A novel marine compound xyloketal B protects against oxidized LDL-induced cell injury in vitro

Chen, Wenliang; Qian, Yan; Meng, Wei-Feng; Pang, Jiyan; Lin, Yongcheng; Guan, Yong‐Yuan; Chen, Sheng-Pin; Liu, Jie; Pei, Zhong; Wang, Guan-Lei

doi:10.1016/j.bcp.2009.05.029

Cited by 76 publications

(104 citation statements)

References 34 publications

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“…Specifically, it attenuated oxLDL-stimulated NADPH oxidase production of ROS [6]. Interestingly, it also decreased the expression of two NADPH oxidase subunits, gp91phox and p47phox [6].…”

Section: Xyloketal B Protects Against Oxldl-induced Cell Injury and Amentioning

confidence: 90%

“…Xyloketal B was found to be cytoprotective and it dosedependently reduced oxLDL-induced damage in human umbilical vein endothelial cells (HUVECs) [6]. Specifically, it attenuated oxLDL-stimulated NADPH oxidase production of ROS [6].…”

Section: Xyloketal B Protects Against Oxldl-induced Cell Injury and Amentioning

confidence: 98%

“…Of these compounds, xyloketal B has shown: 1) to protect endothelial cells against oxidized low-density lipoprotein (oxLDL)-induced cell injury [6], 2) to provide antioxidant activity though heme oxygenase-1 (HO-1) in endothelial cells [7], 3) to reduce oxygen and glucose deprivation (OGD)-induced neuronal cell death in vitro in primary cortical cell culture [8], and for the first time 4) to reduce neonatal hypoxic-ischemic (HI) brain injury in vivo in mice [8]. Recent studies demonstrated that xyloketal B act by targeting free radicals [6,7,9,10], apoptotic proteins and mitochondrion proteins [6][7][8][9][10]. In addition, unpublished data from our lab revealed that xyloketal B was also an inhibitor of transient receptor potential melastatin 7 (TRPM7) which is a nonselective cation channel strongly implicated in neurodegenerative diseases.…”

Section: A Rt I C L E I N F O Abstractmentioning

confidence: 99%

“…Atherosclerosis is one of the leading causes of ischemic stroke and its pathogenesis largely involves the production of excessive reactive oxygen/nitrogen species via activation of NADPH oxidase, reduction of nitric oxide (NO) and decreased expression of the anti-apoptotic protein, B-cell lymphoma 2 (Bcl-2) [6].…”

Section: Xyloketal B Protects Against Oxldl-induced Cell Injury and Amentioning

confidence: 99%

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Effects of marine compound xyloketal B on neuroprotection and potential drug development

2015

J Coast Life Med

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“…Specifically, it attenuated oxLDL-stimulated NADPH oxidase production of ROS [6]. Interestingly, it also decreased the expression of two NADPH oxidase subunits, gp91phox and p47phox [6].…”

Section: Xyloketal B Protects Against Oxldl-induced Cell Injury and Amentioning

confidence: 90%

Section: Xyloketal B Protects Against Oxldl-induced Cell Injury and Amentioning

confidence: 98%

Section: A Rt I C L E I N F O Abstractmentioning

confidence: 99%

Section: Xyloketal B Protects Against Oxldl-induced Cell Injury and Amentioning

confidence: 99%

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Effects of marine compound xyloketal B on neuroprotection and potential drug development

2015

J Coast Life Med

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“…In particular, xyloketal A is a unique ketal compound with C-3 symmetry with cis-junction between tetrahydropyrane and tetrahydrofurane. We have previously demonstrated that xyloketals show a variety of activities, such as antioxidant (21), promoting endothelial cell nitric oxide (NO) production, inhibiting NADPH oxidase, and L-calcium channel blocking in different disease models (22)(23)(24). Xyloketals have been previously reported to inhibit Ca 2+ influx through blockade of L-type calcium channels, which raises the possibility that xyloketals might affect calcium signaling in diseases like chronic hypoxic pulmonary hypertension.…”

mentioning

confidence: 99%

A study on blocking store-operated Ca²⁺ entry in pulmonary arterial smooth muscle cells with xyloketals from marine fungi

Sun

Zheng

et al. 2017

Acta Pharmaceutica

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In this study, the effect of four xyloketals 1-4 on store-operated calcium entry (SOCE) was investigated in primary distal pulmonary arterial smooth muscle cells (PASMCs) isolated from mice. The results showed that xyloketal A (1), an unusual ketal with C-3 symmetry, exhibited strong SOCE blocking activity. Secretion of interleukin-8 (IL-8) was also inhibited by xyloketal A. The parallel artificial membrane permeability assay (PAMPA) of 1-4 suggested that these xyloketals penetrated easily through the cell membrane. Moreover, the molecular docking study of xyloketal A with activation region of the stromal interaction molecule (STIM) 1 and the calcium release-activated calcium modulator (ORAI) 1 (STIM1-ORAI1) protein complex, the key domain of SOCE, revealed that xyloketal A exhibited a noncovalent interaction with the key residue lysine 363 (LYS363) in the identified cytosolic regions in STIM1-C. These findings provided useful information about xyloketal A as a SOCE inhibitor for further evaluation.

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TRPM7 channel regulates ox‐LDL‐induced proliferation and migration of vascular smooth muscle cells via MEK‐ERK pathways

et al. 2016

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Transient receptor potential melastatin 7 (TRPM7) plays a key role in the pathophysiological response of multiple cell types. However, the role of TRPM7 channels in ox-LDL-induced proliferation and migration of VSMC remains unclear. This study used the thoracic aorta VSMCs to explore the effects of ox-LDL on cell proliferation and migration and to investigate the underlying molecular mechanisms and signaling pathways. Data demonstrated that ox-LDL significantly increased TRPM7 activity, and induced VSMC proliferation and migration. VSMC proliferation and migration were inhibited by nonspecific TRPM7 blocker 2-APB or synthetic siRNA targeting TRPM7. Furthermore, the phosphorylation of ERK1/2 and MEK1/2 associated with cell proliferation and migration decreased in TRPM7-deficient VSMC. Therefore, TRPM7 may constitute a useful target for the treatment of atherosclerosis.Keywords: MEK-ERK pathways; migration; proliferation; TRPM7; VSMCs Migration and excess proliferation of vascular smooth muscle cells (VSMCs) are involved in the pathogenesis of various vascular diseases, such as atherosclerosis [1]. Oxidized low-density lipoprotein (Ox-LDL) contributes to the atherosclerotic plaque formation and progression by several mechanisms, including the induction of endothelial cell activation and dysfunction, macrophage foam cell formation, and smooth muscle cell migration and proliferation [2]. Ox-LDL significantly increases VSMC migration and proliferation through the ERK1/2 signaling pathway [3]. However, the mechanisms underlying the effect of ox-LDL on atherosclerosis are not fully understood.Ion channels participate in cell proliferation in diverse types of cells, including vascular endothelial cells [4], cancer cells [5], smooth muscle cells [6], and mesenchymal stem cells [7]. Transient receptor potential melastatin 7 (TRPM7) channel, a member of TRP channel superfamily [8], is a widely expressed nonselective divalent cation (Ca 2+ and Mg 2+ ) channel with protein serine/threonine kinase activity that regulates diverse physiological/pathological processes, such as Mg 2+ homeostasis [9,10], hypoxic neuronal injury [11], and tumor cell growth/proliferation [12]. Activating TRPM7 channels may also contribute to the physiology/pathophysiology of cardiovascular and cerebrovascular diseases, including arterial calcification [13], atrial fibrillation [14], and hypertension [6,15]. However, little is known about the role of TRPM7 channels in atherosclerosis-related vasculopathy.Studies have shown that TRPM7 channels greatly participate in growth/proliferation and nitric oxide production of vascular endothelial cells [4], angiotensin IIinduced phenotype switching, and VSMC proliferation through the ERK pathway [6]. Although the presence and potential function of TRPM7 channels have been Abbreviations 2-APB, 2-aminoethoxydiphenyl borate; ang II, angiotensin II; DMSO, dimethyl sulfoxide; MAPK, mitogen-activated protein kinase; Ox-LDL, oxidized low-density lipoprotein; PDGF, platelet-derived growth factor; PLC, phospholipase C;...

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A novel marine compound xyloketal B protects against oxidized LDL-induced cell injury in vitro

Cited by 76 publications

References 34 publications

Effects of marine compound xyloketal B on neuroprotection and potential drug development

Effects of marine compound xyloketal B on neuroprotection and potential drug development

A study on blocking store-operated Ca²⁺ entry in pulmonary arterial smooth muscle cells with xyloketals from marine fungi

TRPM7 channel regulates ox‐LDL‐induced proliferation and migration of vascular smooth muscle cells via MEK‐ERK pathways

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A novel marine compound xyloketal B protects against oxidized LDL-induced cell injury in vitro

Cited by 76 publications

References 34 publications

Effects of marine compound xyloketal B on neuroprotection and potential drug development

Effects of marine compound xyloketal B on neuroprotection and potential drug development

A study on blocking store-operated Ca2+ entry in pulmonary arterial smooth muscle cells with xyloketals from marine fungi

TRPM7 channel regulates ox‐LDL‐induced proliferation and migration of vascular smooth muscle cells via MEK‐ERK pathways

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A study on blocking store-operated Ca²⁺ entry in pulmonary arterial smooth muscle cells with xyloketals from marine fungi