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. 2015 Sep 10;10(9):e0135988. doi: 10.1371/journal.pone.0135988

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© 2015 Kabir et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Fig 4 — Hearts were treated as in Fig 2 and analyzed at the end of each protocol. A-E. Images are from slices of the same heart in each condition. White areas correspond to the infarcted zone. A. Infarct is minimal in isolated hearts not subjected to I/R. B-D. E2 protected equally well hearts from WT, Esr1 and Esr2 knockouts against infarct induced by I/R. E. Gper1^-/- was the only E2 receptor knockout examined where I/R caused the same degree of infarct in the presence or absence of E2. F. Individual and mean±SEM values of % infarct size. * P<0.05 control versus E2-treated groups (WT, n = 7–8 hearts/group; Esr1^-/-, n = 5 hearts/group; Esr2^-/-, n = 5–6 hearts/group). In Gper1^-/- hearts, E2 treatment did not reduce the infarct size (control = 52±3% vs. E2-treated = 47±4%, n = 6 hearts/group).