Figure 2.
Pulmonary cellular localization of peroxisome proliferator activated receptor γ (PPARγ). Pulmonary histopathology demonstrated by hematoxylin and eosin staining and PPARγ localization determined by immunohistochemical staining of paraffin-embedded lung sections after 48 hour exposure to air (A) or O2 (B). Hyperoxia-induced protein edema in peribronchiolar and perivascular regions and alveolar air space, epithelial proliferation, and inflammatory cell infiltration shown in hematoxylin and eosin stained sections (A, B, upper panels) was markedly greater in Nrf2−/− mice relative to Nrf2+/+ mice. Cellular PPARγ localized by immunohistochemical staining (A, B, bottom panels) using an anti-PPARγ antibody indicated inflammatory cells and bronchiolar epithelial cells (arrows) as the primary sources of PPARγ in the hyperoxia-injured lung. PPARγ-positive cells were more predominantly enhanced in Nrf2+/+ mice relative to Nrf2−/− mice after hyperoxia. Representative light photomicrographs are shown (n = 3/group). Higher magnification photomicrographs displayed fewer occurrences of PPARγ-bearing cells in Nrf2−/− mice relative to Nrf2+/+ mice after O2. AV = alveoli; BR = bronchi or bronchiole; BV = blood vessel; TB = terminal bronchioles. Bars indicate 100 μm.