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. 2020 Oct 23;3(12):e202000821. doi: 10.26508/lsa.202000821

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© 2020 Martins-Marques et al.

This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).

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Figure 5. — (A) Non-reducing WB of HEK293^Cx43+-derived ECM (10 μg total protein/lane). CD63, CD81, CD9, Tsg101, Flotillin-1, and GAPDH was used as EV markers. p53 was used to determine cellular contamination. (B) Representative transmission electron microscopy of HEK293^Cx43+-derived ECM. (C) Levels of Cx43 in ECM (10 μg total protein/lane) from HL-1 cells subjected to 30 min ischemia (ISCH), 1 h or 4 h of reperfusion (I/R; n = 4). (D) Non-reducing WB of heart-derived ECM (10 μg total protein/lane) from sham (ECM^mouseCT), I/R 4H (ECM^{mouseI/R 4H}), and I/R 30′ (ECM^{mouseI/R 30′}). (E) WB analysis of Cx43 in heart-derived ECM (10 μg total protein/lane; n = 6).

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