A 12(
            <i>S</i>
            )-hydroxyeicosatetraenoic acid receptor interacts with steroid receptor coactivator-1

Kurahashi, Yuko; Herbertsson, Helena; Söderström, Mats; Rosenfeld, Michael G.; Hammarström, Sven

doi:10.1073/pnas.97.11.5779

Cited by 16 publications

(7 citation statements)

References 22 publications

(25 reference statements)

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“…These results indicate that 12(S)-HETE signaling through a PTx sensitive GPCR is only partially responsible for this increased VEGF presence and that other mechanisms of ERK1/2 stimulation are at work, such as 12(S)-HETE interaction with some intracellular, as yet uncharacterized, receptor of 12(S)-HETE. In fact 12(S)-HETE can bind to a 50-kDa protein [37] that exists as part of a high molecular weight cytosolic binding complex [38]; however, the functional implications of binding to this receptor remain to be determined. In addition, it is possible that 12(S)-HETE may promote VEGF transcription by binding to the nuclear receptor peroxisome proliferated activating receptor gamma (PPARg) [39], thus bypassing signaling through MAPKs completely.…”

Section: Discussionmentioning

confidence: 99%

Vascular endothelial growth factor production in human prostate cancer cells is stimulated by overexpression of platelet 12-lipoxygenase

2006

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Section: Discussionmentioning

confidence: 99%

Vascular endothelial growth factor production in human prostate cancer cells is stimulated by overexpression of platelet 12-lipoxygenase

2006

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“…The latter high affinity binding sites (K d , 0.5 nM) were found to exist as a 50 kDa subunit within a 650 kDa cytosolic complex that also includes the heat shock proteins hsp70 and hsp90 and has been shown to occur in several cancer cell lines as well as in human platelets [94]. The 12S-HETE binding subunit dissociates from the complex in the presence of ATP and binds to NCOA1 (nuclear receptor coactivator-1) in the presence of 12S-HETE [125], suggesting that it may have a role in regulating gene transcription in the nucleus.…”

Section: Biological Actions Of Hetes and Oxoetesmentioning

confidence: 99%

Biosynthesis, biological effects, and receptors of hydroxyeicosatetraenoic acids (HETEs) and oxoeicosatetraenoic acids (oxo-ETEs) derived from arachidonic acid

Powell

Rokach

2015

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

258

206

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Arachidonic acid can be oxygenated by a variety of different enzymes, including lipoxygenases, cyclooxygenases, and cytochrome P450s, and can be converted to a complex mixture of oxygenated products as a result of lipid peroxidation. The initial products in these reactions are hydroperoxyeicosatetraenoic acids (HpETEs) and hydroxyeicosatetraenoic acids (HETEs). Oxoeicosatetraenoic acids (oxo-ETEs) can be formed by the actions of various dehydrogenases on HETEs or by dehydration of HpETEs. Although a large number of different HETEs and oxo-ETEs have been identified, this review will focus principally on 5-oxo-ETE, 5S-HETE, 12S-HETE, and 15S-HETE. Other related arachidonic acid metabolites will also be discussed in less detail. 5-Oxo-ETE is synthesized by oxidation of the 5-lipoxygenase product 5S-HETE by the selective enzyme, 5-hydroxyeicosanoid dehydrogenase. It actions are mediated by the selective OXE receptor, which is highly expressed on eosinophils, suggesting that it may be important in eosinophilic diseases such as asthma. 5-Oxo-ETE also appears to stimulate tumor cell proliferation and may also be involved in cancer. Highly selective and potent OXE receptor antagonists have recently become available and could help to clarify its pathophysiological role. The 12-lipoxygenase product 12S-HETE acts by the GPR31 receptor and promotes tumor cell proliferation and metastasis and could therefore be a promising target in cancer therapy. It may also be involved as a proinflammatory mediator in diabetes. In contrast, 15S-HETE may have a protective effect in cancer. In addition to GPCRs, higher concentration of HETEs and oxo-ETEs can activate peroxisome proliferator-activated receptors (PPARs) and could potentially regulate a variety of processes by this mechanism.

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“…Based on these findings, it is conceivable that 15(S)-HETE activates Src via a mechanism involving PKC. One study has reported that 12(S)-HETE binds to high affinity binding sites in the cytoplasm of lung carcinoma cells and thereby interacts with steroid receptor coactivator-1 (55). Although no further characterization was provided for these receptors, it is possible that 15(S)-HETE may also possess similar receptors in HRMVEC, which upon binding to 15(S)-HETE, may lead to activation of Src.…”

Section: Discussionmentioning

confidence: 99%

A novel role for activating transcription factor-2 in 15(S)-hydroxyeicosatetraenoic acid-induced angiogenesis

Zhao

Wang

Cheranov

et al. 2009

Journal of Lipid Research

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To investigate the mechanisms underlying 15(S)-HETE-induced angiogenesis, we have studied the role of the small GTPase, Rac1. We find that 15(S)-HETE activated Rac1 in human retinal microvascular endothelial cells (HRMVEC) in a time-dependent manner. Blockade of Rac1 by adenovirus-mediated expression of its dominant negative mutant suppressed HRMVEC migration as well as tube formation and Matrigel plug angiogenesis. 15(S)-HETE stimulated Src in HRMVEC in a time-dependent manner and blockade of its activation inhibited 15(S)-HETE-induced Rac1 stimulation in HRMVEC and the migration and tube formation of these cells as well as Matrigel plug angiogenesis. 15(S)-HETE stimulated JNK1 in Src-Rac1-dependent manner in HRMVEC and adenovirus-mediated expression of its dominant negative mutant suppressed the migration and tube formation of these cells and Matrigel plug angiogenesis. 15(S)-HETE activated ATF-2 in HRMVEC in Src-Rac1-JNK1-dependent manner and interference with its activation via adenovirus-mediated expression of its dominant negative mutant abrogated migration and tube formation of HRMVEC and Matrigel plug angiogenesis. In addition, 15(S)-HETEinduced MEK1 stimulation was found to be dependent on Src-Rac1 activation. Blockade of MEK1 activation inhibited 15(S)-HETE-induced JNK1 activity and ATF-2 phosphorylation. Together, these findings show that 15(S)-HETE activates ATF-2 via the Src-Rac1-MEK1-JNK1 signaling axis in HRMVEC leading to their angiogenic

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A 12( S )-hydroxyeicosatetraenoic acid receptor interacts with steroid receptor coactivator-1

Cited by 16 publications

References 22 publications

Vascular endothelial growth factor production in human prostate cancer cells is stimulated by overexpression of platelet 12-lipoxygenase

Vascular endothelial growth factor production in human prostate cancer cells is stimulated by overexpression of platelet 12-lipoxygenase

Biosynthesis, biological effects, and receptors of hydroxyeicosatetraenoic acids (HETEs) and oxoeicosatetraenoic acids (oxo-ETEs) derived from arachidonic acid

A novel role for activating transcription factor-2 in 15(S)-hydroxyeicosatetraenoic acid-induced angiogenesis

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