Cytochemical Detection of a Senescence-Associated β-Galactosidase in Endothelial and Smooth Muscle Cells from Human and Rabbit Blood Vessels

Loo, Bernd van der; Fenton, Mark; Erusalimsky, Jorge D.

doi:10.1006/excr.1998.4035

Cited by 125 publications

(79 citation statements)

References 16 publications

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“…Senescence of VSMCs has been previously demonstrated using cultures derived from the rabbit (van der Loo et al 1998) This gradual decline in the proliferating fraction of VSMCs is probably associated with telomere shortening, resulting in an increasing likelihood of a cell becoming senescent with each serial passage. Evidence for telomere shortening in VSMCs has been provided by Matthews et al (2006), who also showed that telomere shortening in VSMCs was closely associated with increasing severity of atherosclerosis.…”

Section: Discussionmentioning

confidence: 81%

Microarray analysis of senescent vascular smooth muscle cells: A link to atherosclerosis and vascular calcification

Burton¹,

Giles²,

Sheerin³

et al. 2009

Experimental Gerontology

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International audienceLittle is known about the senescent phenotype of human vascular smooth muscle cells (VSMCs) and the potential involvement of senescent VSMCs in age-related vascular disease, such as atherosclerosis. As such, VSMCs were grown and characterised to generate senescent VSMCs needed for microarray analysis (Affymetrix). Comparative analysis of the transcriptome profiles of early (14 CPD) and late (39-42 CPD) passage VSMCs found a total of 327 probesets called as differentially expressed: 149 are up-regulated in senescence and 178 repressed (-value < 0.5%, minimum effect size of at least 2-fold differential regulation, explore data at www.madras.cf.ac.uk/vsmc). Data mining shows a differential regulation of genes at senescence associated with the development of atherosclerosis and vascular calcification. These included genes with roles in inflammation (IL1β, IL8, ICAM1, TNFAP3, ESM1 and CCL2), tissue remodelling (VEGF, VEGFβ, ADM and MMP14) and vascular calcification (MGP, BMP2, SPP1, OPG and DCN). The microarray data for IL1β, IL8 and MGP were validated by either, ELISA, Western blot analysis or RT-PCR. These data thus provide the first evidence for a role of VSMC senescence in the development of vascular calcification and provides further support for the involvement of senescent VSMCs in the progression of atherosclerosis

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Section: Discussionmentioning

confidence: 81%

Microarray analysis of senescent vascular smooth muscle cells: A link to atherosclerosis and vascular calcification

Burton¹,

Giles²,

Sheerin³

et al. 2009

Experimental Gerontology

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“…Cell morphology was evaluated under an Eclipse TS100 inverted phase microscope from Nikon (Melville, NY). Cytochemical staining of young (P4) and senescent (P18) cells for senescence-associated ␤-galactosidase (SA-␤-gal) was conducted as previously described (35). Total ␤-galactosidase activity in the cell lysates was assayed using a ␤-galactosidase assay kit from Stratagene (LaJolla, CA).…”

Section: Methodsmentioning

confidence: 99%

Identification of CD44 as a senescence-induced cell adhesion gene responsible for the enhanced monocyte recruitment to senescent endothelial cells

Mun

Boo

2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…CR has mixed effects on enzymatic activities associated with aging in lin − SVF Senescence associated β-galactosidase (SA β-gal) has long been used to identify senescence cells in culture (Dimri et al 1995;Serrano et al 1997;van der Loo et al 1998). To determine how age and CR affect − SVF cells with CR, when adjusted for the total amount of tissue, CR significantly increased the lin − cellular density of the white adipose tissue.…”

Section: Resultsmentioning

confidence: 99%

Caloric restriction attenuates the age-associated increase of adipose-derived stem cells but further reduces their proliferative capacity

Schmuck

Mulligan

Saupe

2010

AGE

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White adipose tissue is a promising source of mesenchymal stem cells. Currently, little is known about the effect of age and caloric restriction (CR) on adipose-derived stem cells (ASC). This is important for three reasons: firstly, age and CR cause extensive remodeling of WAT; it is currently unknown how this remodeling affects the resident stem cell population. Secondly, stem cell senescence has been theorized as one of the causes of aging and could reduce the utility of a stem cell as a reagent. Thirdly, the mechanism by which CR extends lifespan is currently not known, one theory postulates that CR maintains the resident stem cell population in youthful "fit" state. For the purpose of this study, we define ASC as lineage negative (lin − )/CD34 +(low) /CD31 − . We show that aging increases the abundance of ASC and the expression of Cdkn2a 9.8-fold and Isl1 60.6-fold.This would suggest that aging causes an accumulation of non-replicative ASC. CR reduced the percentage of ASC in the lin − SVF while also reducing colony forming ability. Therefore, CR appears to have antiproliferative effects on ASC that may be advantageous from the perspective of cancer, but our data raises the possibility that it may be disadvantageous for regenerative medicine applications.

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Cytochemical Detection of a Senescence-Associated β-Galactosidase in Endothelial and Smooth Muscle Cells from Human and Rabbit Blood Vessels

Cited by 125 publications

References 16 publications

Microarray analysis of senescent vascular smooth muscle cells: A link to atherosclerosis and vascular calcification

Microarray analysis of senescent vascular smooth muscle cells: A link to atherosclerosis and vascular calcification

Identification of CD44 as a senescence-induced cell adhesion gene responsible for the enhanced monocyte recruitment to senescent endothelial cells

Caloric restriction attenuates the age-associated increase of adipose-derived stem cells but further reduces their proliferative capacity

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