2014
DOI: 10.18632/aging.100709
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Abstract: Vascular disease is one of the leading causes of death worldwide. Vascular repair, essential for tissue maintenance, is critically reduced during vascular disease and aging. Efficient vascular repair requires functional adult stem cells unimpaired by aging or mutation.One protein candidate for reducing stem cell–mediated vascular repair is progerin, an alternative splice variant of lamin A. Progerin results from erroneous activation of cryptic splice sites within the LMNA gene, and significantly increases duri… Show more

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Cited by 40 publications
(40 citation statements)
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References 58 publications
(78 reference statements)
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“…Immunostaining of cultured skin fibroblasts incubated with labeled elastin demonstrated internalization of extracellular elastin to lysosomes and its degradation by cathepsin K. Induction of its expression in fibroblasts was observed both in vitro and in vivo after exposure to long-wave UVA. In contrast to fibroblasts from young donors, cells from old donors failed to activate cathepsin K in response to UVA [23]. These data suggest a role of intracellular elastin degradation by cathepsin K in the formation of solar elastosis [24].…”
Section: Cathepsin Kmentioning
confidence: 69%
“…Immunostaining of cultured skin fibroblasts incubated with labeled elastin demonstrated internalization of extracellular elastin to lysosomes and its degradation by cathepsin K. Induction of its expression in fibroblasts was observed both in vitro and in vivo after exposure to long-wave UVA. In contrast to fibroblasts from young donors, cells from old donors failed to activate cathepsin K in response to UVA [23]. These data suggest a role of intracellular elastin degradation by cathepsin K in the formation of solar elastosis [24].…”
Section: Cathepsin Kmentioning
confidence: 69%
“…In agreement, disruption of LINC complex integrity, either in Laminopathic patient derived fibroblasts or by the over expression of the dominant negative nesprin KASH domain, triggers altered cell morphology and attenuates cell motility [13,29,30]. We have previously shown that prelamin A accumulation induces VSMC presenescence, yet whether age associated changes in NE architecture impact on VSMC motility remains unknown [28].…”
Section: Introductionmentioning
confidence: 93%
“…HGPS-derived fibroblasts display impaired cell motility, suggesting that coupling between the nuclear lamina and the cytoskeleton is critical for efficient cell migration [29,30]. In agreement, disruption of LINC complex integrity, either in Laminopathic patient derived fibroblasts or by the over expression of the dominant negative nesprin KASH domain, triggers altered cell morphology and attenuates cell motility [13,29,30].…”
Section: Introductionmentioning
confidence: 99%
“…Progerin accumulation is directly involved in the vascular disease associated with the syndrome [227]. FTase inhibition has proved to be beneficial for the alleviation of the condition [228,229]. In the clinical trials of progeric children, FTase inhibitor lonafarnib improved vascular function, bone structure, and audiological status [230].…”
Section: Farnesyltransferase (Protein Farnesyltransferase)mentioning
confidence: 99%