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. 2009 Jan 15;82(1):21–29. doi: 10.1093/cvr/cvp015

Figure 6.

Figure 6

Decreased phosphatase and tensin homologue and increased MMP-2 expression in the infarct region of heart. Mice were subjected to left anterior descending coronary artery ligation for 30 min followed by reperfusion (IR). (A) Representative images showing phosphatase and tensin homologue expression in a section of mouse heart subjected to 7 days post-IR. Localization of phosphatase and tensin homologue (green) in heart sections was achieved using anti-phosphatase and tensin homologue antibody. The sections were counterstained with DAPI (nuclear, blue). Myocytes were stained using anti-alpha-sarcomeric actin antibody (red). (i) Representative image of phosphatase and tensin homologue (green) and DAPI (blue), infarct (I) or non-infarct (NI) regions are indicated; (ii) alpha-sarcomeric actin (red) and DAPI (blue) image. Scale bar = 50 µm. (B) Quantification of phosphatase and tensin homologue signal in infarct (I) vs. non-infarct (NI) regions. Data represent mean ± SD (n = 3). *P < 0.05 compared with NI region. (C) Histologically defined infarct (I) and non-infarct (NI) regions were captured using laser-capture microdissection as described in Figure 2. The laser-captured tissue elements from infarct and non-infarct regions were used for quantification of MMP-2 expression using real-time PCR. Data represent mean ± SD (n = 4). **P < 0.01 compared with control (NI) tissue.