Induction of CRP3/MLP expression during vein arterialization is dependent on stretch rather than shear stress

Aims Cysteine- and glycine-rich protein 3/muscle LIM-domain protein (CRP3/MLP) mediates protein–protein interaction with actin filaments in the heart and is involved in muscle differentiation and vascular remodelling. Here, we assessed the induction of CRP3/MLP expression during arterialization in h...

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Veröffentlicht in:Cardiovascular research 2009-07, Vol.83 (1), p.140-147
Hauptverfasser: Campos, Luciene Cristina Gastalho, Miyakawa, Ayumi Aurea, Barauna, Valerio Garrone, Cardoso, Leandro, Borin, Thaiz Ferraz, Dallan, Luis Alberto de Oliveira, Krieger, Jose Eduardo
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Sprache:eng
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Zusammenfassung:Aims Cysteine- and glycine-rich protein 3/muscle LIM-domain protein (CRP3/MLP) mediates protein–protein interaction with actin filaments in the heart and is involved in muscle differentiation and vascular remodelling. Here, we assessed the induction of CRP3/MLP expression during arterialization in human and rat veins. Methods and results Vascular CRP3/MLP expression was mainly observed in arterial samples from both human and rat. Using quantitative real time RT–PCR, we demonstrated that the CRP3/MLP expression was 10 times higher in smooth muscle cells (SMCs) from human mammary artery (h-MA) vs. saphenous vein (h-SV). In endothelial cells (ECs), CRP3/MLP was scarcely detected in either h-MA or h-SV. Using an ex vivo flow through system that mimics arterial condition, we observed induction of CRP3/MLP expression in arterialized h-SV. Interestingly, the upregulation of CRP3/MLP was primarily dependent on stretch stimulus in SMCs, rather than shear stress in ECs. Finally, using a rat vein in vivo arterialization model, early (1–14 days) CRP3/MLP immunostaining was observed predominantly in the inner layer and later (28–90 days) it appeared more scattered in the vessel layers. Conclusion Here we provide evidence that CRP3/MLP is primarily expressed in arterial SMCs and that stretch is the main stimulus for CRP3/MLP induction in veins exposed to arterial haemodynamic conditions.
ISSN:0008-6363
1755-3245
DOI:10.1093/cvr/cvp108