Difference between revisions of "Albertini 2012 Abstract Bioblast"
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{{Abstract | {{Abstract | ||
|title=Albertini E (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Mitochondr Physiol Network 17.12. | |title=Albertini E, Koziel R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Mitochondr Physiol Network 17.12. | ||
|info=[[MiPNet17.12 Bioblast 2012|MiPNet17.12 Bioblast 2012 - Open Access]] | |info=[[MiPNet17.12 Bioblast 2012|MiPNet17.12 Bioblast 2012 - Open Access]] | ||
|authors=Albertini E, | |authors=Albertini E, Koziel R, Duerr A, Neuhaus M, Jansen-Duerr P | ||
|year=2012 | |year=2012 | ||
|event=[[Bioblast 2012]] | |event=[[Bioblast 2012]] | ||
|abstract=Availability of methionine is known to modulate the rate of aging in model organisms, best illustrated by the observation that dietary methionine restriction extends the lifespan of rodents. However, the underlying mechanisms are incompletely understood. In eukaryotic cells, methionine can be converted to cysteine through the reverse transsulfuration pathway thereby modulating intracellular methionine availability. Whereas previous results obtained in yeast and fruit flies suggest that alterations in the reverse transsulfuration pathway modulate the rate of aging, it is not known whether this function is conserved in evolution. Here we show that depletion of cystathionine beta synthase (CBS), a rate limiting enzyme in the reverse transsulfuration pathway, induces premature senescence in human endothelial cells. We found that CBS depletion induces mild mitochondrial dysfunction and increases the sensitivity of endothelial cells to homocysteine, a known inducer of endothelial cell senescence and an established risk factor for vascular disease. Our finding that CBS deficiency induces endothelial cell senescence in vitro, involving both mitochondrial dysfunction and increased susceptibility of the cells to homocysteine, suggests a new mechanism linking CBS deficiency to vascular aging and disease. Β | |abstract=Availability of methionine is known to modulate the rate of aging in model organisms, best illustrated by the observation that dietary methionine restriction extends the lifespan of rodents. However, the underlying mechanisms are incompletely understood. In eukaryotic cells, methionine can be converted to cysteine through the reverse transsulfuration pathway thereby modulating intracellular methionine availability. Whereas previous results obtained in yeast and fruit flies suggest that alterations in the reverse transsulfuration pathway modulate the rate of aging, it is not known whether this function is conserved in evolution. Here we show that depletion of cystathionine beta synthase (CBS), a rate limiting enzyme in the reverse transsulfuration pathway, induces premature senescence in human endothelial cells. We found that CBS depletion induces mild mitochondrial dysfunction and increases the sensitivity of endothelial cells to homocysteine, a known inducer of endothelial cell senescence and an established risk factor for vascular disease. Our finding that CBS deficiency induces endothelial cell senescence in vitro, involving both mitochondrial dysfunction and increased susceptibility of the cells to homocysteine, suggests a new mechanism linking CBS deficiency to vascular aging and disease. | ||
|keywords=Methionine, Cysteine, Aging, HUVEC, Cystathionine beta synthase Β | |keywords=Methionine, Cysteine, Aging, HUVEC, Cystathionine beta synthase | ||
|mipnetlab=AT Innsbruck Jansen-Duerr P, | |mipnetlab=AT Innsbruck Jansen-Duerr P, | ||
|journal=Mitochondr Physiol Network | |journal=Mitochondr Physiol Network | ||
Revision as of 11:50, 12 November 2012
| Albertini E, Koziel R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Mitochondr Physiol Network 17.12. |
Link: MiPNet17.12 Bioblast 2012 - Open Access
Albertini E, Koziel R, Duerr A, Neuhaus M, Jansen-Duerr P (2012)
Event: Bioblast 2012
Availability of methionine is known to modulate the rate of aging in model organisms, best illustrated by the observation that dietary methionine restriction extends the lifespan of rodents. However, the underlying mechanisms are incompletely understood. In eukaryotic cells, methionine can be converted to cysteine through the reverse transsulfuration pathway thereby modulating intracellular methionine availability. Whereas previous results obtained in yeast and fruit flies suggest that alterations in the reverse transsulfuration pathway modulate the rate of aging, it is not known whether this function is conserved in evolution. Here we show that depletion of cystathionine beta synthase (CBS), a rate limiting enzyme in the reverse transsulfuration pathway, induces premature senescence in human endothelial cells. We found that CBS depletion induces mild mitochondrial dysfunction and increases the sensitivity of endothelial cells to homocysteine, a known inducer of endothelial cell senescence and an established risk factor for vascular disease. Our finding that CBS deficiency induces endothelial cell senescence in vitro, involving both mitochondrial dysfunction and increased susceptibility of the cells to homocysteine, suggests a new mechanism linking CBS deficiency to vascular aging and disease.
β’ Keywords: Methionine, Cysteine, Aging, HUVEC, Cystathionine beta synthase
β’ O2k-Network Lab: AT Innsbruck Jansen-Duerr P
Labels:
HRR: Oxygraph-2k
Affiliations and author contributions
Institute for Biomedical Aging Research, University of Innsbruck, Rennweg 10, 6020 Innsbruck, Austria - e-mail: [email protected]
