Fibronectin expression increases during in vitro cellular senescence: Correlation with increased cell area☆
References (35)
- et al.
Exp. Cell Res
(1961) Exp. Cell Res
(1965)- et al.
Cell Biol. Int. Rep
(1983) - et al.
Mech. Ageing Dev
(1984) - et al.
Mech. Ageing Dev
(1981) - et al.
J. Biol. Chem
(1988) - et al.
Mech. Ageing Dev
(1984) - et al.
Anal. Biochem
(1987) - et al.
Cell
(1987) - et al.
Exp. Cell Res
(1989)
Anal. Biochem
Exp. Cell Res
Mech. Ageing Dev
Cell
Exp. Gerontol
Biochim. Biophys. Acta
J. Cell Biol
Cited by (106)
Role of Xeroderma pigmentosum D (XPD) protein in genome maintenance in human cells under oxidative stress
2022, Mutation Research - Genetic Toxicology and Environmental MutagenesisCitation Excerpt :Morphology of the cells was photographed using an Olympus C-7070 WZ digital camera (Japan). Cells have been shown to increase in size during senescence [46]. On days of harvest, trypsinised cells were observed under a light microscope and measured for cell diameter using a micrometre eyepiece.
The role of senescence in cancer development
2020, Seminars in Cancer BiologyCitation Excerpt :In detail, collagen and collagenous proteins show lower expression in senescent cells, in parallel to the down-regulation of prolyl 4-hydroxylase that catalyzes collagen biosynthesis [103,127,128,130,133,137,141,146,147]. Elastin has been demonstrated to be down-regulated in senescent cells [103,127], as well, in contrast to fibronectin, tenascin and laminin that have been found to be induced [103,146,148–152]. Regarding proteoglycans, they have been mainly shown to be underexpressed and to display modifications concerning their molecular size, binding properties, etc. in senescent fibroblasts, chondrocytes, endothelial cells, VSMCs and IVD cells or in vivo in the skin [132,134,153–158].
In vitro aged, hiPSC-origin engineered heart tissue models with age-dependent functional deterioration to study myocardial infarction
2019, Acta BiomaterialiaCitation Excerpt :They showed that 16% of myocytes and 14% of stem cells found in the aged hearts without any disease condition were senescent. Human cardiomyocytes have been shown to enlarge with age in vivo [56], and the increase in cell area, in general, is another indicator of cellular senescence [57]. We quantified the cell area of iCMs at the early end and later end of 120 day-long culture (Fig. 5C).
Extracellular matrix alterations in senescent cells and their significance in tissue homeostasis
2019, Matrix BiologyCitation Excerpt :Another fibrous protein of ECM, elastin, has a similar fate during cell senescence [55,66], although the enzyme lysyl oxidase (LOX) involved in the cross-linking of elastin and collagen precursors (tropoelastin and tropocollagen, respectively) is up-regulated in senescent VSMCs [83]. On the other hand, fibronectin expression is induced in senescent cells, such as fibroblasts, ECs, and VSMCs [83,90–93], similarly to the expression of tenascin and laminin in senescent ECs [55,94]. Proteoglycan (PG) synthesis at least regarding the small leucine-rich PGs (SLRPs) and the modular PGs [95] has also been reported to decrease as cells approach senescence, in various cell types, such as fibroblasts, chondrocytes, and IVD cells [74,96,97].
Alteration of Golgi structure in senescent cells and its regulation by a G protein γ subunit
2011, Cellular SignallingCitation Excerpt :The consistently altered appearance of the Golgi in both stress induced senescent cells and replicatively senescent cells suggests that the Golgi structure could serve as a useful marker for cellular senescence. Senescent cells show significantly increased secretion of cytokines such as IL-6 and IL-8; growth factors such as VEGF and extracellular matrix proteins such as fibronectin [1,19,27]. One potential reason for the alteration in the structure of the Golgi complex could be that it is a result of the increased secretion of various proteins which traffic from the Golgi to the plasma membrane.
Electric currents of 448 kHz upregulate anti-senescence pathways in human dermal fibroblasts
2024, Journal of Cosmetic Dermatology
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This work was supported in part by grants from the National Institute on Aging, P01-AG07123 and T32-AG00183.