Stereocalpin A inhibits the expression of adhesion molecules in activated vascular smooth muscle cells

Byeon, Hye-Eun; Park, Bong‐Kyun; Yim, Joung Han; Lee, Hong Kum; Moon, Eun‐Yi; Rhee, Dong‐Kwon; Pyo, Suhkneung

doi:10.1016/j.intimp.2011.11.020

Cited by 18 publications

(16 citation statements)

References 45 publications

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“…Ramalina terebrata Hook and Taylor from the Antarctic is the producer of usnic acid, ramalin, stereocalpin A and usimines A–C [40,41,42,43]. Besides, it has been reported from the Ramalina genus isousnic acid, usninic acid, the following depsides sekikaic acid and its 5-OH, 5-Cl derivatives, 4′- O -methylsekikaic acid, 4′- O -demethylsekikaic acid, 4′- O -methylnorsekikaic, 2′- O -methylsekikaic, homosekikaic acid, 4′- O -methylnorhomosekikaic acid, 4′- O -demethylhomosekikaic acid, atranorin, chloroatranorin, divaricatic acid, ramalinolic acid, obtusatic acid, chlorotumidulin, evernic acid, diffractaic acid, 4′- O -demethylbarbatic acid, ramalinaic acid, cryptochlorophaeic acid and its 4,4′-dimethyl derivative, gyrophoric acid, trivaric acid, perlatolic acid, 4′- O -methylpaludosic acid, boninic acid, stenosporic acid, olivetoric acid, paludosic acid, lecanoric acid, and bourgeanic acid.…”

Section: Resultsmentioning

confidence: 99%

Secondary Metabolites in Ramalina terebrata Detected by UHPLC/ESI/MS/MS and Identification of Parietin as Tau Protein Inhibitor

Cornejo

Salgado

Caballero

et al. 2016

IJMS

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Liquid chromatography coupled with mass spectrometry is an outstanding methodology for fast analysis of phenolic compounds in biological samples. Twenty two compounds were quickly and accurately identified in the methanolic extract of the Antarctic lichen Ramalina terebrata for the first time using ultra high pressure liquid chromatography coupled with photodiode array detector and high resolution mass spectrometry (UHPLC-PDA-Q/Orbitrap/MS/MS). In addition, the extract and the four compounds isolated from this species were tested for the inhibitory activity of tau protein aggregation, which is a protein involved in Alzheimer’s disease (AD). All compounds showed null activity with the exception of parietin, which it was able to inhibit aggregation process of tau in a concentration range between 3 µg/mL (10 µM) to 28 µg/mL (100 µM). In addition, we show how parietin interact with tau 306VQIVYK311 hexapeptide inside of the microtubule binding domain (4R) with the help of molecular docking experiments. Finally, the constituents present in the methanolic extract could possibly contribute to the established anti-aggregation activity for this extract and this in-depth analysis of the chemical composition of R. terebrata could guide further research into its medicinal properties and potential uses.

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Section: Resultsmentioning

confidence: 99%

Secondary Metabolites in Ramalina terebrata Detected by UHPLC/ESI/MS/MS and Identification of Parietin as Tau Protein Inhibitor

Cornejo

Salgado

Caballero

et al. 2016

IJMS

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“…17) Briefly, VSMCs were grown in 96-well plates and pretreated with ramalin (0.1-10 μg/mL) for 2 h. The cells were washed with medium to remove ramalin and incubated with fresh growth medium containing TNF-α (10 ng/ mL) for 6 h. The medium was removed from the wells and BCECF [2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein]-labeled THP-1 cells (2.5 × 10 5 cells/ mL) in 0.2 mL medium were added to each well. The test and control samples were tested in triplicate in each experiment.…”

Section: Cell Adhesion Assaymentioning

confidence: 99%

Ramalin inhibits VCAM-1 expression and adhesion of monocyte to vascular smooth muscle cells through MAPK and PADI4-dependent NF-kB and AP-1 pathways

Park

Yim

Lee

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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Cell adhesion molecules play a critical role in inflammatory processes and atherosclerosis. In this study, we investigated the effect of ramalin, a chemical compound from the Antarctic lichen Ramalina terebrata, on vascular cell adhesion molecule-1 (VCAM-1) expression induced by TNF-α in vascular smooth muscular cells (VSMCs). Pretreatment of VSMCs with ramalin (0.1–10 μg/mL) concentration-dependently inhibited TNF-α-induced VCAM-1 expression. Additionally, ramalin inhibited THP-1 (human acute monocytic leukemia cell line) cell adhesion to TNF-α-stimulated VSMCs. Ramalin suppressed TNF-α-induced production of reactive oxygen species (ROS), PADI4 expression, and phosphorylation of p38, ERK, and JNK. Moreover, ramalin inhibited TNF-α-induced translocation of NF-κB and AP-1. Inhibition of PADI4 expression by small interfering RNA or the PADI4-specific inhibitor markedly attenuated TNF-α-induced activation of NF-κB and AP-1 and VCAM-1 expression in VSMCs. Our study provides insight into the mechanisms underlying ramalin activity and suggests that ramalin may be a potential therapeutic agent to modulate inflammation within atherosclerosis.

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“…These results suggest that suppression of intracellular ROS production could be only partially translated into inhibition of NF-κB activation and its downstream adhesion molecule expression in TNF-α-stimulated HASMCs. These findings suggest that smooth muscle cell dysfunction may occur through ROS activation (23,24). In addition, adhesion molecule expression has shown to occur with stimulation of the NF-κB signaling pathway, through the induction of ROS (25).…”

Section: Resultsmentioning

confidence: 98%

“…In addition, adhesion molecule expression has shown to occur with stimulation of the NF-κB signaling pathway, through the induction of ROS (25). Furthermore, ROS activates various transcription factors in vascular cells and may function as a signal in various pathways leading to NF-κB and MAPK activation (24,26-28). To investigate the signaling pathways involved, we tested the effects of P. vulgaris extract on the activation of the mitogen-activated protein kinases (MAPKs) p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK).…”

Section: Resultsmentioning

confidence: 99%

The protective effect of Prunella vulgaris ethanol extract against vascular inflammation in TNF-α-stimulated human aortic smooth muscle cells

Park¹,

Koo²,

Sung³

et al. 2013

BMB Reports

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Atherosclerosis, which manifests as acute coronary syndrome, stroke, and peripheral arterial diseases, is a chronic inflammatory disease of the arterial wall. Prunella vulgaris, a perennial herb with a worldwide distribution, has been used as a traditional medicine in inflammatory disease. Here, we investigated the effects of P. vulgaris ethanol extract on TNF-α-induced inflammatory responses in human aortic smooth muscle cells (HASMCs). We found that P. vulgaris ethanol extract inhibited adhesion of monocyte/macrophage-like THP-1 cells to activated HASMCs. It also decreased expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and ROS, No production in TNF-α-induced HASMCs and reduced NF-kB activation. Furthermore, P. vulgaris extract suppressed TNF-α-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK). These results demonstrate that P. vulgaris possesses antiinflammatory properties and can regulate TNF-α-induced expression of adhesion molecules by inhibiting the p38 MAPK/ ERK signaling pathway. [BMB Reports 2013; 46(7): 352-357]

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Stereocalpin A inhibits the expression of adhesion molecules in activated vascular smooth muscle cells

Cited by 18 publications

References 45 publications

Secondary Metabolites in Ramalina terebrata Detected by UHPLC/ESI/MS/MS and Identification of Parietin as Tau Protein Inhibitor

Secondary Metabolites in Ramalina terebrata Detected by UHPLC/ESI/MS/MS and Identification of Parietin as Tau Protein Inhibitor

Ramalin inhibits VCAM-1 expression and adhesion of monocyte to vascular smooth muscle cells through MAPK and PADI4-dependent NF-kB and AP-1 pathways

The protective effect of Prunella vulgaris ethanol extract against vascular inflammation in TNF-α-stimulated human aortic smooth muscle cells

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