Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT
  Spontaneously immortalized mouse embryo fibroblasts: growth behavior of wild-type and vimentin-deficient cells in relation to mitochondrial structure and activity

Tolstonog, G. V., Belichenko-Weitzmann, I. V., Lu, J.-P., Hartig, R., Shoeman, R. L., Traub, U., et al. (2005). Spontaneously immortalized mouse embryo fibroblasts: growth behavior of wild-type and vimentin-deficient cells in relation to mitochondrial structure and activity. DNA and Cell Biology, 24(11), 680-709. doi:10.1089/dna.2005.24.680.

Item is

Basisdaten

einblenden: ausblenden:
Genre: Zeitschriftenartikel
Alternativer Titel : Spontaneously immortalized mouse embryo fibroblasts: growth behavior of wild-type and vimentin-deficient cells in relation to mitochondrial structure and activity

Dateien

einblenden: Dateien
ausblenden: Dateien
:
DNACellBiol_24_2005_680.pdf (beliebiger Volltext), 2MB
 
Datei-Permalink:
-
Name:
DNACellBiol_24_2005_680.pdf
Beschreibung:
-
OA-Status:
Sichtbarkeit:
Eingeschränkt (Max Planck Institute for Medical Research, MHMF; )
MIME-Typ / Prüfsumme:
application/pdf
Technische Metadaten:
Copyright Datum:
-
Copyright Info:
-
Lizenz:
-

Externe Referenzen

einblenden:
ausblenden:
externe Referenz:
http://online.liebertpub.com/doi/pdf/10.1089/dna.2005.24.680 (beliebiger Volltext)
Beschreibung:
-
OA-Status:
externe Referenz:
https://doi.org/10.1089/dna.2005.24.680 (beliebiger Volltext)
Beschreibung:
-
OA-Status:

Urheber

einblenden:
ausblenden:
 Urheber:
Tolstonog, Genrich V., Autor
Belichenko-Weitzmann, Irina V., Autor
Lu, Jian-Ping, Autor
Hartig, Roland, Autor
Shoeman, Robert L.1, Autor           
Traub, Ulrike, Autor
Traub, Peter, Autor
Affiliations:
1Department of Biomolecular Mechanisms, Max Planck Institute for Medical Research, Max Planck Society, ou_1497700              

Inhalt

einblenden:
ausblenden:
Schlagwörter: -
 Zusammenfassung: Dependent on the presence or absence of vimentin, primary mouse embryo fibroblasts exhibit different growth characteristics in vitro. While most Vim(+/+) fibroblasts stop dividing and die via apoptosis, a substantial fraction of cells immortalize and proliferate almost normally. Vim(-/-) fibroblasts cease to divide earlier, immortalize in vanishingly small numbers and thereafter proliferate extremely slowly. Early after immortalization, Vim(+/+) (imm) fibroblasts appear structurally almost normal, whereas Vim(-/-) (imm) fibroblasts equal postmitotic "crisis" cells, which are characterized by increased cell size, altered cell ultrastructure, nuclear enlargement, genome destabilization, structural degeneration of mitochondria, and diminution of mitochondrial respiratory activity. The differences between immortalized Vim(+/+) (imm) and Vim(-/-) (imm) fibroblasts persist during early cell cloning but disappear during serial subcultivation. At high cell passage, cloned, immortalized vim(-) fibroblasts grow nearly as fast as their cloned vim(+) counterparts, and also resemble them in size, ultrastructure, nuclear volume, and mitochondrial complement; they very likely employ redundancy to cope with the loss of vimentin function when adjusting structure and behavior to that of immortalized vim(+) fibroblasts. Reduction in nuclear size occurs via release of large amounts of filamentous chromatin into extracellular space; because it is complexed with extracellular matrix proteins, it tends to form clusters and to tightly stick to the surface of other cells, thus providing a potential for horizontal gene transfer. On the other hand, cloned vim(+) and vim(-) fibroblasts are equal in showing contact inhibition at young age and becoming anchorage-independent during serial subcultivation, as indicated by the formation of multilayered and -faceted cell sheets and huge spheroids on top of or in soft agar. With this, immortalized vim(-) fibroblasts reduce their adhesiveness to the substratum which, in their precrisis state and early after cloning, is much higher than that of their vim(+) counterparts. In addition, the coupling between the mitochondrial respiratory chain and oxidative phosphorylation is stronger in vim(+) than vim(-) fibroblasts. It appears from these data that after explantation of fibroblasts from the mouse embryo the primary cause of cell and mitochondrial degeneration, including genomic instability, is the mitochondrial production of reactive oxygen species in a vicious circle, and that vimentin provides partial protection from oxidative damage. As a matrix protein with specific in vitro and in vivo affinities for nuclear and mitochondrial, recombinogenic DNA, it may exert this effect preferentially at the genome level via its influence on recombination and repair processes, and in this way also assist the cells in immortalizing. Additional protection of mitochondria by vimentin may occur at the level of mitochondrial fatty acid metabolism.

Details

einblenden:
ausblenden:
Sprache(n): eng - English
 Datum: 2005-05-282005-08-052005-11-01
 Publikationsstatus: Erschienen
 Seiten: 30
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: eDoc: 665503
URI: https://www.ncbi.nlm.nih.gov/pubmed/16274292
DOI: 10.1089/dna.2005.24.680
Anderer: 6515
 Art des Abschluß: -

Veranstaltung

einblenden:

Entscheidung

einblenden:

Projektinformation

einblenden:

Quelle 1

einblenden:
ausblenden:
Titel: DNA and Cell Biology
  Alternativer Titel : DNA Cell Biol.
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 24 (11) Artikelnummer: - Start- / Endseite: 680 - 709 Identifikator: -