The liver, the largest organ of the body, the center of body metabolism and defence, has, like other organs, the capacity to react to increased work load and tissue damage with different means. In the past decades we have obtained a great deal of information thanks to scientific developments in cell biology, molecular biology and pathology. This also applies to the study of prenatal and postnatal liver development, damage and regeneration as part of the repair mechanisms, under various conditions not only in humans but also in different animal models. There is some debate concerning specification of hepatic gene expression for albumin during fetal life as shown by Elmouhoub et al. or immediately after birth. There is also discussion about the changes taking place in the hepatocytes in the early time after birth. It is not clear which mechanisms are involved in changes of gene-expression, cell size and hepatocellular ploidy and in which area of the liver the changes take place. The role of ploidy in cellular metabolism and cellular growth under physiological conditions is still not clear. Its role is also unclear after hepatocellular damage when space generated by the elimination of cellular debris by macrophages has to be refilled to reacquire the original function after a single hit. This can be due to a toxic or infectious agent or to a surgical reduction of the organ volume. Furthermore, the question whether hyperplasia without cell proliferation or real cell proliferation or both are responsible for liver growth under the different conditions is still a matter of debate.
It is also not yet completely understood how liver function can be retained, when these mechanisms are hampered by the persistence of attack and only “scaring” processes are able to keep the organ together. Reduction of the function is then unavoidable after maximal exploitation of the hepatocellular synthetic and clearance capacities has taken place. Similar processes can, however, take place when hepaocytes are not lethally damaged but their function is strongly reduced because of overloading with lipids or other substances due to increased uptake or decreased release into the circulation. Another situation of globally reduced hepatocellular function takes place when an acute massive hepatocellular damage occurs and no repair mechanisms can be put into work.
This picture shows that the albumin-gen is clearly expressed in early fetal liver of the rat as shown at the protein and RNA-level.(with permission)
1. Liver volume and hepatocyte size before and after birth.
2. Acute-phase reaction in hepatoblasts.
3. HIF-gene-expression in hepatoblasts.
4. EPO-gene-expression and regulation in hepatoblasts.
5. Quantitative metabolic power and cell size after birth.
6. Quantitative metabolic power of periportal and pericentral hepatocytes and liver volume after birth.
7. Quantitative gene-expression and ploidy in normal and regenerating liver;correlation with liver volume.
8. Cytokine regulated DNA-synthesis in hepatocytes.
9. Link between ER-stress response, PAMP, DAMP and chemokines in hepatocytes.
10. Changes of synthesis of nuclear proteins, of DNA-synthesis and ribosomal activity.
11. Changes of ribosomal translation speed for different proteins.
12. Mitotic process in normal and in metabolic "stress" immediately after birth.
13. Metabolic load and DNA-synthesis in normal hepatocytes at different times after birth.
14. Changes of DNA-synthesis, ploidy and gene-expression in hepatocytes after surgical reduction of liver volume.
15. Changes of DNA-synthesis, ploidy and gene-expression in hepatocytes after acute hepatocellular damage.
16. Changes of DNA-synthesis, ploidy and gene-expression in hepatocytes after repeated hepatocellular damage.
17. Size and number of non-parenchymal cells before and after birth.
18. Size and number of non-parenchymal cells after surgical reduction of liver volume.
1. Rosa Maria Pascale Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy.
2. Consolato Sergi Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, Canada.
3. Udayan Apte Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, USA.
4. Rui Han Department of Oncology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
5. Benoît Pourcet University Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1011-EGID, 59000 Lille, France.
6. Yao Chen International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai, China.
7. Mariano E Gimenez & Juan Verde IRCAD, Research Institute against Cancer of the Digestive System, Strasbourg, France.
8. Caecilia H. C. Sukowati Department of Medicine, University of Udine, Piazzale M., Udine, Italy.
9. Mei-Hua Qu Department of Pharmacology, Laboratory of Applied Pharmacology, College of Pharmacy, Weifang Medical University, Weifang, China.
10. Vincenza Rita Lo Vasco Department of Diagnostics and Public Health, Unit of Forensic Medicine, University of Verona, Verona, Italy.
11. Giuseppe Servillo Department of Experimental Medicine, School of Medicine, University of Perugia, Perugia, Italy.
12. Madan Mohan Chaturvedi Laboratory for Chromatin Biology, Department of Zoology, University of Delhi, Delhi, India.
13. Kristen A Mitchell Center of Biomedical Research Excellence in Matrix Biology, Boise State University, Boise, ID, USA.
The list is arranged in no particular order and being updated.
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