miR-494. An orthotopic xenograft mouse model was conducted to assess tumor growth and invasion. Results: NTSR1 knockdown attenuated the invasion of glioblastoma cells. Jun was positively regulated by NTSR1, which promoted miR-494 expression through binding to miR-494 promoter. SOCS6 was confirmed as a direct target of miR-494, thus, NTSR1-induced miR-494 upregulation resulted in SOCS6 downregulation. Both miR-494 and SOCS6 were involved in the NTSR1-induced invasion of glioblastoma cells. In vivo, tumor invasion and growth were inhibited by NTSR1 knockdown, but were restored with miR-494 overexpression. Conclusion: NTSR1 knockdown inhibited glioblastoma invasion via the Jun/miR-494/SOCS6 axis.

scholarly journals Deletion of SOCS2 Reduces Post-Colitis Fibrosis via Alteration of the TGFβ Pathway

2020 ◽  
Vol 21 (9) ◽  
pp. 3073
Author(s):  
Amna Al-Araimi ◽  
Amira Al Kharusi ◽  
Asma Bani Oraba ◽  
Matar M Al-Maney ◽  
Shadia Al Sinawi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Recovery Period ◽  
Cytokine Signaling ◽  
Protective Effects ◽  
Wild Type ◽  
Epithelial Proliferation

Inflammatory bowel disease (IBD) is an immunologically mediated chronic intestinal disorder. Growth hormone (GH) administration enhances mucosal repair and decreases intestinal fibrosis in patients with IBD. In the present study, we investigated the effect of cellular sensitivity to GH via suppressor of cytokine signaling 2 (SOCS2) deletion on colitis and recovery. To induce colitis, wild type and SOCS2 knockout (SOCS2−/−) mice were treated with 3% dextran sodium sulphate (DSS), followed by a recovery period. SOCS2−/− mice showed higher disease activity during colitis with increased mRNA expression of the pro-inflammatory cytokines nitric oxide synthase 2 (NOS2) and interleukin 1 β (IL1-β). At recovery time point, SOCS2−/− showed better recovery with less fibrosis measured by levels of α-SMA and collagen deposition. Protein and mRNA expressions of transforming growth factor beta β1 (TGF-β1) receptors were significantly lower in SOCS2−/− mice compared to wild-type littermates. Using an in vivo bromodeoxyuridine (BrdU) proliferation assay, SOCS2−/− mice showed higher intestinal epithelial proliferation compared to wild-type mice. Our results demonstrated that deletion of the SOCS2 protein results in higher growth hormone sensitivity associated with higher pro-inflammatory signaling; however, it resulted in less tissue damage with less fibrotic lesions and higher epithelial proliferation, which are markers of GH-protective effects in IBD. This suggests a pleiotropic effect of SOCS2 and multiple cellular targets. Further study is required to study role of SOCS2 in regulation of TGFβ-mothers against the decapentaplegic homolog (Smad) pathway.

scholarly journals CXCR4-mediated Suppressor of Cytokine Signaling Up-regulation Inactivates Growth Hormone Function

2004 ◽  
Vol 279 (43) ◽  
pp. 44460-44466 ◽  
Author(s):  
Ruth Garzón ◽  
Silvia F. Soriano ◽  
José Miguel Rodríguez-Frade ◽  
Lucio Gómez ◽  
Ana Martín de Ana ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling

scholarly journals Liver X receptor agonist downregulates growth hormone signaling in the liver

2011 ◽  
Vol 8 (2) ◽  
Author(s):  
Fahad Zadjali ◽  
Ruyman Santana-Farre ◽  
Mercedes Mirecki-Garrido ◽  
Ewa Ellis ◽  
Gunnar Norstedt ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hepatic Steatosis ◽  
Hepatic Metabolism ◽  
Liver X Receptor ◽  
Cytokine Signaling ◽  
Hormone Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Lxr Agonists ◽  
Liver X Receptor Agonist ◽  
Gh Receptors

AbstractLiver X receptor (LXR) agonists have been shown to influence the development of hyperlipidemia and atherosclerosis in mouse models. It has also been demonstrated that some LXR agonists can cause hepatic steatosis in experimental animals. Growth hormone (GH) is known to regulate hepatic metabolism and the absence of hepatic GH receptors (GHR) leads to hepatic steatosis. In this study, we analyzed whether the actions of LXR agonists could involve interference with GH signaling. We showed that LXR agonists impair GH signaling in hepatocytes. LXR agonist treatment attenuated GH induction of suppressor of cytokine signaling 2 (

Prolactin and the expression of suppressor of cytokine signaling-3 in the sheep adrenal gland before birth

2006 ◽  
Vol 291 (5) ◽  
pp. R1399-R1405 ◽  
Author(s):  
S. Gentili ◽  
J. S. Schwartz ◽  
M. J. Waters ◽  
I. C. McMillen
Keyword(s):  
Adrenal Gland ◽  
Mrna Expression ◽  
Tissue Growth ◽  
Late Gestation ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Subsequent Increase ◽  
Fetal Sheep

The fetal pituitary-adrenal axis plays a key role in the fetal response to intrauterine stress and in the timing of parturition. The fetal sheep adrenal gland is relatively refractory to stimulation in midgestation (90–120 days) before the prepartum activation, which occurs around 135 days gestation (term = 147 ± 3 days). The mechanisms underlying the switch from adrenal quiescence to activation are unclear. Therefore, we have investigated the expression of suppressor of cytokine signaling-3 (SOCS-3), a putative inhibitor of tissue growth in the fetal sheep adrenal between 50 and 145 days gestation and in the adrenal of the growth-restricted fetal sheep in late gestation. SOCS-3 is activated by a range of cytokines, including prolactin (PRL), and we have, therefore, determined whether PRL administered in vivo or in vitro stimulates SOCS-3 mRNA expression in the fetal adrenal in late gestation. There was a decrease ( P < 0.005) in SOCS-3 expression in the fetal adrenal between 54 and 133 days and between 141 and 144 days gestation. Infusion of the dopaminergic agonist, bromocriptine, which suppressed fetal PRL concentrations but did not decrease adrenal SOCS-3 mRNA expression. PRL administration, however, significantly increased adrenal SOCS-3 mRNA expression ( P < 0.05). Similarly, there was an increase ( P < 0.05) in SOCS-3 mRNA expression in adrenocortical cells in vitro after exposure to PRL (50 ng/ml). Placental and fetal growth restriction had no effect on SOCS-3 expression in the adrenal during late gestation. In summary, the decrease in the expression of the inhibitor SOCS-3 after 133 days gestation may be permissive for a subsequent increase in fetal adrenal growth before birth. We conclude that factors other than PRL act to maintain adrenal SOCS-3 mRNA expression before 133 days gestation but that acute elevations of PRL can act to upregulate adrenal SOCS-3 expression in the sheep fetus during late gestation.

Sign in / Sign up

Export Citation Format

Share Document