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Flow-dependent increase of ICAM-1 on saphenous vein endothelium is sensitive to apamin

journal contribution
posted on 2023-06-08, 19:45 authored by Sabena Sultan, Martin Gosling, Shadi Abu-Hayyeh, Nessa Carey, Janet T Powell
The potassium channel blocker tetraethylammonium blocks the flow-induced increase in endothelial ICAM-1. We have investigated the subtype of potassium channel that modulates flow-induced increased expression of ICAM-1 on saphenous vein endothelium. Cultured human saphenous vein endothelial cells (HSVECs) or intact saphenous veins were perfused at fixed low nd high flows in a laminar shear chamber or flow rig, respectively, in the presence or absence of potassium channel blockers. Expression of K+ channels and endothelial ICAM-1 was measured by real-time polymerase chain reaction and/or immunoassays. In HSVECs, the application of 0.8 N/m2 (8 dyn/cm2) shear stress resulted in a two- to fourfold increase in cellular ICAM-1 within 6 h (P < 0.001). In intact vein a similar shear stress, with pulsatile arterial pressure, resulted in a twofold increase in endothelial ICAM-1/CD31 staining area within 1.5 h (P < 0.001). Both increases in ICAM-1 were blocked by inclusion of 100 nM apamin in the vein perfusate, whereas other K+ channel blockers were less effective. Two subtypes of small conductance Ca 2+-activated K+ channel (selectively blocked by apamin) were expressed in HSVECs and vein endothelium (SK3>SK2). Apamin blocked the upregulation of ICAM-1 on saphenous vein endothelium in response to increased flow to implicate small conductance Ca2+-activated K+ channels in shear stress/flow-mediated signaling pathways.

History

Publication status

  • Published

Journal

American Journal of Physiology - Heart and Circulatory Physiology

ISSN

0363-6135

Publisher

American Physiological Society

Issue

1 56-1

Volume

287

Article number

H22-H28

Department affiliated with

  • Chemistry Publications

Full text available

  • No

Peer reviewed?

  • Yes

Legacy Posted Date

2015-01-28

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