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Figure. Steroid hormones decrease inflammation by inhibiting NFκB. From: Conserved steroid hormone homology converges on NF?B to modulate inflammation in asthma.

Steroid hormones functionthough genomic and non-genomic actions. In classical genomic signaling. glucocorticoids, sex steroids, and secosteroids passively diffuse into the cell and bind to their steroid specific receptor. The glucocorticoids and sex steroids attach to their respective receptors, homodimerize and, translocate to the nucleus. They then bind to steroid specific response elements to alter gene transcription. Similarly, 1,25 dihydroxyvitamin D binds to the vitamin D receptor, but forms a heterodimer with retinoid X receptor (RXR) prior to binding to vitamin D response elements. In non-classical genomic signaling, steroid-hormone receptor complexes transrepress pro-inflammatory mediators, NFκB and activator protein (AP)-1. The rapid, non-genomic actions of steroid hormones involve direct steroid effects on the cell membrane, actions through a steroid specific membrane receptor, and/or the activation of signaling kinases. The rapid fluctuation of sex steroid hormones at puberty and during the menstrual cycle leads to varying levels of estrogen, which may, through non-genomic mechanisms cause altered phosphorylation of IκB, allowing for NFκB mediated inflammation.

Asha S. Payne, et al. J Investig Med. ;60(1):13-17.

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