Dermal microvascular endothelial cells contribute to cutaneous inflammation by secreting proinflammatory cytokines and chemokines. We show here that low extracellular magnesium stimulates the secretion of interleukin 8 and monocyte chemoattractant protein-1 in dermal microvascular endothelial cells. This secretory pattern might result from interplay between NFκB, the master regulator of inflammation, and PPAR, a transcription factor that has emerged as an inhibitor of inflammation. Indeed, both NFκB and PPARγ are activated in dermal microvascular endothelial cells cultured in low magnesiumcontaining medium. In conclusion, we hypothesize that PPARγ and NFκB might contribute to the response of these cells to low Mg.
Potential interplay between NFκB and PPARγ in human dermal microvascular endothelial cells cultured in low magnesium / S. Castiglioni, A. Cazzaniga, J.A..M. Maier. - In: MAGNESIUM RESEARCH. - ISSN 0953-1424. - 27:2(2014), pp. 86-93. [10.1684/mrh.2014.0365]
Potential interplay between NFκB and PPARγ in human dermal microvascular endothelial cells cultured in low magnesium
S. Castiglioni;A. Cazzaniga;J.A..M. Maier
2014
Abstract
Dermal microvascular endothelial cells contribute to cutaneous inflammation by secreting proinflammatory cytokines and chemokines. We show here that low extracellular magnesium stimulates the secretion of interleukin 8 and monocyte chemoattractant protein-1 in dermal microvascular endothelial cells. This secretory pattern might result from interplay between NFκB, the master regulator of inflammation, and PPAR, a transcription factor that has emerged as an inhibitor of inflammation. Indeed, both NFκB and PPARγ are activated in dermal microvascular endothelial cells cultured in low magnesiumcontaining medium. In conclusion, we hypothesize that PPARγ and NFκB might contribute to the response of these cells to low Mg.Pubblicazioni consigliate
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