Antrodia salmonea inhibits TNF-α-induced angiogenesis and atherogenesis in human endothelial cells through the down-regulation of NF-κB and up-regulation of Nrf2 signaling pathways

Yang, Hsin‐Ling; Chang, Hebron C.; Lin, Shu-Wei; Kumar, K. J. Senthil; Liao, Chun-Huei; Wang, Hui‐Min David; Lin, Kai-Yuan; Hseu, You‐Cheng

doi:10.1016/j.jep.2013.10.052

Cited by 30 publications

(19 citation statements)

References 50 publications

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“…MAPK and NF- κ B signaling pathway are typically involved in the downstream function of TNF- α . 40, 41 Consistent with this, our study found that the inhibition of the kinases p38 and p65 reduced TNF- α -induced LRG1 secretion, suggesting that these molecules are implicated in the LRG1 expression in HUVECs. Results suggest that TNF- α is a proinflammatory cytokine of inducing LRG1 expression in OA pathogenesis.…”

Section: Discussionsupporting

confidence: 87%

“…TNF- α has been shown to promote cell proliferation and angiogenesis. 40 Thus, we hypothesized that TNF- α induces the secretion of LRG1 in HUVECs to promote angiogenesis and MSC migration. Consistently, the supernatants of TNF- α -stimulated HUVECs promoted angiogenesis and MSC migration, and this effect was prevented by the supernatants of siLRG1-treated HUVECs.…”

Section: Discussionmentioning

confidence: 99%

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TNF-α-induced LRG1 promotes angiogenesis and mesenchymal stem cell migration in the subchondral bone during osteoarthritis

et al. 2017

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The incomplete understanding of aberrant neovascularization, which contributes to osteoarthritis suggests that additional modulators have yet to be identified. Our objective was to identify the role of Leucine-rich-alpha-2-glycoprotein1 (LRG1), a new regulator of pathogenic angiogenesis, in osteoarthritis progression and to develop effective treatment strategies. In this study, immunohistochemistry showed that LRG1 was increased in the subchondral bone and articular cartilage in anterior cruciate ligament transection (ACLT) mice. Further studies were focused on the role of LRG1 in osteoarthritis. Results showed that LRG1 promoted angiogenesis and mesenchymal stem cells (MSC) migration, which contribute to aberrant bone formation in the subchondral bone. Moreover, tumor necrosis factor-α (TNF-α), not interleukin-1β (IL-1β), IL-6 or IL-17, induced the LRG1 expression in human umbilical vein endothelial cells and this effect was inhibited by p38 mitogen-activated protein kinase or NF-κB inhibitor. Notably, inhibition of TNF-α and LRG1 activity by Lenalidomide, an inhibitor of TNF-α production, in ACLT mice attenuated degeneration of osteoarthritis articular cartilage. This study shows that TNF-α is the predominant proinflammatory cytokine that induces the secretion of LRG1. LRG1 contributes to angiogenesis-coupled de novo bone formation by increasing angiogenesis and recruiting MSCs in the subchondral bone of osteoarthritis joints. Inhibition of TNF-α and LRG1 by Lenalidomide could be a potential therapeutic approach.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

TNF-α-induced LRG1 promotes angiogenesis and mesenchymal stem cell migration in the subchondral bone during osteoarthritis

et al. 2017

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“…However, in Habu GN, CD68+ macrophage infiltration was mainly identified in the renal interstitial space instead of glomeruli. TNF-α is produced from mononuclear cells, and it induces many biological activities such as inducing angiogenesis that are crucial for the development of GN (43). In the acute phase of the Habu model, impairment of mesangial integrity and the loss of endothelial cells lead to ballooning of glomerular capillaries, which are induced by snake venom.…”

Section: Discussionmentioning

confidence: 99%

Suppressor of Cytokine Signaling-1/STAT1 Regulates Renal Inflammation in Mesangial Proliferative Glomerulonephritis Models

Bai

Chen

et al. 2018

Front. Immunol.

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Mesangial proliferative glomerulonephritis (MsGN) is a significant global threat to public health. Inflammation plays a crucial role in MsGN; however, the underlying mechanism remains unknown. Herein, we demonstrate that suppression of the cytokine signaling-1 (SOCS1)/signal transducer and activator of transcription 1 (STAT1) signaling pathway is associated with renal inflammation and renal injury in MsGN. Using MsGN rat (Thy1.1 GN) and mouse (Habu GN) models, renal SOCS1/STAT1 was determined to be associated with CD4+ T cell infiltration and related cytokines. In vitro, SOCS1 overexpression repressed IFN-γ-induced MHC class II and cytokine levels and STAT1 phosphorylation in mesangial cells. SOCS1 and STAT1 inhibitors significantly inhibited IFN-γ-induced CIITA promoter activity and MHC class II expression. In conclusion, our study emphasizes the pivotal role of the SOCS1/STAT1 axis in the regulation of inflammation in MsGN.

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“…The consolidated results suggest that Nrf2 can regulate angiogenesis via HO-1-mediated HIF-1α/VEGF signaling pathways. In addition, certain investigations252829 indeed indicate that HO-1 knockdown by HO-1-specific shRNA or HO-1 inhibitors ZnPP and tin-protoporphyrin may reduce the effects of Nrf2 on angiogenesis. However, the effects of Nrf2 on the pathogenesis of cerebral AVM, particularly under venous hypertension, have yet to be ecaluated mechanistically.…”

Section: Discussionmentioning

confidence: 99%

Interplay between VEGF and Nrf2 regulates angiogenesis due to intracranial venous hypertension

Liu

Pān

Wang

et al. 2016

Sci Rep

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Venous hypertension(VH) plays an important role in the pathogenesis of cerebral arteriovenous malformations (AVMs) and is closely associated with the HIF-1α/VEGF signaling pathway. Nuclear factor erythroid 2-related factor 2(Nrf2) significantly influences angiogenesis; however, the interplay between Nrf2 and VEGF under VH in brain AVMs remains unclear. Therefore, our study aimed to investigate the interplay between Nrf2 and VEGF due to VH in brain AVMs. Immunohistochemistry indicated that Nrf2 and VEGF were highly expressed in human brain AVM tissues. In vivo, we established a VH model in both wild-type (WT) and siRNA-mediated Nrf2 knockdown rats. VH significantly increased the expression of Nrf2 and VEGF. Loss of Nrf2 markedly inhibited the upregulation of VEGF, as determined by Western blot analysis and qRT-PCR. In vitro, primary brain microvascular endothelial cells (BMECs) were isolated from WT and Nrf2−/− mice, and a VEGF-Nrf2 positive feed-back loop was observed in BMECs. By trans well assay and angiogenesis assay, Nrf2 knockout significantly inhibited the migration and vascular tube formation of BMECs. These findings suggest that the interplay between Nrf2 and VEGF can contribute to VH-induced angiogenesis in brain AVMs pathogenesis.

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Antrodia salmonea inhibits TNF-α-induced angiogenesis and atherogenesis in human endothelial cells through the down-regulation of NF-κB and up-regulation of Nrf2 signaling pathways

Cited by 30 publications

References 50 publications

TNF-α-induced LRG1 promotes angiogenesis and mesenchymal stem cell migration in the subchondral bone during osteoarthritis

TNF-α-induced LRG1 promotes angiogenesis and mesenchymal stem cell migration in the subchondral bone during osteoarthritis

Suppressor of Cytokine Signaling-1/STAT1 Regulates Renal Inflammation in Mesangial Proliferative Glomerulonephritis Models

Interplay between VEGF and Nrf2 regulates angiogenesis due to intracranial venous hypertension

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