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The Arachidonate 15-Lipoxygenase Enzyme Product 15-HETE Is Present in Heart Tissue from Patients with Ischemic Heart Disease and Enhances Clot Formation

Artikel i vetenskaplig tidskrift
Författare Annika Lundqvist
Mikael Sandstedt
Joakim Sandstedt
Ruth Wickelgren
G. I. Hansson
Anders Jeppsson
Lillemor Mattsson Hultén
Publicerad i Plos One
Volym 11
Nummer/häfte 8
ISSN 1932-6203
Publiceringsår 2016
Publicerad vid Wallenberglaboratoriet
Institutionen för biomedicin, avdelningen för klinisk kemi och transfusionsmedicin
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Språk en
Länkar dx.doi.org/10.1371/journal.pone.016...
Ämnesord rotation thrombelastography, cardiomyocyte clusters, expression, hypercoagulability, macrophages, samples, Science & Technology - Other Topics
Ämneskategorier Klinisk medicin

Sammanfattning

Ischemic heart disease is a major cause of death and morbidity and the search for novel therapeutic targets is still required. We have previously shown that the enzyme arachidonate 15 lipoxygenase (ALOX15), which catalyzes the conversion of arachidonic acid to 15-hydroxy eicosatetraenoic acid (15-HETE), is highly expressed in ischemic heart tissue, but its role in the pathogenesis of ischemic heart disease is unclear. Here we showed that expression of ALOX15, but not ALOX12 or ALOX15B, was increased in ischemic versus non-ischemic human heart biopsy samples. A similar ALOX expression pattern was found in hypoxic human cardiomyocytes and cardiac endothelial cells. We also showed that levels of 15-HETE were significantly higher in ischemic versus non-ischemic human heart biopsy samples and showed a tendency to increase in serum from the patients with ischemic heart disease. Moreover, hypoxia increased the production of 15-HETE levels from human cardiomyocytes and cardiac endothelial cells. The hypoxia-induced increase in 15-HETE levels from human cardiomyocytes was inhibited by the ALOX15 inhibitor baicalein. Finally, by using intrinsic rotational thromboelastometry, we showed that human whole blood clotted faster in the presence of 15-HETE. In summary, we propose that increased ALOX15 expression in heart tissue under ischemic conditions may lead to increased production of 15-HETE, potentially contributing to thrombosis.

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