TNF-α and TGF-β synergistically stimulate elongation of human endothelial cells without transdifferentiation to smooth muscle cell phenotype

Emmanuel, Catherine; Huynh, Minh; Matthews, Janice; Kelly, Elizabeth; Zoellner, Hans

doi:10.1016/j.cyto.2012.09.017

Cited by 11 publications

(8 citation statements)

References 14 publications

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“…Indeed, low concentrations of TGF-β induced EC activation, whereas high concentrations showed the opposite effects 25 . TGF-β was reported to act synergistically with other cytokines such as leptin, IL-13, TNF-α, epidermal growth factor (EGF), platelet-derived growth factor (PDGF) 26–30 . These synergistical effects were mediated through crosstalk between divergent signaling pathways activated by different receptors.…”

Section: Discussionmentioning

confidence: 99%

Interleukin 37 promotes angiogenesis through TGF-β signaling

Zhao

Jin

et al. 2017

Sci Rep

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IL-37 is a novel pro-angiogenic cytokine that potently promotes endothelial cell activation and pathological angiogenesis in our previous study, but the mechanisms behind the pro-angiogenic effect of IL-37 are less well understood. Extending our observations, we found that TGF-β interacts with IL-37, and potently enhances the binding affinity of IL-37 to the ALK1 receptor complex, thus allowing IL-37 to signal through ALK1 to activate pro-angiogenic responses. We further show that TGF-β and ALK1 are required in IL-37 induced pro-angiogenic response in ECs and in the mouse model of Matrigel plug and oxygen-induced retinopathy. The result suggests that IL-37 induces pro-angiogenic responses through TGF-β, which may act as the bridging molecule that mediates IL-37 binding to the TGF-β receptor complex.

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Section: Discussionmentioning

confidence: 99%

Interleukin 37 promotes angiogenesis through TGF-β signaling

Zhao

Jin

et al. 2017

Sci Rep

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“…Our results had shown that the levels of ROS could not be changed by AT-RvD1, but the morphological changes were reversible. The cultured HUVEC cells are polygonal with the cobblestone morphology ( Jaffe et al ., 1973 ; Emmanuel et al ., 2013 ). TGF-β1 induced elongation and streamlining of endothelium could be reversed by AT-RvD1.These were possible associated with the expression of F-actin.…”

Section: Discussionmentioning

confidence: 99%

Aspirin-Triggered Resolvin D1 Inhibits TGF-β1-Induced EndMT through Increasing the Expression of Smad7 and Is Closely Related to Oxidative Stress

Shu

Liu

Li³

et al. 2016

Biomolecules & Therapeutics

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The endothelial-mesenchymal transition (EndMT) is known to be involved in the transformation of vascular endothelial cells to mesenchymal cells. EndMT has been confirmed that occur in various pathologic conditions. Transforming growth factor β1 (TGF-β1) is a potent stimulator of the vascular endothelial to mesenchymal transition (EMT). Aspirin-triggered resolvin D1 (ATRvD1) has been known to be involved in the resolution of inflammation, but whether it has effects on TGF-β1-induced EndMT is not yet clear. Therefore, we investigated the effects of AT-RvD1 on the EndMT of human umbilical vein vascular endothelial cells line (HUVECs). Treatment with TGF-β1 reduced the expression of Nrf2 and enhanced the level of F-actin, which is associated with paracellular permeability. The expression of endothelial marker VE-cadherin in HUVEC cells was reduced, and the expression of mesenchymal marker vimentin was enhanced. AT-RvD1 restored the expression of Nrf2 and vimentin and enhanced the expression of VE-cadherin. AT-RvD1 did also affect the migration of HUVEC cells. Inhibitory κB kinase 16 (IKK 16), which is known to inhibit the NF-κB pathway, had an ability to increase the expression of Nrf2 and was associated with the inhibition effect of AT-RvD1 on TGF-β1-induced EndMT, but it had no effect on TGF-β1-induced EndMT alone. Smad7, which is a key regulator of TGF-β/Smads signaling by negative feedback loops, was significantly increased with the treatment of AT-RvD1. These results suggest the possibility that AT-RvD1 suppresses the TGF-β1-induced EndMT through increasing the expression of Smad7 and is closely related to oxidative stress.

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“…Based on references, TNF-α may induce endothelial cells elongation [35] and A20 may inhibit the elongation of endothelial cells [18]. To observe whether A20 has impact on the TNF-α induced elongation of endothelial cells, we have checked the cell morphology induced by A20 previously, but no obvious changes were found (data not shown).…”

Section: Resultsmentioning

confidence: 99%

Role of A20 in cIAP-2 Protection against Tumor Necrosis Factor α (TNF-α)-Mediated Apoptosis in Endothelial Cells

Guo

Messmer-Blust

et al. 2014

IJMS

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Tumor necrosis factor α (TNF-α) influences endothelial cell viability by altering the regulatory molecules involved in induction or suppression of apoptosis. However, the underlying mechanisms are still not completely understood. In this study, we demonstrated that A20 (also known as TNFAIP3, tumor necrosis factor α-induced protein 3, and an anti-apoptotic protein) regulates the inhibitor of apoptosis protein-2 (cIAP-2) expression upon TNF-α induction in endothelial cells. Inhibition of A20 expression by its siRNA resulted in attenuating expression of TNF-α-induced cIAP-2, yet not cIAP-1 or XIAP. A20-induced cIAP-2 expression can be blocked by the inhibition of phosphatidyl inositol-3 kinase (PI3-K), but not nuclear factor (NF)-κB, while concomitantly increasing the number of endothelial apoptotic cells and caspase 3 activation. Moreover, TNF-α-mediated induction of apoptosis was enhanced by A20 inhibition, which could be rescued by cIAP-2. Taken together, these results identify A20 as a cytoprotective factor involved in cIAP-2 inhibitory pathway of TNF-α-induced apoptosis. This is consistent with the idea that endothelial cell viability is dependent on interactions between inducers and suppressors of apoptosis, susceptible to modulation by TNF-α.

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TNF-α and TGF-β synergistically stimulate elongation of human endothelial cells without transdifferentiation to smooth muscle cell phenotype

Cited by 11 publications

References 14 publications

Interleukin 37 promotes angiogenesis through TGF-β signaling

Interleukin 37 promotes angiogenesis through TGF-β signaling

Aspirin-Triggered Resolvin D1 Inhibits TGF-β1-Induced EndMT through Increasing the Expression of Smad7 and Is Closely Related to Oxidative Stress

Role of A20 in cIAP-2 Protection against Tumor Necrosis Factor α (TNF-α)-Mediated Apoptosis in Endothelial Cells

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