Lipocytes and transitional cells in alcoholic liver disease: A morphometric study

Mak, Ki M.; Lieber, Charles S.

doi:10.1002/hep.1840080508

Cited by 174 publications

(83 citation statements)

References 12 publications

(9 reference statements)

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“…11 Stellate cells have been shown to transform from fat-storthe 26 patients with PBC in this study showed abnormalities (increases) in concentrations of cholesterol in their sera (re-ing cells to transitional fibroblastic cells capable of collagen synthesis. 18 Whether the fat-storing stellate cells in livers sults not shown). Hypervitaminosis A generates mostly electron-lucid vesicles in stellate cells.…”

Section: Methodsmentioning

confidence: 96%

“…give lipid vesicles that are more electron dense, but the most electron-dense lipids are phospholipids. 15 fibrosis [18][19][20] and via the contraction of their processes in the development of portal hypertension. 21 The significance of the In a separate study of these same 26 PBC patients, 17 we have examined their follow-up liver biopsies, up to 2 years presence of increased numbers of multivesicular stellate cells in livers of patients with PBC requires further longitudinal later, after ursodeoxycholic acid treatment or placebo, and found that the same pattern of increased lipid storage in clinical and laboratory studies.…”

Section: Methodsmentioning

confidence: 99%

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Multivesicular stellate cells in primary biliary cirrhosis

Rg¹,

Mg²,

Shear³

et al. 1997

Hepatology

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little or no steatosis in 24 of 26 (92%) PBC patients. Multive-were from biopsies from the liver pathology reference files of The sicular stellate cells were not seen in female patients with Toronto Hospital. 11 Of the 26 patients with PBC, 16 had been renormal liver histology. These results suggest that there is an corded as having duct lesions and fibrosis without cirrhosis and 10 alteration in hepatic lipid storage that involves stellate cells had cirrhosis. 11 Tissue for TEM examination had been fixed in in PBC that could be an early manifestation of this disease. universal fixative (2% glutaraldehyde and 4% formaldehyde) and processed in a standard way. Numbers of stellate cells were counted

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Section: Methodsmentioning

confidence: 96%

Section: Methodsmentioning

confidence: 99%

Multivesicular stellate cells in primary biliary cirrhosis

Rg¹,

Mg²,

Shear³

et al. 1997

Hepatology

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show abstract

“…8A). As controls, we analyzed expression of tubulin, which does not change during activation, and expression of a-smooth muscle actin (aSMA), which is a marker of activation and expression of which gradually increases (Mak and Lieber 1988). At Day 2, when the cells are still quiescent, there was no detectable expression of RHA by Western blot (Fig.…”

Section: Rha Is Up-regulated During Hepatic Stellate Cell (Hsc) Activmentioning

confidence: 99%

A novel role of RNA helicase A in regulation of translation of type I collagen mRNAs

Manojlovic

Stefanovic²

2011

RNA

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Type I collagen is composed of two a1(I) polypeptides and one a2(I) polypeptide and is the most abundant protein in the human body. Expression of type I collagen is primarily controlled at the level of mRNA stability and translation. Coordinated translation of a(I) and a2(I) mRNAs is necessary for efficient folding of the corresponding peptides into the collagen heterotrimer. In the 59 untranslated region (59 UTR), collagen mRNAs have a unique 59 stem-loop structure (59 SL). La ribonucleoprotein domain family member 6 (LARP6) is the protein that binds 59 SL with high affinity and specificity and coordinates their translation. Here we show that RNA helicase A (RHA) is tethered to the 59 SL of collagen mRNAs by interaction with the C-terminal domain of LARP6. In vivo, collagen mRNAs immunoprecipitate with RHA in an LARP6-dependent manner. Knockdown of RHA prevents formation of polysomes on collagen mRNAs and dramatically reduces synthesis of collagen protein, without affecting the level of the mRNAs. A reporter mRNA with collagen 59 SL is translated three times more efficiently in the presence of RHA than the same reporter without the 59 SL, indicating that the 59 SL is the cis-acting element conferring the regulation. During activation of quiescent cells into collagen-producing cells, expression of RHA is highly up-regulated. We postulate that RHA is recruited to the 59 UTR of collagen mRNAs by LARP6 to facilitate their translation. Thus, RHA has been discovered as a critical factor for synthesis of the most abundant protein in the human body.

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“…26 However, accurate analysis of the cell numbers in the parenchyma failed to show a proliferation of activated HSC. 27,28 Increased desmin positivity and BrdU-or 3 H-thymidine incorporation in desminpositive cells observed in animal experiments were interpreted as proliferation of HSCs. 29,30 Without wanting to reduce the importance of the HSC, two errors might have been made: first, not taking the other mesenchymal cell types into consideration as potential source of connective tissue proteins; and second, a too high degree of confidence in the purity of the HSC cultures by claiming at the same time that collagen production in hepatocyte cultures was due to contaminating mesenchymal cells.…”

Section: Mesenchymal Cells Of the Portal Field And Identification Marmentioning

confidence: 99%

Portal tract fibrogenesis in the liver

Ramadori

Saile

2004

Laboratory Investigation

170

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The portal area is the 'main entrance' and one of the two main exits of the liver lobule. Through the main entrance portal and arterial blood reach the liver sinusoids. Through the exit the bile flows towards the duodenum. The three main structures, portal vein and artery with their own wall (and vascular smooth muscle cells) and bile duct with its basal membrane, are surrounded by loose myofibroblasts and by the first layer of hepatocytes and non-parenchymal cells. Chronic diseases of the liver can lead to development of liver cirrhosis, characterized by formation of fibrotic septa which can be portal-portal in the case of the chronic biliary damage or portal-central in the case of the chronic viral hepatitis. Central-central septa can also be observed under other pathological conditions. When damaging noxae are introduced to the liver, inflammatory cells are first recruited to the portal field, the first layer of hepatocytes may be destroyed (enlargement of the portal field) and portal (myo)fibroblasts become activated. A similar reaction may take place when the target of inflammation is the bile duct with consecutive reduction of the bile flow, activation of the portal (myo)fibroblasts, proliferation of bile ducts and destruction of the hepatocytes around the portal field. Increased matrix deposition may be the consequence. During the past years several publications dealt with the pathomechanisms of portal fibrogenesis as well as with its resolution. One of the most intriguing observations was that it is not hepatic stellate cells of the hepatic sinusoid, but portal (myo)fibroblasts which rapidly acquire the phenotype of 'activated' (myo)fibroblastas in the early stages of cholestatic fibrosis. These may also become the main mesenchymal cells of the porto-portal or porto-central fibrotic septa. This article reviews the similarities as well as differences between the mesenchymal cells of the portal tract and of the fibrotic septa vs 'activated' stellate cells of the hepatic sinusoids, and discusses the debate over their relative contributions to liver fibrogenesis.

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Lipocytes and transitional cells in alcoholic liver disease: A morphometric study

Cited by 174 publications

References 12 publications

Multivesicular stellate cells in primary biliary cirrhosis

Multivesicular stellate cells in primary biliary cirrhosis

A novel role of RNA helicase A in regulation of translation of type I collagen mRNAs

Portal tract fibrogenesis in the liver

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