beta-Galactosidase

Publication Title: 
Oncogene

Cell cycle checkpoints and tumor suppressor gene functions appear to be required for the maintenance of a stable genome in proliferating cells. In this study chromosomal destabilization was monitored in relation to telomere structure, lifespan control and G2 checkpoint function. Replicative senescence was inactivated in secondary cultures of human skin fibroblasts by expressing the human papillomavirus type 16 (HPV-16) E6 oncoprotein to inactivate p53. Chromosome aberrations were enumerated during in vitro aging of isogenic control (F5neo) and HPV-16E6-expressing (F5E6) fibroblasts.

Author(s): 
Filatov, L.
Golubovskaya, V.
Hurt, J. C.
Byrd, L. L.
Phillips, J. M.
Kaufmann, W. K.
Publication Title: 
Biochemical and Biophysical Research Communications

Telomere is the repetitive DNA sequence at the end of chromosomes, which shortens progressively with cell division and limits the replicative potential of normal human somatic cells. L-carnosine, a naturally occurring dipeptide, has been reported to delay the replicative senescence, and extend the lifespan of cultured human diploid fibroblasts. In this work, we studied the effect of carnosine on the telomeric DNA of cultured human fetal lung fibroblast cells.

Author(s): 
Shao, Lan
Li, Qing-Huan
Tan, Zheng
Publication Title: 
Aging Cell

Fetal cardiomyocytes have been proposed as a potential source of cell-based therapy for heart failure. This study examined cellular senescence in cultured human fetal ventricular cardiomyocytes (HFCs). HFCs were isolated and identified by immunocytochemistry and RT-PCR. Cells were found to senesce after 20-25 population doublings, as determined by growth arrest, morphological changes and senescence-associated beta-galactosidase activity. Using the telomeric repeat amplification protocol assay, telomerase activity was undetectable in primary HFCs.

Author(s): 
Ball, Andrew J.
Levine, Fred
Publication Title: 
Free Radical Research

Previous studies have shown that glucose-6-phosphate dehydrogenase (G6PD)-deficient cells are under increased oxidative stress and undergo premature cellular senescence. The present study demonstrates that G6PD-deficient cells cultured under 3% oxygen concentration had an extended replicative lifespan, as compared with those cultured under atmospheric oxygen level. This was accompanied by a reduction in the number of senescence-associated beta-galactosidase (SA-beta-Gal) positive and morphologically senile cells at comparable population doubling levels (PDL).

Author(s): 
Ho, Hung-Yao
Cheng, Mei-Ling
Cheng, Pei-Fen
Chiu, Daniel Tsun-Yee
Publication Title: 
PloS One

BACKGROUND: Recent studies have demonstrated that activation of autophagy increases the lifespan of organisms from yeast to flies. In contrast to the lifespan extension effect in lower organisms, it has been reported that overexpression of unc-51-like kinase 3 (ULK3), the mammalian homolog of autophagy-specific gene 1 (ATG1), induces premature senescence in human fibroblasts. Therefore, we assessed whether the activation of autophagy would genuinely induce premature senescence in human cells.

Author(s): 
Kang, Hyun Tae
Lee, Ki Baek
Kim, Sung Young
Choi, Hae Ri
Park, Sang Chul
Publication Title: 
Methods in Molecular Biology (Clifton, N.J.)

Caloric restriction (CR) has been extensively documented for its profound role in effectively extending maximum lifespan in many different species. However, the accurate mechanisms, especially at the cellular level, for CR-induced aging delay are still under intense investigation. An emerging technique, recently explored in our laboratory, provides precisely controllable caloric intake in a cultured cellular system that allows real-time observation and quantitative analysis of the impact of CR on the molecular cellular level during the aging processes.

Author(s): 
Li, Yuanyuan
Tollefsbol, Trygve O.
Publication Title: 
Cell Cycle (Georgetown, Tex.)

Aging can be viewed as a quasi-programmed phenomenon driven by the overactivation of the nutrient-sensing mTOR gerogene. mTOR-driven aging can be triggered or accelerated by a decline or loss of responsiveness to activation of the energy-sensing protein AMPK, a critical gerosuppressor of mTOR.

Author(s): 
Menendez, Javier A.
Joven, Jorge
AragonËs, Gerard
BarrajÛn-Catal·n, Enrique
Beltr·n-DebÛn, Ra˙l
Borr·s-Linares, Isabel
Camps, Jordi
Corominas-Faja, Bruna
CufÌ, SÌlvia
Fern·ndez-Arroyo, Salvador
Garcia-Heredia, Anabel
Hern·ndez-Aguilera, Anna
Herranz-LÛpez, MarÌa
JimÈnez-S·nchez, Cecilia
LÛpez-Bonet, Eugeni
Lozano-S·nchez, Jes˙s
Luciano-Mateo, Fedra
Martin-Castillo, BegoÒa
Martin-Paredero, Vicente
PÈrez-S·nchez, Almudena
Oliveras-Ferraros, Cristina
Riera-Borrull, Marta
RodrÌguez-Gallego, Esther
Quirantes-PinÈ, Rosa
Rull, Anna
Tom·s-Menor, Laura
Vazquez-Martin, Alejandro
Alonso-Villaverde, Carlos
Micol, Vicente
Segura-Carretero, Antonio
Publication Title: 
Methods in Molecular Biology (Clifton, N.J.)

Caloric restriction (CR) has been extensively documented for its profound role in effectively extending maximum lifespan in many different species. However, the accurate mechanisms, especially at the cellular level, for CR-induced aging delay are still under intense investigation. An emerging technique, recently explored in our laboratory, provides precisely controllable caloric intake in a cultured cellular system that allows real-time observation and quantitative analysis of the impact of CR on the molecular cellular level during the aging processes.

Author(s): 
Li, Yuanyuan
Tollefsbol, Trygve O.
Publication Title: 
Cell Cycle (Georgetown, Tex.)

Aging can be viewed as a quasi-programmed phenomenon driven by the overactivation of the nutrient-sensing mTOR gerogene. mTOR-driven aging can be triggered or accelerated by a decline or loss of responsiveness to activation of the energy-sensing protein AMPK, a critical gerosuppressor of mTOR.

Author(s): 
Menendez, Javier A.
Joven, Jorge
AragonËs, Gerard
BarrajÛn-Catal·n, Enrique
Beltr·n-DebÛn, Ra˙l
Borr·s-Linares, Isabel
Camps, Jordi
Corominas-Faja, Bruna
CufÌ, SÌlvia
Fern·ndez-Arroyo, Salvador
Garcia-Heredia, Anabel
Hern·ndez-Aguilera, Anna
Herranz-LÛpez, MarÌa
JimÈnez-S·nchez, Cecilia
LÛpez-Bonet, Eugeni
Lozano-S·nchez, Jes˙s
Luciano-Mateo, Fedra
Martin-Castillo, BegoÒa
Martin-Paredero, Vicente
PÈrez-S·nchez, Almudena
Oliveras-Ferraros, Cristina
Riera-Borrull, Marta
RodrÌguez-Gallego, Esther
Quirantes-PinÈ, Rosa
Rull, Anna
Tom·s-Menor, Laura
Vazquez-Martin, Alejandro
Alonso-Villaverde, Carlos
Micol, Vicente
Segura-Carretero, Antonio
Publication Title: 
Methods in Molecular Biology (Clifton, N.J.)

Caloric restriction (CR) has been extensively documented for its profound role in effectively extending maximum lifespan in many different species. However, the accurate mechanisms, especially at the cellular level, for CR-induced aging delay are still under intense investigation. An emerging technique, recently explored in our laboratory, provides precisely controllable caloric intake in a cultured cellular system that allows real-time observation and quantitative analysis of the impact of CR on the molecular cellular level during the aging processes.

Author(s): 
Li, Yuanyuan
Tollefsbol, Trygve O.

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