Figure 4

(a) Schema of experimental protocol for deleting Panx1 using CX3Cr1-Cre or LysM-Cre mediated approaches prior to epithelial injury, with (b) in vivo epithelial injury-induced proliferation analysed by EdU incorporation (n=4-5/group Cx3Cr1 Cre, assessed by t-test; n=4/group LysM Cre, assessed by t-test). (c) Schema of local delivery of TAT-Cre into the lungs. (d) Representative flow cytometry plots of YFP expression within epithelium with either PBS (vehicle) or TAT-Cre delivery with (e) confirmation of TAT-Cre-dependent YFP expression within epithelium and (f) analysis of major immune cell populations in response to TAT-Cre. (g) Schema of experimental protocol for expressing Panx1 transgene (Tg) on a global Panx1-deficient mouse (Panx1^-/-) using i.t. TAT-Cre administration. (h) Panx1 protein expression on whole lung extracts analysed in Panx1^-/-/Tg^- and Panx1^-/-/Tg+ mice with and without local TAT-Cre, confirming Panx1 expression in a Tg-dependent and Cre-dependent fashion. (i) In vivo epithelial injury-induced proliferation (analysed by EdU incorporation post-naphthalene) is boosted by re-expression of Panx1 at the site of tissue injury (n=3/group, one experiment, assessed by t-test) with both genotypes treated intra-tracheally with TAT-Cre. *p<0.05.