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Lee, Hyuck Jin,Savelieff, Masha G.,Kang, Juhye,Brophy, Megan Brunjes,Nakashige, Toshiki G.,Lee, Shin Jung C.,Nolan, Elizabeth M.,Lim, Mi Hee The Royal Society of Chemistry 2018 Metallomics Vol.10 No.8
<P>Proteins from the S100 family perform numerous functions and may contribute to Alzheimer's disease (AD). Herein, we report the effects of S100A8/S100A9 heterooligomer calprotectin (CP) and the S100B homodimer on metal-free and metal-bound amyloid-β (Aβ; Aβ40 and Aβ42) aggregation <I>in vitro</I>. Studies performed with CP-Ser [S100A8(C42S)/S100A9(C3S) oligomer] indicate that the protein influences the aggregation profile for Aβ40 in both the absence and presence of metal ions [<I>i.e.</I>, Zn(ii) and Cu(ii)]. Moreover, the detection of Aβ40-CP-Ser complexes by mass spectrometry suggests a direct interaction as a possible mechanism for the involvement of CP in Aβ40 aggregation. Although the interaction of CP-Ser with Aβ40 impacts Aβ40 aggregation <I>in vitro</I>, the protein does not attenuate Aβ-induced toxicity in SH-SY5Y cells. In contrast, S100B has a slight effect on the aggregation of Aβ. Overall, this work supports a potential association of CP with Aβ in the absence and presence of metal ions in AD.</P>
Lee, Yunki,Le Thi, Phuong,Seon, Gyeung Mi,Ryu, Seung Bae,Brophy, Colleen M.,Kim, YongTae,Park, Jong-Chul,Park, Ki Dong,Cheung-Flynn, Joyce,Sung, Hak-Joon Elsevier 2017 Journal of controlled release Vol.266 No.-
<P><B>Abstract</B></P> <P>The leading cause of synthetic graft failure includes thrombotic occlusion and intimal hyperplasia at the site of vascular anastomosis. Herein, we report a co-immobilization strategy of heparin and potent anti-neointimal drug (Mitogen Activated Protein Kinase II inhibitory peptide; MK2i) by using a tyrosinase-catalyzed oxidative reaction for preventing thrombotic occlusion and neointimal formation of synthetic vascular grafts. The binding of heparin–tyramine polymer (HT) onto the polycarprolactone (PCL) surface enhanced blood compatibility with significantly reduced protein absorption (64.7% decrease) and platelet adhesion (85.6% decrease) compared to bare PCL surface. When loading MK2i, 1) the HT depot surface gained high MK2i-loading efficiency through charge-charge interaction, and 2) this depot platform enabled long-term, controlled release over 4weeks (92–272μg/mL of MK2i). The released MK2i showed significant inhibitory effects on VSMC migration through down-regulated phosphorylation of target proteins (HSP27 and CREB) associated with intimal hyperplasia. In addition, it was found that the released MK2i infiltrated into the tissue with a cumulative manner in <I>ex vivo</I> human saphenous vein (HSV) model. This present study demonstrates that enzymatically HT-coated surface modification is an effective strategy to induce long-term MK2i release as well as hemocompatibility, thereby improving anti-neointimal activity of synthetic vascular grafts.</P> <P>Graphical abstract</P> <P>[DISPLAY OMISSION]</P>