The elevation of α-fetoprotein messenger RNA in regenerating rat liver

Chiu, Jen‐Fu; Gabryelak, Teresa; Commers, Patricia A.; Massari, Ronald J.

doi:10.1016/0006-291x(81)91895-7

Cited by 18 publications

(5 citation statements)

References 14 publications

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“…liver regeneration (Krieg et al, 1980;Princen et al, 1982;Petropoulos et al, 1983). The major observation following 68% partial hepatectomy (Krieg et al, 1980;Princen et al, 1982;Petropoulos et al, 1983) or CCl4-induced hepatic necrosis (Chiu et al, 1981; Belayew Petropoulos et al, 1983) has been that a-fetoprotein mRNA increases, but there is no reciprocal change in the albumin mRNA steady-state level. These findings have been taken as evidence for a lack of coordinate or reciprocal regulation of a-fetoprotein and albumin genes once these genes have been induced (Belayew Petropoulos et al, 1983;Fausto, 1984).…”

Section: Discussionmentioning

confidence: 99%

“…It has been postulated (Uriel, 1979;Petropoulos et al, 1983) that if hepatocytes dedifferentiate prior to cell division as part of the proliferative response, then the increase in a-fetoprotein gene expression during liver regeneration should precede DNA synthesis and albumin transcription should be turned off. Although various studies have shown an increase in a-fetoprotein mRNA during liver regeneration (Chiu et al, 1981;Princen et al, 1982; Petropoulos et al, 1983), a reciprocal and specific decrease in albumin mRNA has not been reported (Krieg et al, 1980;Petropoulos et al, 1983). In a most recent study in mice, simultaneously comparing transcription of albumin and a-fetoprotein genes to mRNA steady-state levels (Friedman et al, 1984), there were no significant changes in the transcription or steady-state level of either albumin or a-fetoprotein mRNA following partial hepatectomy.…”

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confidence: 94%

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Transcriptional switch from albumin to .alpha.-fetoprotein and changes in transcription of other genes during carbon tetrachloride-induced liver regeneration

Panduro¹,

Shalaby²,

Weiner³

et al. 1986

Biochemistry

127

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During liver regeneration induced by CCl4 administration to rats, changes in the relative transcription rates of albumin and alpha-fetoprotein genes have been measured in conjunction with other liver-specific and general cellular function genes. Within 24 h following CCl4 administration, albumin gene transcription decreases by 85%, whereas alpha-fetoprotein transcription increases from undetectable levels to 50% of that observed for albumin. These changes precede maximal [3H]thymidine incorporation into DNA which peaks at 48 h. Other genes related to liver-specific functions, such as ligandin, alpha 1-antitrypsin, and cytochrome P-450's, as well as general cellular genes pro alpha 1- and pro alpha 2-collagen, beta-actin, and alpha-tubulin, respond in kinetic patterns often distinct from each other and from albumin and alpha-fetoprotein. Changes in the steady-state levels of albumin and alpha-fetoprotein mRNA correlate with changes in transcription, but there is a lag in alpha-fetoprotein mRNA accumulation, which peaks at 72 h following CCl4 administration. These studies indicate that reciprocal changes in albumin and alpha-fetoprotein gene transcription occur during CCl4-induced liver regeneration, leading to changes in the level of these specific mRNAs. These changes precede DNA synthesis and would appear to represent an alteration in differentiated function of hepatocytes in conjunction with the liver regenerative process.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 94%

Transcriptional switch from albumin to .alpha.-fetoprotein and changes in transcription of other genes during carbon tetrachloride-induced liver regeneration

Panduro¹,

Shalaby²,

Weiner³

et al. 1986

Biochemistry

127

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“…In acute massive loss of liver, e.g., 70% partial hepatectomy (PH), people think liver regeneration relies largely upon increased replication of mature hepatocytes 28 . But the expression of progenitor markers, such as alpha-fetoprotein (AFP) and Fn14 increased, suggesting progenitor cells are also involved in liver regeneration post-PH 29 - 31 . In many types of chronic liver injury, since mature hepatocyte replication is inhibited, it is generally believed that progenitor populations mainly contribute to regeneration of chronically injured livers 28 .…”

Section: Hh Signaling In Liver Regenerationmentioning

confidence: 99%

Role of canonical Hedgehog signaling pathway in liver

Gao¹,

Zhang²,

Zhang³

et al. 2018

Int. J. Biol. Sci.

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Hedgehog (Hh) signaling pathway plays an important role in embryonic development. It becomes reactivated in many types of acute and chronic liver injuries. Hh signaling is required for liver regeneration, regulates capillarisation, controls the fates of hepatic stellate cells, promotes liver fibrosis and liver cancers. In this review, we summarize the current knowledge of the role of canonical Hh signaling pathway in adult liver. This help to understand the pathogenesis of liver diseases and find out the new effective targeted therapeutic strategies for liver diseases treatments.

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“…Such work has consistently demonstrated that striking increases in hepatocyte DNA synthesis occur within the initial 48h post-PH, followed by smaller (but highly significant) increases in hepatocyte mitoses and eventual recovery of liver mass, leading to consensus that liver regeneration after PH relies largely upon increased replication of mature hepatocytes(2–5). Nevertheless, changes in expression of progenitor markers, such as alpha-fetoprotein (AFP) and Fn14, have long been acknowledged to occur during regeneration(6–9). Severe inhibition of liver regeneration after toxic liver injury was recently reported to occur in mice with targeted disruption of Fn14, a member of the tumor necrosis factor receptor superfamily that promotes the growth of bipotent hepatic progenitors (i.e., oval cells)(10).…”

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confidence: 99%

Hedgehog Signaling Is Critical for Normal Liver Regeneration After Partial Hepatectomy in Mice

et al. 2010

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Distinct mechanisms are believed to regulate growth of the liver during fetal development and after injury in adults, because the former relies on progenitors and the latter generally involves replication of mature hepatocytes. However, chronic liver injury in adults increases production of Hedgehog (Hh) ligands, developmental morphogens that control progenitor cell fate and orchestrate various aspects of tissue construction during embryogenesis. This raises the possibility that similar Hh-dependent mechanisms also might regulate adult liver regeneration. The current analysis of murine liver regeneration after 70% partial hepatectomy (PH), an established model of adult liver regeneration, demonstrated that PH induced production of Hh ligands and activated Hh signaling in liver cells. Treatment with a specific Hh signaling inhibitor interfered with several key components of normal liver regeneration, significantly inhibiting progenitor responses, matrix remodeling, proliferation of hepatocytes and ductular cells, and restoration of liver mass. These global inhibitory effects on liver regeneration dramatically reduced survival after PH. Conclusion: Mechanisms that mediate liver organogenesis, such as Hh pathway activation, are retained and promote reconstruction of adult livers after injury. Hepatology 2010

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The elevation of α-fetoprotein messenger RNA in regenerating rat liver

Cited by 18 publications

References 14 publications

Transcriptional switch from albumin to .alpha.-fetoprotein and changes in transcription of other genes during carbon tetrachloride-induced liver regeneration

Transcriptional switch from albumin to .alpha.-fetoprotein and changes in transcription of other genes during carbon tetrachloride-induced liver regeneration

Role of canonical Hedgehog signaling pathway in liver

Hedgehog Signaling Is Critical for Normal Liver Regeneration After Partial Hepatectomy in Mice

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