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Jen Hwey Chiu - One of the best experts on this subject based on the ideXlab platform.
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chrysin suppresses il 6 induced angiogenesis via down regulation of jak1 stat3 and vegf an in vitro and in ovo approach
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Kou-gi Shyu, Bao Wei Wang, Hang Chang, Yenhsu Chen, Jen Hwey ChiuAbstract:Chrysin, 5,7-dihydroxyflavone, possesses many biologic properties. This study aimed to investigate the effects and molecular mechanisms of chrysin on IL-6-induced angiogenesis in vitro and in ovo. Chicken chorioallantoic membrane assay, an in ovo angiogenesis assay, showed chrysin significantly suppressed IL-6-induced neovascularization. Furthermore, chrysin significantly suppressed human umbilical vein endothelial cell (HUVECs) migration and tube formation. The signaling pathway involved in chrysin-related antiangiogenesis was also investigated. The data indicated that chrysin is able to down-regulate the expression of Glycoprotein 130 (gp130), soluble IL-6 receptor (IL-6R), phosphorylated JAK1 and STAT3, and VEGF in HUVECs. The IL-6-induced binding of STAT3 was significantly suppressed by chrysin. Moreover, chrysin did not further suppress VEGF expression with STAT3 knocked down. Taken together, the results show that chrysin suppresses IL-6-induced angiogenesis through modulation of the sIL-6R/gp130/JAK...
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chrysin suppresses il 6 induced angiogenesis via down regulation of jak1 stat3 and vegf an in vitro and in ovo approach
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Chiu Mei Lin, Bao Wei Wang, Hang Chang, Yenhsu Chen, Kou-gi Shyu, Jen Hwey ChiuAbstract:Chrysin, 5,7-dihydroxyflavone, possesses many biologic properties. This study aimed to investigate the effects and molecular mechanisms of chrysin on IL-6-induced angiogenesis in vitro and in ovo. Chicken chorioallantoic membrane assay, an in ovo angiogenesis assay, showed chrysin significantly suppressed IL-6-induced neovascularization. Furthermore, chrysin significantly suppressed human umbilical vein endothelial cell (HUVECs) migration and tube formation. The signaling pathway involved in chrysin-related antiangiogenesis was also investigated. The data indicated that chrysin is able to down-regulate the expression of Glycoprotein 130 (gp130), soluble IL-6 receptor (IL-6R), phosphorylated JAK1 and STAT3, and VEGF in HUVECs. The IL-6-induced binding of STAT3 was significantly suppressed by chrysin. Moreover, chrysin did not further suppress VEGF expression with STAT3 knocked down. Taken together, the results show that chrysin suppresses IL-6-induced angiogenesis through modulation of the sIL-6R/gp130/JAK1/STAT3/VEGF signaling pathway. Chrysin may provide new therapeutic potential for IL-6-induced pathological angiogenesis.
Yasushi Fujio - One of the best experts on this subject based on the ideXlab platform.
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the inhibition of n glycosylation of Glycoprotein 130 molecule abolishes stat3 activation by il 6 family cytokines in cultured cardiac myocytes
PLOS ONE, 2014Co-Authors: Reo Matsuo, Makiko Maeda, Tomomi Mohri, Hiroyuki Nakayama, Hirofumi Morihara, Shiho Murasawa, Kana Takewaki, Yasushi FujioAbstract:Interleukin-6 (IL-6) family cytokines play important roles in cardioprotection against pathological stresses. IL-6 cytokines bind to their specific receptors and activate Glycoprotein 130 (gp130), a common receptor, followed by further activation of STAT3 and extracellular signal-regulated kinase (ERK)1/2 through janus kinases (JAKs); however the importance of glycosylation of gp130 remains to be elucidated in cardiac myocytes. In this study, we examined the biological significance of gp130 glycosylation using tunicamycin (Tm), an inhibitor of enzyme involved in N-linked glycosylation. In cardiomyocytes, the treatment with Tm completely replaced the glycosylated form of gp130 with its unglycosylated one. Tm treatment inhibited leukemia inhibitory factor (LIF)-mediated activation of STAT3 and ERK1/2. Similarly, IL-11 failed to activate STAT3 and ERK1/2 in the presence of Tm. Interestingly, Tm inhibited the activation of JAKs 1 and 2, without influencing the expression of suppressor of cytokine signalings (SOCSs) and protein-tyrosine phosphatase 1B (PTP1B), which are endogenous inhibitors of JAKs. To exclude the possibility that Tm blocks LIF and IL-11 signals by inhibiting the glycosylation of their specific receptors, we investigated whether the stimulation with IL-6 plus soluble IL-6 receptor (sIL-6R) could transduce their signals in Tm-treated cardiomyocytes and found that this stimulation was unable to activate the downstream signals. Collectively, these findings indicate that glycosylation of gp130 is essential for signal transduction of IL-6 family cytokines in cardiomyocytes.
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Glycoprotein 130 cytokine signal as a therapeutic target against cardiovascular diseases
Journal of Pharmacological Sciences, 2011Co-Authors: Yasushi Fujio, Makiko Maeda, Tomomi Mohri, Masanori Obana, Tomohiko Iwakura, Akiko Hayama, Tomomi Yamashita, Hiroyuki Nakayama, Junichi AzumaAbstract:Postnatal cardiomyocytes have only limited capacity of proliferation. Therefore, the myocardium is intrinsically equipped with cardioprotective machineries and protects itself from pathological stresses. One of the most important cardioprotective systems is the signal network of autocrine/paracrine factors, including neurohumoral factors, growth factors, and cytokines. In this review, we focus on the roles of interleukin-6 (IL-6) family cytokines, also known as Glycoprotein 130 (gp130) cytokines, in cardioprotection. These cytokines make a complex with their specific cytokine receptor α-subunits. The cytokine-receptor α-subunit complex binds to gp130, a common receptor of the IL-6 family, followed by the activation of JAK/STAT, ERK, and PI3 kinase/Akt pathways. In cardiomyocytes, signals through gp130 promote cell survival and angiogenesis through the JAK/STAT pathway. Activation of gp130 in cardiac stem cells induces their endothelial transdifferentiation, leading to neovascularization. Recently, accumulating evidence has revealed that altered JAK/STAT activity is associated with heart failure, suggesting that the JAK/STAT pathway is a therapeutic target against cardiovascular diseases. Interestingly, activation of the JAK/STAT pathway with interleukin-11 (IL-11) exhibits preconditioning effects in ischemia/reperfusion model. Moreover, IL-11 treatment after coronary ligation prevents cardiac remodeling through the JAK/STAT pathway. Since IL-11 is used for patients with thrombocytopenia, we propose that IL-11 is a candidate cytokine clinically available for cardioprotection therapy.
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signals through Glycoprotein 130 regulate the endothelial differentiation of cardiac stem cells
Arteriosclerosis Thrombosis and Vascular Biology, 2009Co-Authors: Tomomi Mohri, Yasushi Fujio, Makiko Maeda, Masanori Obana, Tomohiko Iwakura, Koichi Matsuda, Junichi AzumaAbstract:Objective— Cardiac Sca-1+ cells were originally identified as multipotent stem cells. To address the regulation of their differentiation, we investigated the effects of the proinflammatory cytokines on their endothelial differentiation. Methods and Results— We examined the effects of the proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-11, and cardiotrophin-1 (CT-1) on the cardiac Sca-1+ cell differentiation. IL-11 and CT-1, whose receptor systems use Glycoprotein 130 (gp130), induced endothelial-specific genes in Sca-1+ cells, but not TNF-α, IL-1β, or IL-6, analyzed by RT-PCR and by immunocytochemistry. Immnunoblot analyses showed that IL-11 and CT-1 activated signal transducer and activator of transcription 3 (STAT3), a downstream target of gp130, but not other cytokines. Though IL-6 receptor is not endogenously expressed in Sca-1+ cells, IL-6 exhibited the activity to induce the endothelial markers in the presence of soluble IL-6 receptor, an agonistic receptor, associated with STAT3 phosphorylation. Moreover, the inhibition of STAT3, by its dominant-negative form or siRNA, suppressed the induction of endothelial specific genes by IL-11 and CT-1. Finally, LIF and IL-11 transcripts were upregulated in postinfarct myocardium, accompanied by the induction of Sca-1+/VE-cadherin+ cells. Conclusions— Gp130/STAT3 pathway plays critical roles in the regulation of endothelial differentiation of cardiac Sca-1+ cells.
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abstract 328 signals through Glycoprotein 130 promote the endothelial differentiation of cardiac sca 1 cells
Circulation, 2007Co-Authors: Tomomi Mohri, Yasushi Fujio, Makiko Maeda, Masanori Obana, Tomohiko Iwakura, Koichi Matsuda, Takashi Ito, Yasuhiro Yamamoto, Nozomi Hayata, Junichi AzumaAbstract:Background: Cardiac Sca-1+ cells were originally identified as multipotent stem cells that can be differentiated into various types of cardiac cells, including cardiomyocytes and endothelial cells....
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Glycoprotein 130 regulates cardiac myocyte survival in doxorubicin induced apoptosis through phosphatidylinositol 3 kinase akt phosphorylation and bcl xl caspase 3 interaction
Circulation, 2001Co-Authors: Shinji Negoro, Tadamitsu Kishimoto, Hidemasa Oh, Eiroh Tone, Keita Kunisada, Yasushi Fujio, Kenneth Walsh, Keiko YamauchitakiharaAbstract:Background—We recently reported that the activation of Glycoprotein (gp) 130 by leukemia inhibitory factor (LIF) upregulates Bcl-xL and exerts antiapoptotic effects in cardiac myocytes. In addition, LIF induces activation of phosphatidylinositol (PI) 3-kinase and Akt, which are known to be required for cell survival. However, their regulatory roles in cell death remain unknown. Methods and Results—We investigated the fate of these proteins and the cytoprotective effects of LIF on doxorubicin (DOX)-induced apoptosis in cultured neonatal rat cardiac myocytes. Myocyte apoptosis increased significantly in DOX-treated cells but was significantly reduced by LIF pretreatment. The kinase activities of PI 3-kinase and Akt declined below basal levels but were partially recovered with LIF. Moreover, DOX-induced caspase-3 activation and decrease in Bcl-xL abundance are completely inhibited by LIF and caspase inhibitor. LIF phosphorylates Bad through PI 3-kinase and reduces the heterodimerization of Bad with Bcl-xL. A...
Stefan Rosejohn - One of the best experts on this subject based on the ideXlab platform.
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due to interleukin 6 type cytokine redundancy only Glycoprotein 130 receptor blockade efficiently inhibits myeloma growth
Haematologica, 2017Co-Authors: Renate Burger, Andreas Gunther, Katja Klausz, Matthias Staudinger, Matthias Peipp, Eva Maria Murga Penas, Stefan Rosejohn, John Wijdenes, Martin GramatzkiAbstract:Interleukin-6 has an important role in the pathophysiology of multiple myeloma where it supports the growth and survival of the malignant plasma cells in the bone marrow. It belongs to a family of cytokines which use the Glycoprotein 130 chain for signal transduction, such as oncostatin M or leukemia inhibitory factor. Targeting interleukin-6 in plasma cell diseases is currently evaluated in clinical trials with monoclonal antibodies. Here, efforts were made to elucidate the contribution of interleukin-6 and Glycoprotein 130 signaling in malignant plasma cell growth in vivo. In the xenograft severe combined immune deficiency model employing our interleukin-6-dependent plasma cell line INA-6, the lack of human interleukin-6 induced autocrine interleukin-6 production and a proliferative response to other cytokines of the Glycoprotein 130 family. Herein, mice were treated with monoclonal antibodies against human interleukin-6 (elsilimomab/B-E8), the interleukin-6 receptor (B-R6), and with an antibody blocking Glycoprotein 130 (B-R3). While treatment of mice with interleukin-6 and interleukin-6 receptor antibodies resulted in a modest delay in tumor growth, the development of plasmacytomas was completely prevented with the anti-Glycoprotein 130 antibody. Importantly, complete inhibition was also achieved using F(ab’)2-fragments of monoclonal antibody B-R3. Tumors harbor activated signal transducer and activator of transcription 3, and in vitro, the antibody inhibited leukemia inhibitory factor stimulated signal transducer and activator of transcription 3 phosphorylation and cell growth, while being less effective against interleukin-6. In conclusion, the growth of INA-6 plasmacytomas in vivo under interleukin-6 withdrawal remains strictly dependent on Glycoprotein 130, and other Glycoprotein 130 cytokines may substitute for interleukin-6. Antibodies against Glycoprotein 130 are able to overcome this redundancy and should be explored for a possible therapeutic window.
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Glycoprotein 130 receptor signaling mediates α cell dysfunction in a rodent model of type 2 diabetes
Diabetes, 2014Co-Authors: Samuel Z Chow, Stefan Rosejohn, Madeleine Speck, Piriya Yoganathan, Dominika Nackiewicz, Ann Maria Kruse Hansen, Mette Ladefoged, Bjorn Rabe, Peter J Voshol, Francis C LynnAbstract:Dysregulated glucagon secretion accompanies islet inflammation in type 2 diabetes. We recently discovered that interleukin (IL)-6 stimulates glucagon secretion from human and rodent islets. IL-6 family cytokines require the Glycoprotein 130 (gp130) receptor to signal. In this study, we elucidated the effects of α-cell gp130 receptor signaling on glycemic control in type 2 diabetes. IL-6 family cytokines were elevated in islets in rodent models of this disease. gp130 receptor activation increased STAT3 phosphorylation in primary α-cells and stimulated glucagon secretion. Pancreatic α-cell gp130 knockout (αgp130KO) mice showed no differences in glycemic control, α-cell function, or α-cell mass. However, when subjected to streptozotocin plus high-fat diet to induce islet inflammation and pathophysiology modeling type 2 diabetes, αgp130KO mice had reduced fasting glycemia, improved glucose tolerance, reduced fasting insulin, and improved α-cell function. Hyperinsulinemic-euglycemic clamps revealed no differences in insulin sensitivity. We conclude that in a setting of islet inflammation and pathophysiology modeling type 2 diabetes, activation of α-cell gp130 receptor signaling has deleterious effects on α-cell function, promoting hyperglycemia. Antagonism of α-cell gp130 receptor signaling may be useful for the treatment of type 2 diabetes.
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interleukin 6 receptor specific rna aptamers for cargo delivery into target cells
RNA Biology, 2012Co-Authors: Cindy Meyer, Stefan Rosejohn, Joachim Grotzinger, Katja Eydeler, Eileen Magbanua, Tijana Zivkovic, Nicolas Piganeau, Inken Lorenzen, Gunter Mayer, Ulrich HahnAbstract:Aptamers represent an emerging strategy to deliver cargo molecules, including dyes, drugs, proteins or even genes, into specific target cells. Upon binding to specific cell surface receptors aptamers can be internalized, for example by macropinocytosis or receptor mediated endocytosis. Here we report the in vitro selection and characterization of RNA aptamers with high affinity (Kd = 20 nM) and specificity for the human IL-6 receptor (IL-6R). Importantly, these aptamers trigger uptake without compromising the interaction of IL-6R with its natural ligands the cytokine IL-6 and Glycoprotein 130 (gp130). We further optimized the aptamers to obtain a shortened, only 19-nt RNA oligonucleotide retaining all necessary characteristics for high affinity and selective recognition of IL-6R on cell surfaces. Upon incubation with IL-6R presenting cells this aptamer was rapidly internalized. Importantly, we could use our aptamer, to deliver bulky cargos, exemplified by fluorescently labeled streptavidin, into IL-6R pre...
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activation of interleukin 6 induced Glycoprotein 130 signal transducer and activator of transcription 3 pathway in mesenchymal stem cells enhances hepatic differentiation proliferation and liver regeneration
Liver Transplantation, 2010Co-Authors: Shuk Pik Lam, John M Luk, Kwan Man, Cindy K Cheung, Stefan RosejohnAbstract:Adult bone marrow-derived mesenchymal stem cells (MSCs) exist in all living species and are capable of differentiating into different types of specific cells. In this study, we demonstrate the therapeutic effectiveness of rat MSC transplantation in D-galactosamine (GalN)-induced acute liver injury and identified the novel pathways which are involved in hepatic differentiation of MSCs. In vivo, intraportal transplantation with 5 × 10(6) MSCs at 24 hours after GalN administration resulted in significant reduction in serum levels of alanine aminotransferase, aspartate aminotransferase, and total bilirubin compared to the control group. Engrafted MSCs actively proliferated, differentiated, and further enhanced hepatocyte proliferation activity. In vitro, coculture of MSCs with GalN-induced injured hepatocytes showed efficient differentiation and was evidenced by progressive increase in messenger RNA levels of hepatic markers, including albumin, α-fetoprotein, CCAAT-enhancer binding protein α, α-1-antitryspin, and hepatocyte nuclear factor-3β. Immunofluorescent staining revealed that these cells were positive for albumin, α-fetoprotein, and cytokeratin 18, but not clusters of differentiation 34, cytokeratin 19, or OV6. During hepatic differentiation, signal transducer and activator of transcription 3 (STAT3) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling were constantly activated, and a gradual down-regulation of β-catenin expression in messenger RNA and protein levels was detected. Hyper-interleukin-6 fusion protein but not interleukin-6 (IL-6) alone caused reduction in β-catenin expression associated with the up-regulation of Wnt-5a in MSCs via activating the Glycoprotein 130 (gp130)-mediated STAT3 signaling pathway, which indicates the operation of the trans-signaling mechanism. Activation of IL-6/gp130-mediated STAT3 signaling pathway in MSCs triggered wound healing, cell migration, and proliferation. In conclusion, transplantation of MSCs promotes cell proliferation and organ repair, and activation of IL-6/gp130-mediated STAT3 signaling pathway via soluble IL-6 receptor is crucial in hepatic differentiation of MSCs.
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soluble il 6 receptor governs il 6 activity in experimental arthritis blockade of arthritis severity by soluble Glycoprotein 130
Journal of Immunology, 2003Co-Authors: Mari Ann Nowell, Stefan Rosejohn, Peter James Richards, Sankichi Horiuchi, Naoki Yamamoto, Nicholas Topley, Anwen Sian Williams, Simon Arnett JonesAbstract:Studies in IL-6-deficient (IL-6(-/-)) mice highlight that IL-6 contributes to arthritis progression. However, the molecular mechanism controlling its activity in vivo remains unclear. Using an experimental arthritis model in IL-6(-/-) mice, we have established a critical role for the soluble IL-6R in joint inflammation. Although intra-articular administration of IL-6 itself was insufficient to reconstitute arthritis within these mice, a soluble IL-6R-IL-6 fusion protein (HYPER-IL-6) restored disease activity. Histopathological assessment of joint sections demonstrated that HYPER-IL-6 increased arthritis severity and controlled intrasynovial mononuclear leukocyte recruitment through the CC-chemokine CCL2. Activation of synovial fibroblasts by soluble IL-6R and IL-6 emphasized that these cells may represent the source of CCL2 in vivo. Specific blockade of soluble IL-6R signaling in wild-type mice using soluble gp130 ameliorated disease. Consequently, soluble IL-6R-mediated signaling represents a promising therapeutic target for the treatment of rheumatoid arthritis.
Kou-gi Shyu - One of the best experts on this subject based on the ideXlab platform.
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chrysin suppresses il 6 induced angiogenesis via down regulation of jak1 stat3 and vegf an in vitro and in ovo approach
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Kou-gi Shyu, Bao Wei Wang, Hang Chang, Yenhsu Chen, Jen Hwey ChiuAbstract:Chrysin, 5,7-dihydroxyflavone, possesses many biologic properties. This study aimed to investigate the effects and molecular mechanisms of chrysin on IL-6-induced angiogenesis in vitro and in ovo. Chicken chorioallantoic membrane assay, an in ovo angiogenesis assay, showed chrysin significantly suppressed IL-6-induced neovascularization. Furthermore, chrysin significantly suppressed human umbilical vein endothelial cell (HUVECs) migration and tube formation. The signaling pathway involved in chrysin-related antiangiogenesis was also investigated. The data indicated that chrysin is able to down-regulate the expression of Glycoprotein 130 (gp130), soluble IL-6 receptor (IL-6R), phosphorylated JAK1 and STAT3, and VEGF in HUVECs. The IL-6-induced binding of STAT3 was significantly suppressed by chrysin. Moreover, chrysin did not further suppress VEGF expression with STAT3 knocked down. Taken together, the results show that chrysin suppresses IL-6-induced angiogenesis through modulation of the sIL-6R/gp130/JAK...
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chrysin suppresses il 6 induced angiogenesis via down regulation of jak1 stat3 and vegf an in vitro and in ovo approach
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Chiu Mei Lin, Bao Wei Wang, Hang Chang, Yenhsu Chen, Kou-gi Shyu, Jen Hwey ChiuAbstract:Chrysin, 5,7-dihydroxyflavone, possesses many biologic properties. This study aimed to investigate the effects and molecular mechanisms of chrysin on IL-6-induced angiogenesis in vitro and in ovo. Chicken chorioallantoic membrane assay, an in ovo angiogenesis assay, showed chrysin significantly suppressed IL-6-induced neovascularization. Furthermore, chrysin significantly suppressed human umbilical vein endothelial cell (HUVECs) migration and tube formation. The signaling pathway involved in chrysin-related antiangiogenesis was also investigated. The data indicated that chrysin is able to down-regulate the expression of Glycoprotein 130 (gp130), soluble IL-6 receptor (IL-6R), phosphorylated JAK1 and STAT3, and VEGF in HUVECs. The IL-6-induced binding of STAT3 was significantly suppressed by chrysin. Moreover, chrysin did not further suppress VEGF expression with STAT3 knocked down. Taken together, the results show that chrysin suppresses IL-6-induced angiogenesis through modulation of the sIL-6R/gp130/JAK1/STAT3/VEGF signaling pathway. Chrysin may provide new therapeutic potential for IL-6-induced pathological angiogenesis.
Bao Wei Wang - One of the best experts on this subject based on the ideXlab platform.
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chrysin suppresses il 6 induced angiogenesis via down regulation of jak1 stat3 and vegf an in vitro and in ovo approach
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Kou-gi Shyu, Bao Wei Wang, Hang Chang, Yenhsu Chen, Jen Hwey ChiuAbstract:Chrysin, 5,7-dihydroxyflavone, possesses many biologic properties. This study aimed to investigate the effects and molecular mechanisms of chrysin on IL-6-induced angiogenesis in vitro and in ovo. Chicken chorioallantoic membrane assay, an in ovo angiogenesis assay, showed chrysin significantly suppressed IL-6-induced neovascularization. Furthermore, chrysin significantly suppressed human umbilical vein endothelial cell (HUVECs) migration and tube formation. The signaling pathway involved in chrysin-related antiangiogenesis was also investigated. The data indicated that chrysin is able to down-regulate the expression of Glycoprotein 130 (gp130), soluble IL-6 receptor (IL-6R), phosphorylated JAK1 and STAT3, and VEGF in HUVECs. The IL-6-induced binding of STAT3 was significantly suppressed by chrysin. Moreover, chrysin did not further suppress VEGF expression with STAT3 knocked down. Taken together, the results show that chrysin suppresses IL-6-induced angiogenesis through modulation of the sIL-6R/gp130/JAK...
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chrysin suppresses il 6 induced angiogenesis via down regulation of jak1 stat3 and vegf an in vitro and in ovo approach
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Chiu Mei Lin, Bao Wei Wang, Hang Chang, Yenhsu Chen, Kou-gi Shyu, Jen Hwey ChiuAbstract:Chrysin, 5,7-dihydroxyflavone, possesses many biologic properties. This study aimed to investigate the effects and molecular mechanisms of chrysin on IL-6-induced angiogenesis in vitro and in ovo. Chicken chorioallantoic membrane assay, an in ovo angiogenesis assay, showed chrysin significantly suppressed IL-6-induced neovascularization. Furthermore, chrysin significantly suppressed human umbilical vein endothelial cell (HUVECs) migration and tube formation. The signaling pathway involved in chrysin-related antiangiogenesis was also investigated. The data indicated that chrysin is able to down-regulate the expression of Glycoprotein 130 (gp130), soluble IL-6 receptor (IL-6R), phosphorylated JAK1 and STAT3, and VEGF in HUVECs. The IL-6-induced binding of STAT3 was significantly suppressed by chrysin. Moreover, chrysin did not further suppress VEGF expression with STAT3 knocked down. Taken together, the results show that chrysin suppresses IL-6-induced angiogenesis through modulation of the sIL-6R/gp130/JAK1/STAT3/VEGF signaling pathway. Chrysin may provide new therapeutic potential for IL-6-induced pathological angiogenesis.