Branches of the NF-κB signaling pathway regulate proliferation of oval cells in rat liver regeneration.
Genet Mol Res
; 15(1)2016 Mar 24.
Article
en En
| MEDLINE
| ID: mdl-27050988
ABSTRACT
The NF-kB (nuclear factor kB) pathway is involved in the proliferation of many cell types. To explore the mechanism of the NF-kB signaling pathway underlying the oval cell proliferation during rat liver regeneration, the Rat Genome 230 2.0 Array was used to detect expression changes of NF-kB signaling pathway-related genes in oval cells. The results revealed that the expression levels of many genes in the NF-kB pathway were significantly changed. This included 48 known genes and 16 homologous genes, as well as 370 genes and 85 homologous genes related to cell proliferation. To further understand the biological significance of these changes, an expression profile function was used to analyze the potential biological processes. The results showed that the NF-kB pathway promoted oval cell proliferation mainly through three signaling branches; the tumor necrosis factor alpha branch (TNF-a pathway), the growth factor branch, and the chemokine branch. An integrated statistics method was used to define the key genes in the NF-kB pathway. Seven genes were identified to play vital roles in the NF-kB pathway. To confirm these results, the protein content, including two key genes (TNF and FGF11) and two non-key genes (CCL2 and TNFRSF12A), were analyzed using two-dimensional gel electrophoresis and MALDI-TOF/TOF mass spectrometry. The results were generally consistent with those of the array data. To conclude, three branches and seven key genes were involved in the NF-kB signaling pathway that regulates oval cell proliferation during rat liver regeneration.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Transducción de Señal
/
FN-kappa B
/
Proliferación Celular
/
Hígado
/
Regeneración Hepática
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Genet Mol Res
Asunto de la revista:
BIOLOGIA MOLECULAR
/
GENETICA
Año:
2016
Tipo del documento:
Article
País de afiliación:
China