Segregated hepatocyte proliferation and metabolic states within the regenerating mouse liver.

Détails

Ressource 1Télécharger: Minocha_et_al-2017-Hepatology_Communications.pdf (1908.23 [Ko])
Etat: Serval
Version: Final published version
ID Serval
serval:BIB_6C2F58697FCC
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Segregated hepatocyte proliferation and metabolic states within the regenerating mouse liver.
Périodique
Hepatology Communications
Auteur(s)
Minocha S., Villeneuve D., Rib L., Moret C., Guex N., Herr W.
ISSN
2471-254X (Electronic)
ISSN-L
2471-254X
Statut éditorial
Publié
Date de publication
2017
Peer-reviewed
Oui
Volume
1
Numéro
9
Pages
871-885
Langue
anglais
Résumé
Mammalian partial hepatectomy (PH) induces an orchestrated compensatory hyperplasia, or regeneration, in remaining tissue to restore liver mass; during this process, liver functions are maintained. We probed this process in mice with feeding- and light/dark-entrained animals subjected to sham or PH surgery. Early on (i.e., 10 hours), irrespective of sham or PH surgery, hepatocytes equidistant from the portal and central veins (i.e., midlobular) accumulated the G1-phase cell-division-cycle marker cyclin D1. By 24 hours, however, cyclin D1 disappeared absent PH but was reinforced in midlobular hepatocytes after PH. At 48 hours after PH and 2 hours fasting, synchronously mitotic hepatocytes possessed less glycogen than surrounding nonproliferating hepatocytes. The differential glycogen content generated a conspicuous entangled pattern of proliferating midlobular and nonproliferating periportal and pericentral hepatocytes. The nonproliferating hepatocytes maintained aspects of normal liver properties. Conclusion: In the post-PH regenerating mouse liver, a binary switch segregates midlobular cells to proliferate side-by-side with nonproliferating periportal and pericentral cells, which maintain metabolic functions. Our results also indicate that mechanisms of liver regeneration display evolutionary flexibility. (Hepatology Communications 2017;1:871-885).

Pubmed
Open Access
Oui
Création de la notice
08/02/2018 11:32
Dernière modification de la notice
08/05/2019 20:01
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