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. 2022 Feb 11;10:830671. doi: 10.3389/fchem.2022.830671

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Copyright © 2022 Hintze, Schnabelrauch and Rother.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanisms of GAG action on TIMP-3. (A) GAG control ECM remodelling via stabilizing and accruing TIMP-3, interfering with TIMP/LRP-1 complex formation and increasing extracellular TIMP-3 level; SPR sensorgram: binding analysis of solute TIMP-3 with immobilized LRP-1 cluster II in the absence or presence of differently sulfated sHA (black line: interaction of TIMP-3 alone, grey and blue line: interaction with TIMP-3 after preincubation with sHA1 and sHA3, respectively). (B) GAG control endothelial cell activation by interfering with VEGFR-2 complexation via VEGF-A and TIMP- (Reprinted with permission from Rother S. et al. 2016 Biomacromolecules 17, 3252-3261 and Rother S. et al. 2017 ACS Appl. Mater. Interfaces 9, 9539-9550. Copyright ũ 2016/2017 American Chemical Society).