Increasing extracellular Ca2+ sensitizes TNF-alpha-induced vascular cell adhesion molecule-1 (VCAM-1) via a TRPC1/ERK1/2/NFκB-dependent pathway in human vascular endothelial cells

Li, Songtao; Hua, Ning; Ye, Yaxin; Wei, Wei; Guo, Rui; Song, Qing; Liu, Lei; Liu, Yunyun; Na, Lixin; Niu, Yucun; Chu, Xia; Feng, Rennan; Moustaid‐Moussa, Naima; Liu, Ying; Sun, Chongde

doi:10.1016/j.bbamcr.2017.06.001

Cited by 14 publications

(9 citation statements)

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“…As a pleiotropic proinflammatory cytokine, TNFα could be used to establish a model of endothelial dysfunction in vitro and in vivo 32, 33, 34, 35. Likewise, in our experiments, we found that TNFα markedly induced the expression of endothelial dysfunction biomarkers (VCAM-1, ICAM-1, and E-selectin),36, 37, 38 directly providing evidence of the important role of TNFα in endothelial dysfunction 39, 40, 41.…”

Section: Discussionsupporting

confidence: 75%

MicroRNA-29a-3p Reduces TNFα-Induced Endothelial Dysfunction by Targeting Tumor Necrosis Factor Receptor 1

Deng

Chu

Wang

et al. 2019

Molecular Therapy - Nucleic Acids

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miR-29a-3p has been shown to be associated with cardiovascular diseases; however, the effect of miR-29a-3p on endothelial dysfunction is unclear. This study aimed to reveal the effects and mechanisms of miR-29a-3p on endothelial dysfunction. The levels of vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), and E-selectin were determined by real-time PCR and immunofluorescence staining to reveal the degree of tumor necrosis factor alpha (TNFα)-induced endothelial dysfunction. A luciferase activity assay and cell transfection with a miR-29a-3p mimic or an inhibitor were used to reveal the underlying mechanisms of miR-29a-3p action. Furthermore, the effects of miR-29a-3p on endothelial dysfunction were assessed in C57BL/6 mice injected with TNFα and/or a miR-29a-3p agomir. The results showed that the expression of TNFα-induced adhesion molecules in vascular endothelial cells (EA.hy926 cells, human aortic endothelial cells [HAECs], and primary human umbilical vein endothelial cells [pHUVECs]) and smooth muscle cells (human umbilical vein smooth muscle cells [HUVSMCs]) was significantly decreased following transfection with miR-29a-3p. This effect was reversed by cotransfection with a miR-29a-3p inhibitor. As a key target of miR-29a-3p, tumor necrosis factor receptor 1 mediated the effect of miR-29a-3p. Moreover, miR-29a-3p decreased the plasma levels of TNFα-induced VCAM-1 (32.62%), ICAM-1 (38.22%), and E-selectin (39.32%) in vivo. These data indicate that miR-29a-3p plays a protective role in TNFα-induced endothelial dysfunction, suggesting that miR-29a-3p is a novel target for the prevention and treatment of atherosclerosis.

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Section: Discussionsupporting

confidence: 75%

MicroRNA-29a-3p Reduces TNFα-Induced Endothelial Dysfunction by Targeting Tumor Necrosis Factor Receptor 1

Deng

Chu

Wang

et al. 2019

Molecular Therapy - Nucleic Acids

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“…Interesting, VCAM and MAPK1 were decreased in COMMD10 depleting cells in CRC cells. VCAM-1 is stimulated by TNF- α and accelerated monocyte adhesion in a NF- κ B-dependent manner ( Li et al , 2017 ). MAPK1 is involved in a wide variety of cellular processes, such as proliferation, differentiation, transcription regulation and development.…”

Section: Discussionmentioning

confidence: 99%

FMNL2 destabilises COMMD10 to activate NF-κB pathway in invasion and metastasis of colorectal cancer

Yang

et al. 2017

Br J Cancer

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Background:Diaphanous-related formins (DRFs), actin necleator, have been known to participate in the progression of cancer cells. We previously reported that FMNL2 (Formin-like2), a member of DRFs, was a positive regulator in colorectal cancer (CRC) metastasis, yet proteins and pathways required for the function of this pro-invasive DRFs remain to be identified.Methods:The relationship between FMNL2 and COMMD10 was examined using Co-IP, GST pull-down, immunofluorescence and in vitro ubiquitination assay. The in vitro and in vivo function of COMMD10 in CRC was evaluated using CCK-8 proliferation assay, plate colony formation, cell cycle, apoptosis and animal models. The inhibition of NF-κB signalling by COMMD10 was detected using dual-luciferase reporter assay and western blotting. Co-IP, GST pull-down and nuclear protein extraction assay were performed to evaluate the effect on p65 by COMMD10. Real-time PCR and western blotting were performed to detect expressions of FMNL2, COMMD10 and p65 in paired tissues.Results:FMNL2 targets COMMD10 for ubiquitin-mediated proteasome degradation in CRC cells. COMMD10 targets p65 NF-κB (nuclear factor-κB) subunit and reduces its nuclear translocation, thereby leading to the inactivation of NF-κB pathway and suppression of CRC invasion and metastasis. Inhibition of NF-κB signalling by COMMD10 is necessary for FMNL2-mediated CRC cell behaviours. Downregulation of COMMD10 predicts poor prognosis of CRC patients. The expressions of FMNL2, COMMD10 and p65 are highly linked in CRC tissues.Conclusions:These data demonstrate that the FMNL2/COMMD10/p65 axis acts as a critical regulator in the maintenance of metastatic phenotypes and is strongly associated with negative clinical outcomes.

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“…Suppressing the MAPK/NF-κB signaling pathway protects HUVECs from lipopolysaccharide-induced oxidative stress and inflammation (32). Advanced glycation end products (AGE) impair the functions of saphenous vein through the AGE receptor/MAPK signaling pathway in diabetes (43). Studies have also demonstrated that the activation of the MAPK/ERK pathway can enhance the proliferation and migration of HUVECs (44), whereas disrupting MAPK signaling pathway inhibits angiogenesis in HUVECs (45).…”

Section: Discussionmentioning

confidence: 99%

Expression profile of tRNA‑derived fragments and their potential roles in human varicose veins

Wang

Yun

et al. 2019

Mol Med Report

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Varicose veins (VVs) is a common disease presenting with chronic venous insufficiency. tRNA-derived fragments (tRFs) are associated with a variety of pathological conditions. However, the functions of tRFs in VVs have not been elucidated to date. The present study aimed to identify the key tRFs and investigate their potential roles in VVs. Small RNA sequencing (RNA-seq) was performed to investigate the expression of tRFs in tissues of patients with VVs and their matched adjacent normal veins tissues (ANVs). Reverse transcription-quantitative PCR (RT-qPCR) was used to confirm the differential expression of tRFs. A total of 13,789 tRFs were identified by small RNA-seq, including 45 differentially expressed tRFs (DETs), which comprised 14 upregulated and 31 downregulated tRFs in VV tissues compared with ANVs. In addition, DETs were mainly involved in the function of epidermal growth factor receptor and vascular endothelial growth factor receptor signaling pathways in VVs. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the target genes of DETs were predominantly involved in Wnt and mitogen-activated protein kinase (MAPK) signaling pathways, as well as calcium signaling. Additionally, two upregulated tRFs (tRF-36-F900BY4D84KRIME and tRF-23-87R8WP9IY) and one downregulated tRF (tRF-40-86J8WPMN1E8Y7Z2R) were further validated by RT-qPCR, and a signaling pathway regulation network of their target genes confirmed their involvement in the calcium, Wnt and MAPK signaling pathways. The results of the present study identified three DETs (tRF-36-F900BY4D84KRIME, tRF-23-87R8WP9IY and tRF-40-86J8WPMN1E8Y7Z2R), which may have crucial roles in the occurrence and progression of VVs by regulating Wnt and MAPK signaling, as well as calcium signaling. The present results may provide a basis for further investigation of the functional roles of tRFs in VVs.

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Increasing extracellular Ca2+ sensitizes TNF-alpha-induced vascular cell adhesion molecule-1 (VCAM-1) via a TRPC1/ERK1/2/NFκB-dependent pathway in human vascular endothelial cells

Cited by 14 publications

References 51 publications

MicroRNA-29a-3p Reduces TNFα-Induced Endothelial Dysfunction by Targeting Tumor Necrosis Factor Receptor 1

MicroRNA-29a-3p Reduces TNFα-Induced Endothelial Dysfunction by Targeting Tumor Necrosis Factor Receptor 1

FMNL2 destabilises COMMD10 to activate NF-κB pathway in invasion and metastasis of colorectal cancer

Expression profile of tRNA‑derived fragments and their potential roles in human varicose veins

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