In:
Cell Biology International, Wiley, Vol. 44, No. 1 ( 2020-01), p. 80-88
Abstract:
At the normal physiological conditions, hepatocytes predominantly reside in G0 phase of cell cycle; they actively proceed to G1 phase upon damage to the organ. As it was shown in experiments with restoration of liver mass in rats after subtotal hepatectomy (resection of 80% of the organ mass may be considered as a model of the ‘small for size’ liver syndrome), the growth inhibition is due to prolonged arrest of hepatocyte proliferation, molecular mechanisms of which remain understudied. In a rat model of liver regeneration after surgical removal of 80% of its mass, we observe a delayed onset of hepatocyte proliferation: Ki67 + hepatocytes begin to appear as late as at 30 h after liver subtotal resection. Their appearance coincides with the beginning of transcription of genes for cyclins A2, B1, D 1 , and E 1 at 24–30 h after surgery. The corresponding increase in concentrations of cyclin D 1 and E proteins is further delayed till 48 h after liver resection. We have also observed a prolonged decrease in the expression of proto‐oncogene c‐met (the hepatocyte growth factor receptor‐encoding gene Met ), an increase in expression of the transforming growth factor β1 (TGFβ 1 ) receptor‐encoding gene Tgfbr2 . At the same time, irreversible block of hepatocyte proliferation is prevented by expression of certain factors, notably of the TWEAK/Fn14 signaling pathway: concentrations of the corresponding proteins in remnant livers have peaked from 24 to 48 h after liver subtotal resection.
Type of Medium:
Online Resource
ISSN:
1065-6995
,
1095-8355
Language:
English
Publisher:
Wiley
Publication Date:
2020
detail.hit.zdb_id:
1462519-2
SSG:
12
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