Endotoxin-induced vascular endothelial cell migration is dependent on TLR4/NF-κB pathway, NAD(P)H oxidase activation, and transient receptor potential melastatin 7 calcium channel activity

Sarmiento, Daniela; Montorfano, Ignacio; Cáceres, Mónica; Echeverría, César; Fernández, Ricardo; Cabello-Verrugio, Claudio; Cerda, Oscar; Tapía, Pablo; Simón, Felipe

doi:10.1016/j.biocel.2014.08.001

Cited by 37 publications

(36 citation statements)

References 53 publications

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“…These results are consistent with those from the study by Sarmiento et al [21], which showed that EC migration is dependent on TRPM4 [21]. In addition, TRPM7 also modulates EC migration caused by oxidative stress [34, 35]. These in vitro results are consistent with the notion that TRPM4 is an important contributor to oxidative stress-induced endothelium dysfunction.…”

Section: Discussionsupporting

confidence: 83%

Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

Ding

Ban

Liu

et al. 2017

Cell Physiol Biochem

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Background/Aims: The present study investigated whether the transient receptor potential melastatin 4 (TRPM4) channel plays a role in high salt diet (HSD)-induced endothelial injuries. Methods: Western blotting and immunofluorescence were used to examine TRPM4 expression in the mesenteric endothelium of Dahl salt-sensitive (SS) rats fed a HSD. The MTT, TUNEL, and transwell assays were used to evaluate the cell viability, cell apoptosis, and cell migration, respectively, of human umbilical vein endothelial cells (HUVECs). Enzyme-linked immunosorbent assays were used to determine the concentrations of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), and E-selectin. Carboxy-H2DCFDA, a membrane-permeable reactive oxygen species (ROS)-sensitive fluorescent probe, was used to detect intracellular ROS levels. Results: TRPM4 was mainly expressed near the plasma membrane of mesenteric artery endothelial cells, and its expression level increased in SS hypertensive rats fed a HSD. Its protein expression was significantly upregulated upon treatment with exogenous hydrogen peroxide (H₂O₂) and aldosterone in cultured HUVECs. Cell viability decreased upon treatment with both agents in a concentration-dependent manner, which could be partially reversed by 9-phenanthrol, a specific TRPM4 inhibitor. Exogenous H₂O₂ induced apoptosis, enhanced cell migration, and increased the release of adhesion molecules, including ICAM-1, VCAM-1, and E-selectin, all of which were significantly attenuated upon treatment with 9-phenanthrol. Aldosterone and H₂O₂ induced the accumulation of intracellular ROS, which was significantly inhibited by 9-phenanthrol, suggesting that oxidative stress is one of the mechanisms underlying aldosterone-induced endothelial injury. Conclusions: Given the fact that oxidative stress and high levels of circulating aldosterone are present in hypertensive patients, we suggest that the upregulation of TRPM4 in the vascular endothelium may be involved in endothelial injuries caused by these stimuli.

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Section: Discussionsupporting

confidence: 83%

Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

Ding

Ban

Liu

et al. 2017

Cell Physiol Biochem

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“…That is, in situations of magnesium deficiency, calcium competes with magnesium and enters the cells. 51,52 Magnesium deficiency appears to increase the production of free radicals and the sensitivity of cells to the attack of reactive oxygen species. 53,54 Hypomagnesemia favors the infiltration of neutrophils and macrophages in the affected cells, which potentiates the activity of the enzyme nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), increasing the production of the superoxide radical.…”

Section: Metabolic and Physiological Aspects Of Magnesiummentioning

confidence: 99%

Hypomagnesemia and its relation with chronic low-grade inflammation in obesity

Oliveira

Cruz

Silva³

et al. 2017

Rev. Assoc. Med. Bras.

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“…Furthermore, TRPM4 is involved in endothelial cell migration, which is a typical feature of activated fibroblasts that is mediated by intracellular calcium changes. It has been demonstrated that TRPM4 plays a decisive role in the enhancement of endothelial cell migration induced by oxidative stress [42,43].…”

Section: Transient Receptor Potential Melastatin 4 Participates In Camentioning

confidence: 99%

Suppression of transient receptor potential melastatin 4 expression promotes conversion of endothelial cells into fibroblasts via transforming growth factor/activin receptor-like kinase 5 pathway

Echeverría

Montorfano

Cabello-Verrugio³

et al. 2015

Journal of Hypertension

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Endotoxin-induced vascular endothelial cell migration is dependent on TLR4/NF-κB pathway, NAD(P)H oxidase activation, and transient receptor potential melastatin 7 calcium channel activity

Cited by 37 publications

References 53 publications

Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

Hypomagnesemia and its relation with chronic low-grade inflammation in obesity

Suppression of transient receptor potential melastatin 4 expression promotes conversion of endothelial cells into fibroblasts via transforming growth factor/activin receptor-like kinase 5 pathway

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