Figure 4.

Effect of uPA plasma membrane receptor (uPAR) expression on bleomycin (BLM)-induced ATII cell epithelial–mesenchymal transitions. A: ATII cells isolated from mice lacking uPAR expression were exposed to PBS, BLM, BLM+CSP, or BLM+CP in vitro. The lysates were immunoblotted for the expression of collagen-I, α-SMA, E-cadherin, ZO-1, and β-actin antigens. The lysates from uPAR-deficient ATII cells treated with transforming growth factor β (TGF-β) were used as a control. The densities of individual bands were compiled and normalized against corresponding values of β-actin loading controls. The fold changes in proteins are presented as a bar graph, and the differences between treatments versus control were statistically significant. B: uPAR-deficient mice were treated with saline or BLM and 24 hours after the initial exposure to BLM, mice with BLM injury were i.p. injected with or without caveolin-1 scaffolding domain peptide (CSP) or control peptide (CP). Three days after the initiation of BLM injury, ATII cells were isolated from these mice, and the cell lysates were immunoblotted for altered expression of collagen-I, α-SMA, E-cadherin, ZO-1, and β-actin. The fold changes of proteins are presented as a bar graph. C: ATII cell RNA from uPAR-deficient mice exposed to saline, BLM, BLM+CSP, or CP were tested for changes in the expression of E-cadherin, collagen-I, ZO-1, and α-SMA mRNAs by real-time PCR. The fold changes of mRNA are presented as a bar graph. ^∗∗∗∗P < 0.0001 versus control.