Post by Max on Jul 17, 2005 6:33:32 GMT -5
Retinoids are known to produce water loss. Synthetic retinoids produce dose-dependent alterations in transepidermal water loss [4].
TNF-alpha and the Na+-K+-2Cl- cotransporter
Retinoic acid is known to in a dose dependent manner inhibit TNF-alpha in various cell types. In endothelial cells derived from microvessels, ATRA significantly inhibited TNFalpha-induced TF expression in HMEC-1 as well as HUVEC [2]. RA-induced inhibition of TNF-alpha and iNOS mRNA expression in activated microglia was accompanied by the concomitant reduction in release of iNOS and TNF-alpha proteins as revealed by nitrite assay and ELISA, respectively [3]. In cultured caco-2 cells, TNF-alpha inhibited net water and chloride absorption, down-regulated in both surface and crypt colonocytes the Na+-K+-2Cl- cotransporter, and reduced the protein expression and activity of the Na+-K+ ATPase. It was concluded that the effect of the cytokine on colonocytes is mediated via PGE2. By inhibiting the Na+-K+ ATPase, it reduces the Na+ gradient needed for NaCl absorption, and by down-regulating the expression of the Na+-K+-2Cl- symporter, it reduces basolateral Cl- entry and luminal Cl- secretion. The inhibitory effect on absorption is more significant than the inhibitory effect on secretion resulting in a decrease in net electrolyte uptake and consequently in more water retention in the lumen [1].
TNF-alpha and the Na+-K+-2Cl- cotransporter
Retinoic acid is known to in a dose dependent manner inhibit TNF-alpha in various cell types. In endothelial cells derived from microvessels, ATRA significantly inhibited TNFalpha-induced TF expression in HMEC-1 as well as HUVEC [2]. RA-induced inhibition of TNF-alpha and iNOS mRNA expression in activated microglia was accompanied by the concomitant reduction in release of iNOS and TNF-alpha proteins as revealed by nitrite assay and ELISA, respectively [3]. In cultured caco-2 cells, TNF-alpha inhibited net water and chloride absorption, down-regulated in both surface and crypt colonocytes the Na+-K+-2Cl- cotransporter, and reduced the protein expression and activity of the Na+-K+ ATPase. It was concluded that the effect of the cytokine on colonocytes is mediated via PGE2. By inhibiting the Na+-K+ ATPase, it reduces the Na+ gradient needed for NaCl absorption, and by down-regulating the expression of the Na+-K+-2Cl- symporter, it reduces basolateral Cl- entry and luminal Cl- secretion. The inhibitory effect on absorption is more significant than the inhibitory effect on secretion resulting in a decrease in net electrolyte uptake and consequently in more water retention in the lumen [1].