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http://purl.uniprot.org/citations/22231515http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Objective

Mutations in LMNA encoding the A-type lamins cause several diseases, including those with features of premature aging and skeletal abnormalities. The aim of this study was to examine the expression of lamin A in cartilage from patients with osteoarthritis (OA) and the effects of its overexpression on chondrocyte senescence and apoptosis.

Methods

Human chondrocyte-like cells (SW-1353) were used. RNA isolated from human OA and non-OA cartilage was used for profiling messenger RNA expression, using Affymetrix microarray analysis. The effects of lamin A overexpression on mitochondrial function and apoptosis were examined by assessing mitochondrial membrane potential, ATP levels, and cytochrome c release, and with a TUNEL assay. Western blotting was performed to determine protein expression.

Results

Lamin A expression was markedly elevated in OA cartilage samples compared with non-OA control samples. Western blot analysis confirmed increased expression of lamin A in OA compared with non-OA cartilage. Interleukin-1β treatment inhibited lamin A accumulation, whereas treatment with prostaglandin E(2) (PGE(2) ) caused a marked increase in lamin A accumulation. These effects of exogenous PGE(2) on lamin A expression were mediated via the EP(2) /EP(4) receptors. Transfected chondrocytes that expressed lamin A displayed markers of early senescence/apoptosis.

Conclusion

The results of this study suggest that lamin A is up-regulated in OA chondrocytes, and that increased nuclear accumulation of lamin A in response to catabolic stress may account for the premature aging phenotype and apoptosis of OA chondrocytes."xsd:string
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http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/author"Yang Q."xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/author"Abramson S.B."xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/author"Palmer G."xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/author"Worman H.J."xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/author"Attur M."xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/author"Al-Mussawir H.E."xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/author"Ben-Artzi A."xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/name"Arthritis Rheum"xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/pages"1940-1949"xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/title"Perturbation of nuclear lamin A causes cell death in chondrocytes."xsd:string
http://purl.uniprot.org/citations/22231515http://purl.uniprot.org/core/volume"64"xsd:string
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