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Anti‐transforming growth factor‐β1 antibody transiently enhances DNA synthesis during liver regeneration after partial hepatectomy in rats
Author(s) -
Enami Yuta,
Kato Hirohisa,
Murakami Masahiko,
Fujioka Toshihiro,
Aoki Takeshi,
Niiya Takashi,
Murai Noriyuki,
Ohtsuka Koji,
Kusano Mitsuo
Publication year - 2001
Publication title -
journal of hepato‐biliary‐pancreatic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 0944-1166
DOI - 10.1007/s005340170025
Subject(s) - liver regeneration , regeneration (biology) , hepatectomy , dna synthesis , transforming growth factor , antibody , chemistry , microbiology and biotechnology , dna , medicine , biology , immunology , biochemistry , surgery , resection
The regulation of liver regeneration after partial hepatectomy (PHx) is complex and involves many different cytokines. We investigated the role of one of these, transforming growth factor‐β1 (TGF‐β1), an inhibitor of liver regeneration, in a Wistar male rat model, in which anti‐TGF‐β1 antibody was injected immediately or 24 h after 70% PHx. Livers from treated animals contained an increased number of cells in S phase, according to 5‐bromo‐2′‐deoxyuridine (BrdU) labeling 36 h after PHx. Antibody administration 24 h after PHx resulted in the highest peak of proliferation; moreover, peak MIB‐5 labeling was also observed at that time. However, neither residual liver‐weight‐to‐body‐weight ratios nor regeneration rates differed significantly between any of the animals. Therefore, we also measured levels of serum TGF‐β1 and hepatocyte growth factor (HGF; an activator). With antibody administration at 0 or 24 h, TGF‐β1 levels were diminished at 24 or 36 h as compared with levels in control rats, but then rebounded, reaching a delayed peak at 48 or 72 h after PHx, respectively. Interestingly, there were also similar trends in HGF levels. These results indicate that TGF‐β1 may inhibit the G1 checkpoint, and serum TGF‐β1 concentration may influence HGF to regulate liver regeneration and to maintain homeostasis of proliferation after PHx.