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Reuter, B.; Rodemer, C.; Grudzenski, S.; Couraud, P.-O.; Weksler, B.; Romero, Ignacio A; Meairs, S.; Bugert, P.; Hennerici, M. G and Fatar, M.
(2013).
DOI: https://doi.org/10.1159/000350731
Abstract
The objective of our study was to determine the contribution of human BMECs to the MMP metabolism under in vitro OGD conditions simulating ischemic stroke. Our results suggest that human BMECs switch to a proinflammatory state by means of an enhanced production of MMP-2, attenuated release of TIMP-1, and unaffected production of TIMP-2. Thus, human BMECs might participate in the MMP-mediated BBB breakdown during ischemic stroke. However, our data does not support human BMECs to be a source of MMP-9.