Posted On: 02/02/2015 9:50:02 PM
Post# of 30066
Here's a couple of key points:
"Our results also indicate that recombinant MANF suppressed the expression of NF-κB target genes and inhibited the proliferation of inflammatory FLS."
"The longevity and intensity of inflammation is detrimental to cells and tissues. In order to restrict inflammation, MANF may be induced as a compensatory mechanism. Therefore, we speculate that MANF induction governed by ER stress may aim to limit tissue damage and aid in tissue repair via inhibiting an inflammatory response. Taken together, our data indicate that MANF may be a novel negative regulator of inflammation that mediates the crosstalk between the NF-κB pathway and ER stress as well as can prevent the proliferation of inflamed cells."
"Our results also indicate that recombinant MANF suppressed the expression of NF-κB target genes and inhibited the proliferation of inflammatory FLS."
"The longevity and intensity of inflammation is detrimental to cells and tissues. In order to restrict inflammation, MANF may be induced as a compensatory mechanism. Therefore, we speculate that MANF induction governed by ER stress may aim to limit tissue damage and aid in tissue repair via inhibiting an inflammatory response. Taken together, our data indicate that MANF may be a novel negative regulator of inflammation that mediates the crosstalk between the NF-κB pathway and ER stress as well as can prevent the proliferation of inflamed cells."
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