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Open AccessFeature PaperArticle

Contribution of the Potassium Channels KV1.3 and KCa3.1 to Smooth Muscle Cell Proliferation in Growing Collateral Arteries

1
Walter-Brendel-Centre of Experimental Medicine, University Hospital, LMU Munich, 80539 Munich, Germany
2
Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital, LMU Munich, 80539 Munich, Germany
3
Department of Internal Medicine I, Faculty of Medicine, University Hospital, LMU Munich, 80539 Munich, Germany
4
Department of Obstetrics and Gynaecology, University Hospital, LMU Munich, 80539 Munich, Germany
*
Author to whom correspondence should be addressed.
Cells 2020, 9(4), 913; https://doi.org/10.3390/cells9040913
Received: 19 February 2020 / Revised: 21 March 2020 / Accepted: 3 April 2020 / Published: 8 April 2020
(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)
Collateral artery growth (arteriogenesis) involves the proliferation of vascular endothelial cells (ECs) and smooth muscle cells (SMCs). Whereas the proliferation of ECs is directly related to shear stress, the driving force for arteriogenesis, little is known about the mechanisms of SMC proliferation. Here we investigated the functional relevance of the potassium channels KV1.3 and KCa3.1 for SMC proliferation in arteriogenesis. Employing a murine hindlimb model of arteriogenesis, we found that blocking KV1.3 with PAP-1 or KCa3.1. with TRAM-34, both interfered with reperfusion recovery after femoral artery ligation as shown by Laser-Doppler Imaging. However, only treatment with PAP-1 resulted in a reduced SMC proliferation. qRT-PCR results revealed an impaired downregulation of α smooth muscle-actin (αSM-actin) and a repressed expression of fibroblast growth factor receptor 1 (Fgfr1) and platelet derived growth factor receptor b (Pdgfrb) in growing collaterals in vivo and in primary murine arterial SMCs in vitro under KV1.3. blockade, but not when KCa3.1 was blocked. Moreover, treatment with PAP-1 impaired the mRNA expression of the cell cycle regulator early growth response-1 (Egr1) in vivo and in vitro. Together, these data indicate that KV1.3 but not KCa3.1 contributes to SMC proliferation in arteriogenesis. View Full-Text
Keywords: arteriogenesis; collateral artery growth; SMC proliferation; potassium channel; KV1.3; KCa3.1; FGFR-1; Egr-1; PDFG-R; αSM-actin arteriogenesis; collateral artery growth; SMC proliferation; potassium channel; KV1.3; KCa3.1; FGFR-1; Egr-1; PDFG-R; αSM-actin
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MDPI and ACS Style

Lasch, M.; Caballero Martinez, A.; Kumaraswami, K.; Ishikawa-Ankerhold, H.; Meister, S.; Deindl, E. Contribution of the Potassium Channels KV1.3 and KCa3.1 to Smooth Muscle Cell Proliferation in Growing Collateral Arteries. Cells 2020, 9, 913. https://doi.org/10.3390/cells9040913

AMA Style

Lasch M, Caballero Martinez A, Kumaraswami K, Ishikawa-Ankerhold H, Meister S, Deindl E. Contribution of the Potassium Channels KV1.3 and KCa3.1 to Smooth Muscle Cell Proliferation in Growing Collateral Arteries. Cells. 2020; 9(4):913. https://doi.org/10.3390/cells9040913

Chicago/Turabian Style

Lasch, Manuel; Caballero Martinez, Amelia; Kumaraswami, Konda; Ishikawa-Ankerhold, Hellen; Meister, Sarah; Deindl, Elisabeth. 2020. "Contribution of the Potassium Channels KV1.3 and KCa3.1 to Smooth Muscle Cell Proliferation in Growing Collateral Arteries" Cells 9, no. 4: 913. https://doi.org/10.3390/cells9040913

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