-
Something wrong with this record ?
Brassinosteroids inhibit in vitro angiogenesis in human endothelial cells
L. Rárová, S. Zahler, J. Liebl, V. Kryštof, D. Sedlák, P. Bartůněk, L. Kohout, M. Strnad,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Estrogen Receptor alpha metabolism MeSH
- Estrogen Receptor beta metabolism MeSH
- Brassinosteroids metabolism pharmacology MeSH
- Human Umbilical Vein Endothelial Cells drug effects metabolism MeSH
- Neovascularization, Physiologic drug effects MeSH
- Angiogenesis Inhibitors metabolism pharmacology MeSH
- Humans MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Antiangiogenic activity of the brassinosteroid plant hormones (BRs) and their derivative cholestanon was investigated in human umbilical vein endothelial cells (HUVEC) and in human microvascular endothelial cells (HMEC-1). 24-Epibrassinolide and 28-homocastasterone from group of 21 tested natural BRs inhibited migration of HUVEC cells. Seven tested BRs decreased the number of tubes significantly. Synthetic analogue cholestanon inhibited angiogenesis in vitro more effectively than natural BRs. Because of the similarity of BRs to human steroids, we have also studied interactions of BRs with human steroid receptors. Synthetic BRs cholestanon showed agonistic effects on estrogen-receptor-α, estrogen-receptor-β and androgen receptor. Of the natural BRs, 24-epibrassinolide was found to be a weak antagonist of estrogen-receptor-α (ERα). Our results provide the first evidence that large group of BRs can inhibit in vitro angiogenesis of primary endothelial cells. BRs constitute a novel group of human steroid receptor activators or inhibitors with capacity to inhibit angiogenesis.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc13024310
- 003
- CZ-PrNML
- 005
- 20130709103337.0
- 007
- ta
- 008
- 130703s2012 xxu f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1016/j.steroids.2012.08.011 $2 doi
- 035 __
- $a (PubMed)22974826
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xxu
- 100 1_
- $a Rárová, Lucie $u Centre of Region Haná for Biotechnological and Agricultural Research, Department of Growth Regulators, Faculty of Science, Palacký University, Šlechtitelů 11, 783 71 Olomouc, Czech Republic.
- 245 10
- $a Brassinosteroids inhibit in vitro angiogenesis in human endothelial cells / $c L. Rárová, S. Zahler, J. Liebl, V. Kryštof, D. Sedlák, P. Bartůněk, L. Kohout, M. Strnad,
- 520 9_
- $a Antiangiogenic activity of the brassinosteroid plant hormones (BRs) and their derivative cholestanon was investigated in human umbilical vein endothelial cells (HUVEC) and in human microvascular endothelial cells (HMEC-1). 24-Epibrassinolide and 28-homocastasterone from group of 21 tested natural BRs inhibited migration of HUVEC cells. Seven tested BRs decreased the number of tubes significantly. Synthetic analogue cholestanon inhibited angiogenesis in vitro more effectively than natural BRs. Because of the similarity of BRs to human steroids, we have also studied interactions of BRs with human steroid receptors. Synthetic BRs cholestanon showed agonistic effects on estrogen-receptor-α, estrogen-receptor-β and androgen receptor. Of the natural BRs, 24-epibrassinolide was found to be a weak antagonist of estrogen-receptor-α (ERα). Our results provide the first evidence that large group of BRs can inhibit in vitro angiogenesis of primary endothelial cells. BRs constitute a novel group of human steroid receptor activators or inhibitors with capacity to inhibit angiogenesis.
- 650 _2
- $a inhibitory angiogeneze $x metabolismus $x farmakologie $7 D020533
- 650 _2
- $a brassinosteroidy $x metabolismus $x farmakologie $7 D060406
- 650 _2
- $a alfa receptor estrogenů $x metabolismus $7 D047628
- 650 _2
- $a beta receptor estrogenů $x metabolismus $7 D047629
- 650 _2
- $a endoteliální buňky pupečníkové žíly (lidské) $x účinky léků $x metabolismus $7 D061307
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a fyziologická neovaskularizace $x účinky léků $7 D018919
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Zahler, Stefan $u -
- 700 1_
- $a Liebl, Johanna $u -
- 700 1_
- $a Kryštof, Vladimír $u -
- 700 1_
- $a Sedlák, David $u -
- 700 1_
- $a Bartůněk, Petr $u -
- 700 1_
- $a Kohout, Ladislav $u -
- 700 1_
- $a Strnad, Miroslav $u -
- 773 0_
- $w MED00004438 $t Steroids $x 1878-5867 $g Roč. 77, č. 13 (2012), s. 1502-9
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/22974826 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20130703 $b ABA008
- 991 __
- $a 20130709103800 $b ABA008
- 999 __
- $a ok $b bmc $g 987990 $s 822690
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2012 $b 77 $c 13 $d 1502-9 $i 1878-5867 $m Steroids $n Steroids $x MED00004438
- LZP __
- $a Pubmed-20130703
