Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Albertini 2012 Abstract Bioblast"

From Bioblast
ย 
(10 intermediate revisions by 5 users not shown)
Line 7: Line 7:
|abstract=[[File:Eva albertini.jpg|right|150px|Eva Albertini]]
|abstract=[[File:Eva albertini.jpg|right|150px|Eva Albertini]]
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.
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.
# [[Albertini 2012 Aging (Albany NY)|Albertini E, Kozieล‚ R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Aging (Albany NY) (Epub ahead of print)]]
# [[Albertini 2012 Aging (Albany NY)|Albertini E, Kozieล‚ R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Aging (Albany NY) 4:664-73.]]
|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,
|journal=Mitochondr Physiol Network
|journal=Mitochondr Physiol Network
Line 14: Line 14:
}}
}}
{{Labeling
{{Labeling
|area=Respiration, Genetic knockout;overexpression
|diseases=Aging;senescence
|tissues=Endothelial;epithelial;mesothelial cell, HUVEC
|preparations=Intact cells
|topics=mt-Membrane potential
|couplingstates=LEAK, ROUTINE, ET
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Aging; Senescence, Genetic Defect; Knockdown; Overexpression
|model cell lines=HUVEC
|preparations=Intact Cell; Cultured; Primary
|couplingstates=LEAK, ROUTINE, ETS
|substratestates=CI, CIII
|topics=mt-Membrane potential
|journal=Mitochondr Physiol Network
|journal=Mitochondr Physiol Network
|articletype=Abstract
|articletype=Abstract
Line 32: Line 32:


== Help ==
== Help ==
* [[Abstracts help]]
* [[MitoPedia: Terms and abbreviations]]
* [[MitoPedia Glossary: Terms and abbreviations]]

Latest revision as of 13:14, 26 March 2018

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

Eva Albertini

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.

  1. Albertini E, Kozieล‚ R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Aging (Albany NY) 4:664-73.

โ€ข Keywords: Methionine, Cysteine, Cystathionine beta synthase

โ€ข O2k-Network Lab: AT Innsbruck Jansen-Duerr P


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


Tissue;cell: Endothelial;epithelial;mesothelial cell, HUVEC  Preparation: Intact cells 

Regulation: mt-Membrane potential  Coupling state: LEAK, ROUTINE, ET 

HRR: Oxygraph-2k 




Affiliations and author contributions

Institute for Biomedical Aging Research, University of Innsbruck, Rennweg 10, 6020 Innsbruck, Austria - e-mail: [email protected]

Help