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Activation of Cell Surface Bound 20S Proteasome Inhibits Vascular Cell Growth and Arteriogenesis

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Activation of Cell Surface Bound 20S Proteasome Inhibits Vascular Cell Growth and Arteriogenesis. / Ito, Wulf D; Lund, Natalie; Zhang, Ziyang; Buck, Friedrich; Lellek, Heinrich; Horst, Andrea; Machens, Hans-Günther; Schunkert, Heribert; Schaper, Wolfgang; Meinertz, Thomas.

In: BIOMED RES INT , Vol. 2015, 2015, p. 719316.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ito, WD, Lund, N, Zhang, Z, Buck, F, Lellek, H, Horst, A, Machens, H-G, Schunkert, H, Schaper, W & Meinertz, T 2015, 'Activation of Cell Surface Bound 20S Proteasome Inhibits Vascular Cell Growth and Arteriogenesis', BIOMED RES INT , vol. 2015, pp. 719316. https://doi.org/10.1155/2015/719316

APA

Ito, W. D., Lund, N., Zhang, Z., Buck, F., Lellek, H., Horst, A., Machens, H-G., Schunkert, H., Schaper, W., & Meinertz, T. (2015). Activation of Cell Surface Bound 20S Proteasome Inhibits Vascular Cell Growth and Arteriogenesis. BIOMED RES INT , 2015, 719316. https://doi.org/10.1155/2015/719316

Vancouver

Ito WD, Lund N, Zhang Z, Buck F, Lellek H, Horst A et al. Activation of Cell Surface Bound 20S Proteasome Inhibits Vascular Cell Growth and Arteriogenesis. BIOMED RES INT . 2015;2015:719316. https://doi.org/10.1155/2015/719316

Bibtex

@article{241eebe316a943c4b5111c3dd0f76a8f,
title = "Activation of Cell Surface Bound 20S Proteasome Inhibits Vascular Cell Growth and Arteriogenesis",
abstract = "Arteriogenesis is an inflammatory process associated with rapid cellular changes involving vascular resident endothelial progenitor cells (VR-EPCs). Extracellular cell surface bound 20S proteasome has been implicated to play an important role in inflammatory processes. In our search for antigens initially regulated during collateral growth mAb CTA 157-2 was generated against membrane fractions of growing collateral vessels. CTA 157-2 stained endothelium of growing collateral vessels and the cell surface of VR-EPCs. CTA 157-2 bound a protein complex (760 kDa) that was identified as 26 kDa α7 and 21 kDa β3 subunit of 20S proteasome in mass spectrometry. Furthermore we demonstrated specific staining of 20S proteasome after immunoprecipitation of VR-EPC membrane extract with CTA 157-2 sepharose beads. Functionally, CTA 157-2 enhanced concentration dependently AMC (7-amino-4-methylcoumarin) cleavage from LLVY (N-Succinyl-Leu-Leu-Val-Tyr) by recombinant 20S proteasome as well as proteasomal activity in VR-EPC extracts. Proliferation of VR-EPCs (BrdU incorporation) was reduced by CTA 157-2. Infusion of the antibody into the collateral circulation reduced number of collateral arteries, collateral proliferation, and collateral conductance in vivo. In conclusion our results indicate that extracellular cell surface bound 20S proteasome influences VR-EPC function in vitro and collateral growth in vivo.",
author = "Ito, {Wulf D} and Natalie Lund and Ziyang Zhang and Friedrich Buck and Heinrich Lellek and Andrea Horst and Hans-G{\"u}nther Machens and Heribert Schunkert and Wolfgang Schaper and Thomas Meinertz",
year = "2015",
doi = "10.1155/2015/719316",
language = "English",
volume = "2015",
pages = "719316",
journal = "BIOMED RES INT ",
issn = "2314-6133",
publisher = "Hindawi Publishing Corporation",

}

RIS

TY - JOUR

T1 - Activation of Cell Surface Bound 20S Proteasome Inhibits Vascular Cell Growth and Arteriogenesis

AU - Ito, Wulf D

AU - Lund, Natalie

AU - Zhang, Ziyang

AU - Buck, Friedrich

AU - Lellek, Heinrich

AU - Horst, Andrea

AU - Machens, Hans-Günther

AU - Schunkert, Heribert

AU - Schaper, Wolfgang

AU - Meinertz, Thomas

PY - 2015

Y1 - 2015

N2 - Arteriogenesis is an inflammatory process associated with rapid cellular changes involving vascular resident endothelial progenitor cells (VR-EPCs). Extracellular cell surface bound 20S proteasome has been implicated to play an important role in inflammatory processes. In our search for antigens initially regulated during collateral growth mAb CTA 157-2 was generated against membrane fractions of growing collateral vessels. CTA 157-2 stained endothelium of growing collateral vessels and the cell surface of VR-EPCs. CTA 157-2 bound a protein complex (760 kDa) that was identified as 26 kDa α7 and 21 kDa β3 subunit of 20S proteasome in mass spectrometry. Furthermore we demonstrated specific staining of 20S proteasome after immunoprecipitation of VR-EPC membrane extract with CTA 157-2 sepharose beads. Functionally, CTA 157-2 enhanced concentration dependently AMC (7-amino-4-methylcoumarin) cleavage from LLVY (N-Succinyl-Leu-Leu-Val-Tyr) by recombinant 20S proteasome as well as proteasomal activity in VR-EPC extracts. Proliferation of VR-EPCs (BrdU incorporation) was reduced by CTA 157-2. Infusion of the antibody into the collateral circulation reduced number of collateral arteries, collateral proliferation, and collateral conductance in vivo. In conclusion our results indicate that extracellular cell surface bound 20S proteasome influences VR-EPC function in vitro and collateral growth in vivo.

AB - Arteriogenesis is an inflammatory process associated with rapid cellular changes involving vascular resident endothelial progenitor cells (VR-EPCs). Extracellular cell surface bound 20S proteasome has been implicated to play an important role in inflammatory processes. In our search for antigens initially regulated during collateral growth mAb CTA 157-2 was generated against membrane fractions of growing collateral vessels. CTA 157-2 stained endothelium of growing collateral vessels and the cell surface of VR-EPCs. CTA 157-2 bound a protein complex (760 kDa) that was identified as 26 kDa α7 and 21 kDa β3 subunit of 20S proteasome in mass spectrometry. Furthermore we demonstrated specific staining of 20S proteasome after immunoprecipitation of VR-EPC membrane extract with CTA 157-2 sepharose beads. Functionally, CTA 157-2 enhanced concentration dependently AMC (7-amino-4-methylcoumarin) cleavage from LLVY (N-Succinyl-Leu-Leu-Val-Tyr) by recombinant 20S proteasome as well as proteasomal activity in VR-EPC extracts. Proliferation of VR-EPCs (BrdU incorporation) was reduced by CTA 157-2. Infusion of the antibody into the collateral circulation reduced number of collateral arteries, collateral proliferation, and collateral conductance in vivo. In conclusion our results indicate that extracellular cell surface bound 20S proteasome influences VR-EPC function in vitro and collateral growth in vivo.

U2 - 10.1155/2015/719316

DO - 10.1155/2015/719316

M3 - SCORING: Journal article

C2 - 26146628

VL - 2015

SP - 719316

JO - BIOMED RES INT

JF - BIOMED RES INT

SN - 2314-6133

ER -