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. 2014 Nov 25;15:148. doi: 10.1186/s12931-014-0148-4

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© Yang et al.; licensee BioMed Central Ltd. 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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HMGB1 induced ET-1 release from HPAECs and proliferation of HPASMCs. (A) HMGB1-stimulated ET-1 release from HPAECs. Release of ET-1 was approximately 10% higher in the HMGB1-treated (40 ng/ml) group than in the control group (*p <0.001). (B, C) ET-1 release from HPAECs was attenuated by treatment antibodies against HMGB1 or RAGE in a dose-dependent manner (†p = 0.011; ‡p = 0.006). (D) HPASMCs were cultured with serum-free medium alone or 10% FBS, or in the presence of 30 ng/ml HMGB1. HMGB1 induced proliferation of HPASMCs (p <0.001). Data are presented as means ± SEM.