@article {1168,
	title = {Sterile Inflammation Enhances ECM Degradation in Integrin β1 KO Embryonic Skin.},
	journal = {Cell Rep},
	volume = {16},
	year = {2016},
	month = {2016 09 20},
	pages = {3334-3347},
	abstract = {<p>Epidermal knockout of integrin β1 results in complete disorganization of the basement membrane (BM), resulting in neonatal lethality. Here, we report that this disorganization is exacerbated by an early\&nbsp;embryonic inflammatory response involving the recruitment of tissue-resident and monocyte-derived macrophages to the dermal-epidermal junction, associated with increased matrix metalloproteinase activity. Remarkably, the skin barrier in the integrin β1 knockout animals is intact, suggesting that this inflammatory response is initiated in a sterile environment. We demonstrate that the molecular mechanism involves de novo expression of integrin αvβ6 in the basal epidermal cells, which activates a TGF-β1 driven inflammatory cascade resulting in upregulation of dermal NF-κB in a Tenascin C-dependent manner. Importantly, treatment of β1 KO embryos in utero with small molecule inhibitors of TGF-βR1 and NF-κB results in marked rescue of the BM defects and amelioration of immune response, revealing an unconventional immuno-protective role for integrin β1 during BM remodeling.</p>
},
	keywords = {Animals, Extracellular Matrix, Inflammation, Integrin beta1, Macrophages, Mice, Mice, Knockout, Signal Transduction, Skin},
	issn = {2211-1247},
	doi = {10.1016/j.celrep.2016.08.062},
	author = {Kurbet, Ambika S and Hegde, Samarth and Bhattacharjee, Oindrila and Marepally, Srujan and Vemula, Praveen K and Raghavan, Srikala}
}
