By con trast ?brosis was markedly decreased in galectin 32 2 mice, as quanti?ed for collagen written content by sircol assay and ?brosis scoring. In WT mice, galectin three expression was observed in alveolar macrophages and while in the bronchial epi thelium and was temporally and spatially related to ?brosis. Ad TGF b1 made precisely the same marked greater ex pression of lively TGF b1 while in the bronchoalveolar lavage ?uid from Days two 6 following instillation plus the similar modest degree of in?ammation, in?ammatory cell recruitment, and combined in?ammatory score in WT and galectin 32 two mice. Thus galectin 32 two mice showed signi?cant attenuation of TGF b1 induced ?brosis despite equivalent initial tissue responses and in?ammatory cell recruitment. Galectin 32 two Fibroblasts Demonstrate Lowered Activation and Collagen Production in Response to TGF b1 Equal yields of ?broblasts have been obtained from WT and galectin 32 2 mice. TGF b1 induced a marked transform in morphology and increase in collagen synthesis in primary lung ?broblasts iso lated from WT mice that was abrogated in galectin 32 2 lung ?bro blasts.
Myo?broblast activation in response to TGF b1 was signi?cantly decreased with markedly reduced collagen one and a SMA expression in galectin 32 2 compared with WT lung ?broblasts as judged by Western blot examination and sircol assay. There was no big difference in prolifera tion in between WT and galectin 32 2 key lung ?broblasts. Galectin 32 two AECs Display Decreased EMT in Response to TGF b1 EMT is really a leading supply of pathogenic myo?broblasts all through pul monary ?brogenesis. our site EMT myo?broblast activation in re sponse to TGF b1 was established in AECs isolated from WT and galectin 32 two mice. Equal yields of AECs had been obtained from WT and galectin 32 two mice. At Day two after isolation AECs formed the full details islands of cobblestone shaped clusters with E cadherin staining on the cell junctions. TGF b1 remedy for 72 hrs altered WT AEC morphology from a con?uent cobble stone visual appeal with surface E cadherin staining to spindle shaped with reduction of cell cell contacts and enhanced a SMA immuno?uo rescence staining.
Treatment with TGF b1 also enhanced galectin 3 secretion in WT AECs as measured by ELISA. By contrast, galectin 32 2AECs maintained E cadherin surface stain ing and decreased up regulation of the SMA. This was con?rmed by Western blot examination,

which showed that TGF b1 induced a marked up regulation of mesenchymal markers a SMA and vimentin and down regulation of the epithelial marker E cadherin in WT AECs, which was evident just after 48 hrs. By contrast, TGF b1 did not stimulate a SMA expression or down regulate E cadherin in galectin 32 two AECs. Western blot analysis and reverse transcriptase polymerase chain reaction demonstrate that TGF b1 induced a SMA up regulation is re duced in galectin 32 two AECs and restored by the addition of 25 mg ml of recombinant galectin three.