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Difference between revisions of "Albertini 2012 Aging (Albany NY)"

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{{Publication
{{Publication
|title=Albertini E, Kozieł R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Aging (Albany NY) 4: 664-673.
|title=Albertini E, Kozieł R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Aging (Albany NY) 4:664-73.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23117410 PMID: 23117410 Open Access]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23117410 PMID: 23117410 Open Access]
|authors=Albertini E, Kozieł R, Duerr A, Neuhaus M, Jansen-Duerr P
|authors=Albertini E, Koziel R, Duerr A, Neuhaus M, Jansen-Duerr P
|year=2012
|year=2012
|journal=Aging (Albany NY)
|journal=Aging (Albany NY)
|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.
|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
|keywords=Methionine, Cysteine, Cystathionine beta synthase
|mipnetlab=AT Innsbruck Jansen-Duerr P,
|mipnetlab=AT Innsbruck Jansen-Duerr P,
}}
}}
{{Labeling
{{Labeling
|model cell lines=HUVEC
|area=Respiration, Genetic knockout;overexpression
|diseases=Aging;senescence
|organism=Human
|tissues=Endothelial;epithelial;mesothelial cell, HUVEC
|preparations=Intact cells
|preparations=Intact cells
|enzymes=Complex I, Complex III
|enzymes=Complex I, Complex III
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Aging; Senescence, Genetic Defect; Knockdown; Overexpression
|topics=mt-Membrane potential
|topics=mt-Membrane potential
|couplingstates=LEAK, ROUTINE, ETS
|couplingstates=LEAK, ROUTINE, ET
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
}}
}}

Latest revision as of 13:06, 26 March 2018

Publications in the MiPMap
Albertini E, Kozieł R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Aging (Albany NY) 4:664-73.

» PMID: 23117410 Open Access

Albertini E, Koziel R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Aging (Albany NY)

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, Cystathionine beta synthase

O2k-Network Lab: AT Innsbruck Jansen-Duerr P


Labels: MiParea: Respiration, Genetic knockout;overexpression  Pathology: Aging;senescence 

Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell, HUVEC  Preparation: Intact cells  Enzyme: Complex I, Complex III  Regulation: mt-Membrane potential  Coupling state: LEAK, ROUTINE, ET 

HRR: Oxygraph-2k