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. 2018 Jul;59(1):104–113. doi: 10.1165/rcmb.2017-0025OC

Figure 5.

Figure 5.

(A) Relative expression of collagen I and α-SMA by HLFs conditioned with primary BECs derived from healthy donors (n = 13) after inhibition of BEC secretion of FSTL3 via Dox-inducible lentiviral shRNA knockdown. After knockdown of FSTL3 production by healthy BECs, collagen I expression was 92% greater in HLFs cocultured with BECs exposed to Dox compared with BECs not exposed to Dox (P = 0.001). α-SMA expression was 88% greater in HLFs cocultured with BECs exposed to Dox compared with BECs not exposed to Dox (P = 0.02). (B) Expression of collagen I and α-SMA by HLFs conditioned with primary BECs derived from donors with asthma (n = 12) after inhibition of BEC secretion of activin A via Dox-inducible lentiviral shRNA knockdown. After knockdown of activin A secretion by asthmatic BECs, collagen I expression was not significantly lower in HLFs cocultured with BECs exposed to Dox compared with BECs not exposed to Dox (P = 0.1). α-SMA expression was 22% lower in HLFs cocultured with BECs exposed to Dox compared with BECs not exposed to Dox (P = 0.02). (C and D) Representative immunostaining for collagen I (red), α-SMA (green), and DAPI (blue) in a representative healthy BEC-HLF coculture FSTL3 shRNA knockdown experiment (C, Dox-negative; D, Dox-positive).