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  Arginase inhibition attenuates arteriogenesis and interferes with M2 macrophage accumulation

Lasch, M., Caballero-Martinez, A., Troidl, K., Schloegl, I., Lautz, T., & Deindl, E. (2016). Arginase inhibition attenuates arteriogenesis and interferes with M2 macrophage accumulation. LABORATORY INVESTIGATION, 96(8), 830-838. doi:10.1038/labinvest.2016.62.

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Datensatz-Permalink: https://hdl.handle.net/21.11116/0000-0001-BD28-E Versions-Permalink: https://hdl.handle.net/21.11116/0000-0001-D78B-0
Genre: Zeitschriftenartikel

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 Urheber:
Lasch, Manuel, Autor
Caballero-Martinez, Amelia, Autor
Troidl, Kerstin1, Autor           
Schloegl, Irmengard, Autor
Lautz, Thomas, Autor
Deindl, Elisabeth, Autor
Affiliations:
1Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591696              

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Schlagwörter: NITRIC-OXIDE SYNTHASE; COLLATERAL ARTERY GROWTH; ANGIOTENSIN-II; IN-VIVO; ACTIVATION; ANGIOGENESIS; INFLAMMATION; ISCHEMIA; PATHWAY; STRESSResearch & Experimental Medicine; Pathology;
 Zusammenfassung: L-Arginine is the common substrate for nitric oxide synthases (NOS) and arginase. Whereas the contribution of NOS to collateral artery growth (arteriogenesis) has been demonstrated, the functional role of arginase remains to be elucidated and was topic of the present study. Arteriogenesis was induced in mice by ligation of the femoral artery. Laser Doppler perfusion measurements demonstrated a significant reduction in arteriogenesis in mice treated with the arginase inhibitor nor-NOHA (N-omega-hydroxy-nor-arginine). Accompanying in vitro results on murine primary arterial endothelial cells and smooth muscle cells revealed that nor-NOHA treatment interfered with cell proliferation and resulted in increased nitrate/nitrite levels, indicative for increased NO production. Immuno-histological analyses on tissue samples demonstrated that nor-NOHA administration caused a significant reduction in M2 macrophage accumulation around growing collateral arteries. Gene expression studies on isolated growing collaterals evidenced that nor-NOHA treatment abolished the differential expression of Icam1 (intercellular adhesion molecule 1). From our data we conclude that arginase activity is essential for arteriogenesis by promoting perivascular M2 macrophage accumulation as well as arterial cell proliferation.

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Sprache(n): eng - English
 Datum: 2016
 Publikationsstatus: Erschienen
 Seiten: 9
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: ISI: 000380772900002
DOI: 10.1038/labinvest.2016.62
 Art des Abschluß: -

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Titel: LABORATORY INVESTIGATION
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA : NATURE PUBLISHING GROUP
Seiten: - Band / Heft: 96 (8) Artikelnummer: - Start- / Endseite: 830 - 838 Identifikator: ISSN: 0023-6837