Selective enrichment and biochemical characterization of seven human skin fibroblasts cell types in vitro

Hp, Rodemann; Bayreuther, Klaus; Pi, Francz; Dittmann, Klaus; Albiez, M

doi:10.1016/0014-4827(89)90214-0

Cited by 127 publications

(55 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Such stressful conditions include UV light (Bayreuther et al, 1988;Rodemann et al, 1989). To study the effect of UV light on caveolin-1 protein expression, NIH 3T3 cells were irradiated with subLDs of UV-C light (10 J/m 2 ).…”

Section: Uv Irradiation Up-regulates Caveolin-1 Protein Expressionmentioning

confidence: 99%

“…However, stressful stimuli can harmfully accelerate the process. Stressful conditions include exposure to hydrogen peroxide (H 2 O 2 ; Chen and Ames, 1994;Chen et al, 1998;Frippiat et al, 2001), UV light (Bayreuther et al, 1988;Rodemann et al, 1989), tert-butylhydroperoxide (Toussaint et al, 1992), hyperoxia (von Zglinicki et al, 1995), and radioactivity (Bumann et al, 1995). Cellular senescence may also be achieved when cells are passaged for a long period of time in culture (Thomas et al, 1997).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Expression of Caveolin-1 Induces Premature Cellular Senescence in Primary Cultures of Murine Fibroblasts

Volonté

Zhang

Lisanti

et al. 2002

MBoC

201

194

View full text Add to dashboard Cite

Caveolae are vesicular invaginations of the plasma membrane. Caveolin-1 is the principal structural component of caveolae in vivo. Several lines of evidence are consistent with the idea that caveolin-1 functions as a "transformation suppressor" protein. In fact, caveolin-1 mRNA and protein expression are lost or reduced during cell transformation by activated oncogenes. Interestingly, the human caveolin-1 gene is localized to a suspected tumor suppressor locus (7q31.1). We have previously demonstrated that overexpression of caveolin-1 arrests mouse embryonic fibroblasts in the G 0 /G 1 phase of the cell cycle through activation of a p53/p21-dependent pathway, indicating a role of caveolin-1 in mediating growth arrest. However, it remains unknown whether overexpression of caveolin-1 promotes cellular senescence in vivo. Here, we demonstrate that mouse embryonic fibroblasts transgenically overexpressing caveolin-1 show: 1) a reduced proliferative lifespan; 2) senescence-like cell morphology; and 3) a senescence-associated increase in ␤-galactosidase activity. These results indicate for the first time that the expression of caveolin-1 in vivo is sufficient to promote and maintain the senescent phenotype. Subcytotoxic oxidative stress is known to induce premature senescence in diploid fibroblasts. Interestingly, we show that subcytotoxic level of hydrogen peroxide induces premature senescence in NIH 3T3 cells and increases endogenous caveolin-1 expression. Importantly, quercetin and vitamin E, two antioxidant agents, successfully prevent the premature senescent phenotype and the up-regulation of caveolin-1 induced by hydrogen peroxide. Also, we demonstrate that hydrogen peroxide alone, but not in combination with quercetin, stimulates the caveolin-1 promoter activity. Interestingly, premature senescence induced by hydrogen peroxide is greatly reduced in NIH 3T3 cells harboring antisense caveolin-1. Importantly, induction of premature senescence is recovered when caveolin-1 levels are restored. Taken together, these results clearly indicate a central role for caveolin-1 in promoting cellular senescence and they suggest the hypothesis that premature senescence may represent a tumor suppressor function mediated by caveolin-1 in vivo. INTRODUCTIONCaveolae are vesicular invaginations of the plasma membrane. Caveolins are the structural components of caveolae. It has been proposed that caveolins participate in vesicular trafficking events and signal transduction processes (Lisanti et al., 1994;Couet et al., 1997a;Okamoto et al., 1998). Several independent lines of evidence suggest that signaling molecules are sequestered, organized, and functionally regulated by caveolae microdomains. These caveolin-interacting proteins include HaRas, Src-family tyrosine kinases, G protein ␣ subunits, endothelial nitric oxide synthase, epidermal growth factor receptor, Neu, protein kinase A, and protein kinase C (Smart et ., 1993;Lisanti et al., 1994;Shenoy-Scaria et al., 1994;Li et al., 1995;Schnitzer et al., 1995;Feron et al., 1996;Li...

show abstract

Section: Uv Irradiation Up-regulates Caveolin-1 Protein Expressionmentioning

confidence: 99%

mentioning

confidence: 99%

Expression of Caveolin-1 Induces Premature Cellular Senescence in Primary Cultures of Murine Fibroblasts

Volonté

Zhang

Lisanti

et al. 2002

MBoC

201

194

View full text Add to dashboard Cite

show abstract

“…Alternatively, it could be the result of the presence of increased numbers of specific fibroblast subpopulations with distinct growth characteristics as has been suggested in the setting of lung fibrosis and scleroderma (15,20,21,24,32). However, it is not known whether the pulmonary artery (PA) adventitia is composed of heterogeneous fibroblast subpopulations with unique functional characteristics and, if so, whether these fibroblast subpopulations contribute selectively to the fibroproliferative vascular changes observed in cases of severe hypoxia-induced pulmonary hypertension.The existence of phenotypic and functional heterogeneity among the resident fibroblast populations of different organs has been well described (6,19,26,34,36,37,39,43). Evidence of fibroblast heterogeneity within the same anatomical site or organ system has also been well documented (2,11,15,16,18,20,34).…”

mentioning

confidence: 99%

“…The existence of phenotypic and functional heterogeneity among the resident fibroblast populations of different organs has been well described (6,19,26,34,36,37,39,43). Evidence of fibroblast heterogeneity within the same anatomical site or organ system has also been well documented (2,11,15,16,18,20,34).…”

mentioning

confidence: 99%

Selective expansion of fibroblast subpopulations from pulmonary artery adventitia in response to hypoxia

Das

Dempsey

Reeves

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

mark. Selective expansion of fibroblast subpopulations from pulmonary artery adventitia in response to hypoxia. Am J Physiol Lung Cell Mol Physiol 282: L976-L986, 2002; 10.1152/ajplung.00382.2001.-Proliferation of fibroblasts contributes to the adventitial thickening observed during the development of hypoxia-induced pulmonary hypertension. However, whether all or only specific subpopulations of fibroblasts proliferate during this process is unknown. Because lung, skin, and gingiva contain multiple fibroblast subpopulations, we hypothesized that the pulmonary artery (PA) adventitia of neonatal calves is composed of multiple fibroblast subpopulations and that only selective subpopulations expand under chronic hypoxic conditions. Fibroblast subpopulations were isolated from PA adventitia of control calves using limited dilution cloning techniques. These subpopulations exhibited marked differences in morphology, actin expression, and serum-stimulated growth. Only select fibroblast subpopulations demonstrated the ability to proliferate in response to hypoxia. Fibroblast subpopulations were similarly isolated from calves exposed to hypoxia (14 days). With regard to morphology, actin expression, and serumstimulated growth of subpopulations, there were no obvious differences in fibroblast subpopulations between the hypoxic and the control calves. However, the number of fibroblast subpopulations with about a twofold increase in hypoxiainduced DNA synthesis was significantly greater in the hypoxic calves (26%) compared with control calves (10%). We conclude that the bovine PA adventitia comprises numerous phenotypically and biochemically distinct fibroblast subpopulations and that select subpopulations expand in response to chronic hypoxia. fibrosis; vascular disease; vascular remodeling; fibroblast growth; hypoxia-induced proliferation HYPOXIA-INDUCED pulmonary hypertension complicates the clinical course of many important lung diseases in both children and adults (23,42,46). The pulmonary hypertension and accompanying structural remodeling is particularly severe in infants, and often the earliest and most dramatic structural changes are found in the adventitial compartment of the vessel wall (31,46). In animal models, the resident adventitial fibroblasts have been shown to exhibit early and sustained increases in proliferation and matrix protein synthesis under hypoxic conditions, and these changes have been associated with luminal narrowing and a progressive decrease in the ability of the vessel wall to respond to vasodilating stimuli (3,23,30,45,46). Furthermore, in response to different stimuli, adventitial fibroblasts isolated from hypoxia-induced pulmonary hypertensive neonatal calves demonstrate greater growth capabilities than those from control animals (8), which could be the result of a generalized or polyclonal activation of resident adventitial fibroblasts. Alternatively, it could be the result of the presence of increased numbers of specific fibroblast subpopulations with distinct growth characteristics a...

show abstract

“…Among the multiple papers which dealt with the effects of UVB on different cell types, very few studies were aimed at the long-term effect of UVB on the appearance of SIPS in HDFs. Earlier studies used UV light but without discriminating the wavelength used and were very descriptive since they were restricted to the description of morphological changes and appearance/disappearance of spots on two-dimensional electrophoreses [13]. Short subcytotoxic oxidative stress protocols have already been used to induce SIPS (for a review, see [2]).…”

Section: Discussionmentioning

confidence: 99%

UVB-induced premature senescence of human diploid skin fibroblasts

Chainiaux

Magalhães

Eliaers

et al. 2002

The International Journal of Biochemistry & Cell Biology

View full text Add to dashboard Cite

In this work, we show that repeated stresses with UVB (290-320 nm) induce stress-induced premature senescence (SIPS) of skin human diploid fibroblasts (HDFs). HDFs at early cumulative population doublings were exposed three or five times to increasing subcytotoxic doses of UVB with one stress per day. After 2 days of recovery, several biomarkers of replicative senescence were established. First, there was an increase in the proportion of cells positive for senescence-associated ␤-galactosidase activity. Second, there was a loss of replicative potential as assessed by a very low level of [ 3 H]-thymidine incorporation. Third, the steady-state level of the mRNA of three senescence-associated genes, i.e. fibronectin, osteonectin and SM22, was increased in HDFs at 72 h after three and five exposures to UVB. In conclusion, these results suggest that it is possible to induce SIPS in HDFs after repeated exposures to subcytotoxic doses of UVB. This model could be used to test whether HDFs in UVB-induced premature senescence are able to promote epithelial cell growth and tumorigenesis in skin, as shown recently with HDFs in H 2 O 2 -induced premature senescence.

show abstract

Selective enrichment and biochemical characterization of seven human skin fibroblasts cell types in vitro

Cited by 127 publications

References 6 publications

Expression of Caveolin-1 Induces Premature Cellular Senescence in Primary Cultures of Murine Fibroblasts

Expression of Caveolin-1 Induces Premature Cellular Senescence in Primary Cultures of Murine Fibroblasts

Selective expansion of fibroblast subpopulations from pulmonary artery adventitia in response to hypoxia

UVB-induced premature senescence of human diploid skin fibroblasts

Contact Info

Product

Resources

About