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. 2008 Feb 18;205(2):295–303. doi: 10.1084/jem.20071297

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Copyright © 2008, The Rockefeller University Press

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Figure 2. — Cardiac rupture after AMI is caused by periostin disruption. (A) Schema of the targeting strategy deletes the first exon of periostin locus. (B) Decreased survival of periostin ^−/− mice (n = 91) compared with the survival of ^+/+ mice (n = 80) after AMI. **, P < 0.0001. (C) Infarct LV wall stiffness was more reduced in periostin ^−/− mice than in ^+/+ mice after AMI (left). Mean passive stiffness was also significantly lower in the ^−/− mice than in the ^+/+ mice after AMI (right). Open columns, ^+/+; filled columns, ^−/−. **, P < 0.005, compared with ^+/+ mice. (D) Loss of periostin attenuated cardiac dilation after AMI, as shown by echocardiography. Open columns, ^+/+; filled columns, ^−/−. *, P < 0.05 compared with ^+/+ mice. (E) Histological analysis of heart sections from periostin ^−/− and ^+/+ mice stained with toluidine blue 5 d after AMI, showing a lower number of cardiac fibroblasts and lower ECM density in ^−/− mice. (right) The number of vimentin-positive cells. *, P < 0.02, compared with ^+/+ mice. (F) Images of the infarct border stained with anti-collagen I (left), and TEM images of infarct border, showing evidence of smaller and less abundant collagen in tissues from periostin ^−/− mice 5 d after AMI compared with the collagen of the ^+/+ infarct heart. Bar, 50 μm. (G) CSA distribution of collagen fibrils in the infarct border of ^+/+ and ^−/− mice, measured from TEM images. (H) Biochemical analysis of the collagen amount and cross-linking. *, P < 0.05; **, P < 0.01, compared with ^+/+ mice. (I) The number of αSMA-positive cells in the infarct area was reduced in periostin ^−/− mice 5 d after AMI. (right) The number of αSMA-positive cells. **, P < 0.01, compared with ^+/+ mice. Error bars represent the mean ± the SEM. Bars, 200 μm.