Quantitative analysis of macrophages and perisinusoidal cells in primary biliary cirrhosis

Mathew, Joseph P.; Hines, Julie E.; Toole, Kieran; Johnson, Sarah J.; James, Oliver; Burt, Alastair D.

doi:10.1111/j.1365-2559.1994.tb00599.x

Cited by 35 publications

(24 citation statements)

References 19 publications

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“…Kupffer cells are positive for CD68. 27 We found that spindle-shaped CD68-positive cells were present in the sinusoids in the intact human liver, indicating that these cells were Kupffer cells. These cells were predominantly located along the sinusoids (Figure 3a).…”

Section: Specificity Of the Anti-cygb Antibodymentioning

confidence: 83%

Cytoglobin is expressed in hepatic stellate cells, but not in myofibroblasts, in normal and fibrotic human liver

Motoyama

Komiya

Thủy

et al. 2014

Laboratory Investigation

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Cytoglobin (CYGB) is ubiquitously expressed in the cytoplasm of fibroblastic cells in many organs, including hepatic stellate cells. As yet, there is no specific marker with which to distinguish stellate cells from myofibroblasts in the human liver. To investigate whether CYGB can be utilized to distinguish hepatic stellate cells from myofibroblasts in normal and fibrotic human liver, human liver tissues damaged by infection with hepatitis C virus (HCV) and at different stages of fibrosis were obtained by liver biopsy. Immunohistochemistry was performed on histological sections of liver tissues using antibodies against CYGB, cellular retinol-binding protein-1 (CRBP-1), a-smooth muscle actin (a-SMA), thymocyte differentiation antigen 1 (Thy-1), and fibulin-2 (FBLN2). CYGB-and CRBP-1-positive cells were counted around fibrotic portal tracts in histological sections of the samples. The expression of several of the proteins listed above was examined in cultured mouse stellate cells. Quiescent stellate cells, but not portal myofibroblasts, expressed both CYGB and CRBP-1 in normal livers. In fibrotic and cirrhotic livers, stellate cells expressed both CYGB and a-SMA, whereas myofibroblasts around the portal vein expressed a-SMA, Thy-1, and FBLN2, but not CYGB. Development of the fibrotic stage was positively correlated with increases in Sirius red-stained, a-SMA-positive, and Thy-1-positive areas, whereas the number of CYGB-and CRBP-1-positive cells decreased with fibrosis development. Primary cultured mouse stellate cells expressed cytoplasmic CYGB at day 1, whereas they began to express a-SMA at the cellular margins at day 4. Thy-1 was undetectable throughout the culture period. In human liver tissues, quiescent stellate cells are CYGB positive. When activated, they also become a-SMA positive; however, they are negative for Thy-1 and FBLN2. Thus, CYGB is a useful marker with which to distinguish stellate cells from portal myofibroblasts in the damaged human liver.

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Section: Specificity Of the Anti-cygb Antibodymentioning

confidence: 83%

Cytoglobin is expressed in hepatic stellate cells, but not in myofibroblasts, in normal and fibrotic human liver

Motoyama

Komiya

Thủy

et al. 2014

Laboratory Investigation

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“…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%

“…13 The statistiIn this study we describe multivesicular stellate cells as a cal comparison of groups was by Student's t test. A P value of P õ prominent feature of both noncirrhotic and cirrhotic PBC.…”

mentioning

confidence: 99%

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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“…Elimination of activated HSCs plays key role in resolution of liver fibrosis (163). However, since it is not easy to clearly define the fate of activated HSCs during resolution of fibrosis in human (164), most of conclusions are based on studies in animal models of liver fibrosis.…”

Section: Resolution Of Livermentioning

confidence: 99%

Bioconjugation of Oligonucleotides for Treating Liver Fibrosis

Houssein

Mahato

2007

Oligonucleotides

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Liver fibrosis results from chronic liver injury due to hepatitis B and C, excessive alcohol ingestion, and metal ion overload. Fibrosis culminates in cirrhosis and results in liver failure. Therefore, a potent antifibrotic therapy is in urgent need to reverse scarring and eliminate progression to cirrhosis. Although activated hepatic stellate cells (HSCs) remains the principle cell type responsible for liver fibrosis, perivascular fibroblasts of portal and central veins as well as periductular fibroblasts are other sources of fibrogenic cells. This review will critically discuss various treatment strategies for liver fibrosis, including prevention of liver injury, reduction of inflammation, inhibition of HSC activation, degradation of scar matrix, and inhibition of aberrant collagen synthesis. Oligonucleotides (ODNs) are short, single-stranded nucleic acids, which disrupt expression of target protein by binding to complementary mRNA or forming triplex with genomic DNA. Triplex forming oligonucleotides (TFOs) provide an attractive strategy for treating liver fibrosis. A series of TFOs have been developed for inhibiting the transcription of α1(I) collagen gene, which opens a new area for antifibrotic drugs. There will be in depth discussion on the use of TFOs and how different bioconjugation strategies can be utilized for their site-specific delivery to HSCs or hepatocytes for enhanced antifibrotic activities. Various insights developed in individual strategy and the need for multipronged approaches will also be discussed.

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Quantitative analysis of macrophages and perisinusoidal cells in primary biliary cirrhosis

Cited by 35 publications

References 19 publications

Cytoglobin is expressed in hepatic stellate cells, but not in myofibroblasts, in normal and fibrotic human liver

Cytoglobin is expressed in hepatic stellate cells, but not in myofibroblasts, in normal and fibrotic human liver

Multivesicular stellate cells in primary biliary cirrhosis

Bioconjugation of Oligonucleotides for Treating Liver Fibrosis

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