Cyclin expression in the atrophying and proliferating lobes of the liver after portal vein branch ligation and hepatectomy in rats

Junji Ueda, Kazuo Chijiiwa, kenji nakano

    Research output: Contribution to journalArticle

    9 Citations (Scopus)

    Abstract

    Background Portal vein branch ligation causes atrophy of the portal vein ligated lobes (PVL) and proliferation of the nonligated lobes (PVNL) of the liver. However, the mechanisms underlying atrophy of the PVL and proliferation of PVNL after portal vein branch ligation have not been clarified except that interleukin-6 (IL-6), nuclear factor kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), and immediate-early gene expression are similarly induced in both the PVL and the PVNL. Thus, it is still unclear what factors cause the subsequent atrophy and proliferation. Materials and methods Male Wistar rats were randomly separated into a portal vein branch ligation group and partial hepatectomy group. In the portal vein branch ligation group, the branch of portal vein supplying the median and left lateral lobes of the liver was ligated. In the partial hepatectomy group, the correspondent lobes of the liver were excised. We examined cyclin expression in the PVL and PVNL after portal vein branch ligation in comparison to cyclin expression in the remaining liver (HEP) after partial hepatectomy. Cyclin D1, E, and A mRNA and protein expressions were analyzed by RT-PCR and Western blotting, respectively. Results The mRNA and protein expressions of cyclin D1 and A were not up-regulated in the PVL, whereas those in the PVNL and HEP were up-regulated. Cyclin D1 mRNA and protein expressions were significantly lower in the PVL than in the PVNL and HEP at 18 h. The levels of mRNA and protein expression of cyclin A were significantly lower in the PVL than in the PVNL and HEP at 36 h. Liver regeneration, assessed by the relative liver weight, thymidine incorporation into DNA, and proliferating cell nuclear antigen (PCNA) labeling index was delayed significantly in the PVNL compared to that in the HEP. Cyclin D1 mRNA and protein expressions were significantly lower in the PVNL than in the HEP at 12 and 18 h, respectively. Conclusions Cell-cycle progression might be inhibited at G1-phase accompanied by impaired cyclin D1 expression in the PVL, which results in atrophy. The fact that liver proliferation of the PVNL is delayed in comparison to that of the HEP is likely due to delayed expression of cyclin D1.

    Original languageEnglish
    Pages (from-to)89-96
    Number of pages8
    JournalJournal of Surgical Research
    Volume120
    Issue number1
    DOIs
    Publication statusPublished - Jul 1 2004

    Fingerprint

    Cyclins
    Hepatectomy
    Portal Vein
    Ligation
    Liver
    Cyclin D1
    Cyclin A
    Atrophy
    Messenger RNA
    Proteins
    CCAAT-Enhancer-Binding Protein-beta
    STAT3 Transcription Factor
    Cyclin E
    Liver Regeneration
    Immediate-Early Genes
    NF-kappa B
    Proliferating Cell Nuclear Antigen
    G1 Phase
    Thymidine
    Wistar Rats

    All Science Journal Classification (ASJC) codes

    • Surgery

    Cite this

    Cyclin expression in the atrophying and proliferating lobes of the liver after portal vein branch ligation and hepatectomy in rats. / Ueda, Junji; Chijiiwa, Kazuo; nakano, kenji.

    In: Journal of Surgical Research, Vol. 120, No. 1, 01.07.2004, p. 89-96.

    Research output: Contribution to journalArticle

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    abstract = "Background Portal vein branch ligation causes atrophy of the portal vein ligated lobes (PVL) and proliferation of the nonligated lobes (PVNL) of the liver. However, the mechanisms underlying atrophy of the PVL and proliferation of PVNL after portal vein branch ligation have not been clarified except that interleukin-6 (IL-6), nuclear factor kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), and immediate-early gene expression are similarly induced in both the PVL and the PVNL. Thus, it is still unclear what factors cause the subsequent atrophy and proliferation. Materials and methods Male Wistar rats were randomly separated into a portal vein branch ligation group and partial hepatectomy group. In the portal vein branch ligation group, the branch of portal vein supplying the median and left lateral lobes of the liver was ligated. In the partial hepatectomy group, the correspondent lobes of the liver were excised. We examined cyclin expression in the PVL and PVNL after portal vein branch ligation in comparison to cyclin expression in the remaining liver (HEP) after partial hepatectomy. Cyclin D1, E, and A mRNA and protein expressions were analyzed by RT-PCR and Western blotting, respectively. Results The mRNA and protein expressions of cyclin D1 and A were not up-regulated in the PVL, whereas those in the PVNL and HEP were up-regulated. Cyclin D1 mRNA and protein expressions were significantly lower in the PVL than in the PVNL and HEP at 18 h. The levels of mRNA and protein expression of cyclin A were significantly lower in the PVL than in the PVNL and HEP at 36 h. Liver regeneration, assessed by the relative liver weight, thymidine incorporation into DNA, and proliferating cell nuclear antigen (PCNA) labeling index was delayed significantly in the PVNL compared to that in the HEP. Cyclin D1 mRNA and protein expressions were significantly lower in the PVNL than in the HEP at 12 and 18 h, respectively. Conclusions Cell-cycle progression might be inhibited at G1-phase accompanied by impaired cyclin D1 expression in the PVL, which results in atrophy. The fact that liver proliferation of the PVNL is delayed in comparison to that of the HEP is likely due to delayed expression of cyclin D1.",
    author = "Junji Ueda and Kazuo Chijiiwa and kenji nakano",
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    T1 - Cyclin expression in the atrophying and proliferating lobes of the liver after portal vein branch ligation and hepatectomy in rats

    AU - Ueda, Junji

    AU - Chijiiwa, Kazuo

    AU - nakano, kenji

    PY - 2004/7/1

    Y1 - 2004/7/1

    N2 - Background Portal vein branch ligation causes atrophy of the portal vein ligated lobes (PVL) and proliferation of the nonligated lobes (PVNL) of the liver. However, the mechanisms underlying atrophy of the PVL and proliferation of PVNL after portal vein branch ligation have not been clarified except that interleukin-6 (IL-6), nuclear factor kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), and immediate-early gene expression are similarly induced in both the PVL and the PVNL. Thus, it is still unclear what factors cause the subsequent atrophy and proliferation. Materials and methods Male Wistar rats were randomly separated into a portal vein branch ligation group and partial hepatectomy group. In the portal vein branch ligation group, the branch of portal vein supplying the median and left lateral lobes of the liver was ligated. In the partial hepatectomy group, the correspondent lobes of the liver were excised. We examined cyclin expression in the PVL and PVNL after portal vein branch ligation in comparison to cyclin expression in the remaining liver (HEP) after partial hepatectomy. Cyclin D1, E, and A mRNA and protein expressions were analyzed by RT-PCR and Western blotting, respectively. Results The mRNA and protein expressions of cyclin D1 and A were not up-regulated in the PVL, whereas those in the PVNL and HEP were up-regulated. Cyclin D1 mRNA and protein expressions were significantly lower in the PVL than in the PVNL and HEP at 18 h. The levels of mRNA and protein expression of cyclin A were significantly lower in the PVL than in the PVNL and HEP at 36 h. Liver regeneration, assessed by the relative liver weight, thymidine incorporation into DNA, and proliferating cell nuclear antigen (PCNA) labeling index was delayed significantly in the PVNL compared to that in the HEP. Cyclin D1 mRNA and protein expressions were significantly lower in the PVNL than in the HEP at 12 and 18 h, respectively. Conclusions Cell-cycle progression might be inhibited at G1-phase accompanied by impaired cyclin D1 expression in the PVL, which results in atrophy. The fact that liver proliferation of the PVNL is delayed in comparison to that of the HEP is likely due to delayed expression of cyclin D1.

    AB - Background Portal vein branch ligation causes atrophy of the portal vein ligated lobes (PVL) and proliferation of the nonligated lobes (PVNL) of the liver. However, the mechanisms underlying atrophy of the PVL and proliferation of PVNL after portal vein branch ligation have not been clarified except that interleukin-6 (IL-6), nuclear factor kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), and immediate-early gene expression are similarly induced in both the PVL and the PVNL. Thus, it is still unclear what factors cause the subsequent atrophy and proliferation. Materials and methods Male Wistar rats were randomly separated into a portal vein branch ligation group and partial hepatectomy group. In the portal vein branch ligation group, the branch of portal vein supplying the median and left lateral lobes of the liver was ligated. In the partial hepatectomy group, the correspondent lobes of the liver were excised. We examined cyclin expression in the PVL and PVNL after portal vein branch ligation in comparison to cyclin expression in the remaining liver (HEP) after partial hepatectomy. Cyclin D1, E, and A mRNA and protein expressions were analyzed by RT-PCR and Western blotting, respectively. Results The mRNA and protein expressions of cyclin D1 and A were not up-regulated in the PVL, whereas those in the PVNL and HEP were up-regulated. Cyclin D1 mRNA and protein expressions were significantly lower in the PVL than in the PVNL and HEP at 18 h. The levels of mRNA and protein expression of cyclin A were significantly lower in the PVL than in the PVNL and HEP at 36 h. Liver regeneration, assessed by the relative liver weight, thymidine incorporation into DNA, and proliferating cell nuclear antigen (PCNA) labeling index was delayed significantly in the PVNL compared to that in the HEP. Cyclin D1 mRNA and protein expressions were significantly lower in the PVNL than in the HEP at 12 and 18 h, respectively. Conclusions Cell-cycle progression might be inhibited at G1-phase accompanied by impaired cyclin D1 expression in the PVL, which results in atrophy. The fact that liver proliferation of the PVNL is delayed in comparison to that of the HEP is likely due to delayed expression of cyclin D1.

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    JO - Journal of Surgical Research

    JF - Journal of Surgical Research

    SN - 0022-4804

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