Effects of hypocrellin A on expression of vascular endothelial growth factor and endothelin-1 in human umbilical endothelial cells

Dang, L; Seale, PJ; Qu, X

Effects of hypocrellin A on expression of vascular endothelial growth factor and endothelin-1 in human umbilical endothelial cells

Dang, L Seale, PJ Qu, X

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Publication Type:: Journal Article
Citation:: American Journal of Chinese Medicine, 2007, 35 (4), pp. 713 - 723
Issue Date:: 2007-08-30

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Field	Value	Language
dc.contributor.author	Dang, L	en_US
dc.contributor.author	Seale, PJ	en_US
dc.contributor.author	Qu, X	en_US
dc.date.issued	2007-08-30	en_US
dc.identifier.citation	American Journal of Chinese Medicine, 2007, 35 (4), pp. 713 - 723	en_US
dc.identifier.issn	0192-415X	en_US
dc.identifier.uri	http://hdl.handle.net/10453/4651
dc.description.abstract	Increased endothelin-1 (ET-1), vascular endothelial growth factor (VEGF) and activation of protein kinase C (PKC) are co-contributors to endothelial hyperpermeability in diabetes. Several lines of evidence have suggested a hypothesis that activation of specific PKC isoforms are the causative factor in ET-1 and VEGF mediated endothelial dysfunction. In the present study, we tested this hypothesis with hypocrellin A, a naturally occurring PKC inhibitor from a Chinese plant. Human umbilical vein endothelial cells (HUVECs) were incubated with 20 mM glucose in both the presence and absence of hypocrellin A, after which, the protein expression and release of VEGF and mRNA expression and release of ET-1 were measured. VEGF and ET-1 were released into the medium and expressions of VEGF protein and ET-1 mRNA were significantly increased in HUVECs incubated with 20 mM glucose. Hypocrellin A (150 nM) significantly decreased VEGF release (117 ± 3 vs. 180 ± 11 pg/mg, p <0.05) and VEGF protein expression (from 130 ± 14% to 88 ± 18.5%, p <0.05). ET-1 release was also reduced in hypocrellin A treated HUVECs (63.3 ± 9.9 vs. 75.2 ± 12.6 ng/mg). Hypocrellin A significantly reversed the effect of high glucose on ET-1 mRNA expression (p < 0.05). The results revealed that PKC activation plays a pivotal role in VEGF and ET-1 mediated endothelial permeability. The naturally occurring compound hypocrellin A may be a potentially novel treatment for endothelial dysfunction in diabetes. © 2007 World Scientific Publishing Company Institute for Advanced Research in Asian Science and Medicine.	en_US
dc.relation.ispartof	American Journal of Chinese Medicine	en_US
dc.relation.isbasedon	10.1142/S0192415X0700520X	en_US
dc.subject.classification	Complementary & Alternative Medicine	en_US
dc.subject.mesh	Endothelium, Vascular	en_US
dc.subject.mesh	Cells, Cultured	en_US
dc.subject.mesh	Umbilical Cord	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Hypocreales	en_US
dc.subject.mesh	Mannitol	en_US
dc.subject.mesh	Quinones	en_US
dc.subject.mesh	Perylene	en_US
dc.subject.mesh	Protein Kinase C	en_US
dc.subject.mesh	Glucose	en_US
dc.subject.mesh	Vascular Endothelial Growth Factor A	en_US
dc.subject.mesh	Endothelin-1	en_US
dc.subject.mesh	RNA, Messenger	en_US
dc.subject.mesh	Drugs, Chinese Herbal	en_US
dc.subject.mesh	Enzyme Activation	en_US
dc.title	Effects of hypocrellin A on expression of vascular endothelial growth factor and endothelin-1 in human umbilical endothelial cells	en_US
dc.type	Journal Article
utslib.citation.volume	4	en_US
utslib.citation.volume	35	en_US
utslib.for	1104 Complementary and Alternative Medicine	en_US
utslib.for	11 Medical and Health Sciences	en_US
dc.location.activity	ISI:000249451000016	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	closed_access
pubs.issue	4	en_US
pubs.publication-status	Published	en_US
pubs.volume	35	en_US

Abstract:

Increased endothelin-1 (ET-1), vascular endothelial growth factor (VEGF) and activation of protein kinase C (PKC) are co-contributors to endothelial hyperpermeability in diabetes. Several lines of evidence have suggested a hypothesis that activation of specific PKC isoforms are the causative factor in ET-1 and VEGF mediated endothelial dysfunction. In the present study, we tested this hypothesis with hypocrellin A, a naturally occurring PKC inhibitor from a Chinese plant. Human umbilical vein endothelial cells (HUVECs) were incubated with 20 mM glucose in both the presence and absence of hypocrellin A, after which, the protein expression and release of VEGF and mRNA expression and release of ET-1 were measured. VEGF and ET-1 were released into the medium and expressions of VEGF protein and ET-1 mRNA were significantly increased in HUVECs incubated with 20 mM glucose. Hypocrellin A (150 nM) significantly decreased VEGF release (117 ± 3 vs. 180 ± 11 pg/mg, p <0.05) and VEGF protein expression (from 130 ± 14% to 88 ± 18.5%, p <0.05). ET-1 release was also reduced in hypocrellin A treated HUVECs (63.3 ± 9.9 vs. 75.2 ± 12.6 ng/mg). Hypocrellin A significantly reversed the effect of high glucose on ET-1 mRNA expression (p < 0.05). The results revealed that PKC activation plays a pivotal role in VEGF and ET-1 mediated endothelial permeability. The naturally occurring compound hypocrellin A may be a potentially novel treatment for endothelial dysfunction in diabetes. © 2007 World Scientific Publishing Company Institute for Advanced Research in Asian Science and Medicine.

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