Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

Figure 8

Ultrastructural morphology after TSP-2 overexpression in the ARDS mouse model. Mouse tissue sections from normal mice or mice treated with LPS for 4, 12, 24, and 72 h and overexpressing either empty vector (vehicle group), TSP-1 (TSP-1 group), or TSP-2 (TSP-2 group) were analyzed for ultrastructural morphology using electron microscopy. (a–d) Ultrastructure of pulmonary capillaries under normal conditions. Arrow in (a) shows normal blood vessel epithelial cells (ECs), blue arrow in (b) shows the side of the bronchium, and the red arrow shows the side of the capillary at the air-blood barrier having a continuous thin basement membrane. (c) Macrophages within the blood vessel. Arrow in (d) shows alveolar epithelial cells (AECs) with clear lamellar bodies. (e–h) Electron micrographs in the vehicle group demonstrated disruption of the basement membrane in capillaries (e); thickened air-blood barrier (f); perivascular edema and inflammatory cell infiltration (g); and an apoptotic AEC with visible empty lamellar bodies, swollen cell organs, and contracted nuclei with condensed and fragmented nuclear chromatin (arrow) (h). (i–l) Ultrastructural morphology of EC (i), thickened air-blood barrier (j), perivascular edema (k), and apoptotic AEC (l) in the TSP-1 overexpression group, which was similar to the vehicle group. (m–p) Depiction of normal ultrastructural morphology of EC (m), AEC (p), air-blood barrier (n), and alleviated perivascular edema (o) in the TSP-2 overexpression group. The scale bars in (a, c, e, f, i, j, l, and n) are 1 μm; the scale bars in (b, d, g, h, k, m, o, and p) are 2 μm ( per group).