CD10 immunostaining of bile canaliculi in liver biopsies: change of staining pattern with the development of cirrhosis

Shousha, S; F, Gadir; Peston, David; Bansi, D; Thillainaygam, A V; Murray-Lyon, I M

doi:10.1111/j.1365-2559.2004.01927.x

Cited by 34 publications

(35 citation statements)

References 9 publications

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“…25 None of the patients whom we studied was known to have hepatitis C virus infection, while most of those in whom fibrosis was associated with loss of canalicular CD10 expression were thus infected. 21 These disparate findings suggest that loss of canalicular CD10 expression in patients with fibrosis owing to hepatitis C virus infection may not be simply due to increasing fibrosis. Rather, viral infection may affect expression of CD10.…”

Section: Nc1 Ags1 Ags2 Ags4 Ags5mentioning

confidence: 66%

“…21 However, while CD10 was absent from canaliculi in some foci of hepatocellular nodular regeneration, no association between increasing fibrosis scores and loss of CD10 expression was observed; AGS patients lacking CD10 expression had grade 2 or grade 3 fibrosis (scale 0-4), but canaliculi from adults without AGS and with similar or worse fibrosis expressed CD10 well. 15 These observations suggest that fibrosis alone does not account for lack of canalicular CD10 expression in AGS.…”

Section: Nc1 Ags1 Ags2 Ags4 Ags5mentioning

confidence: 99%

“…Such loss of CD10 expression may not be due to chronic viral infection alone, as CD10 loss reportedly was much less pronounced in patients with hepatitis B virus infection. 21 Our work sheds light on the ontogenic regulation of both CD10 and MME in granulocytes. Newborn babies have 55% lower levels of CD10 expression on granulocytes than do adults.…”

Section: Nc1 Ags1 Ags2 Ags4 Ags5mentioning

confidence: 99%

“…To correlate CD10 expression with the degree of fibrosis, 21 sections stained for reticulin fibres were assessed. Fibrosis scores for selected patients are shown in Table 3, along with CD10 and control-antigen (CD13 and BSEP) staining results.…”

Section: Immunohistochemical Evaluation Of Cd10 Expression In the Livermentioning

confidence: 99%

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Lack of hepatocellular CD10 along bile canaliculi is physiologic in early childhood and persistent in Alagille syndrome

Byrne

Meara

Rayner

et al. 2007

Laboratory Investigation

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Many tissues, including hepatobiliary cells, express neutral endopeptidase (CD10), encoded by MME. Serum neutral endopeptidase activity (NEA) has been recommended as a marker of cholestasis in adults but not in children with Alagille syndrome (AGS). We investigated ontogenic and disease-related differences in the expression of CD10. CD10 was found on canalicular surfaces of hepatocytes throughout the lobule in 16 adults and in 31 children aged Z24 months, with and without cholestasis, but not in 39 children aged o24 months, with and without cholestasis. Ten AGS children aged 2 months to 6 years lacked any canalicular CD10 expression. Cholangiocyte apices and/or intrasinusoidal granulocytes marked for CD10 in all subjects. Liver membrane fractions from a child with cholestasis aged o24 months and from 2 AGS patients aged 424 months contained reduced levels of CD10. In contrast, AGS children and all controls expressed CD10 similarly on granulocytes. MME mRNA was found in the liver of children aged o24 months and of adults, all with cholestasis, and of AGS patients. Granulocyte MME mRNA levels were similar among all study subjects; however, liver MME mRNA levels were 6-to 140-fold less than in normal adults in all cholestatic subjects, including AGS children. Methylation of the MME promoter was not detected in the liver of AGS children. In conclusion, hepatocytes in early childhood physiologically lack immunohistochemically detectable CD10. Reduced MME mRNA in AGS is not due to MME promoter methylation. Liver CD10 in childhood appears to undergo reduced synthesis or rapid degradation, which persists in AGS. Absence of CD10 expression thus may limit NEA as a marker of cholestasis in young patients and in AGS.

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Section: Nc1 Ags1 Ags2 Ags4 Ags5mentioning

confidence: 66%

Section: Nc1 Ags1 Ags2 Ags4 Ags5mentioning

confidence: 99%

Section: Nc1 Ags1 Ags2 Ags4 Ags5mentioning

confidence: 99%

Section: Immunohistochemical Evaluation Of Cd10 Expression In the Livermentioning

confidence: 99%

See 2 more Smart Citations

Lack of hepatocellular CD10 along bile canaliculi is physiologic in early childhood and persistent in Alagille syndrome

Byrne

Meara

Rayner

et al. 2007

Laboratory Investigation

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“…Concerning staining pattern changes with the development of cirrhosis, the report by Shousha et al is of much interest [42]. They mentioned that the CD10 staining patterns of bile canaliculi in liver biopsies are preserved in cases with mild fibrosis and inflammation, but become increasingly reduced with the advance of fibrosis or the presence of severe lobular inflammation or extensive metastasis [42].…”

Section: Distribution In Normal Tissuesmentioning

confidence: 99%

Availability of CD10 as a Histopathological Diagnostic Marker

Yasuda

Itoh

Satoh³

et al. 2005

Acta Histochem. Cytochem

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Wnt/β‐Catenin Signaling Plays a Protective Role in the Mdr2 Knockout Murine Model of Cholestatic Liver Disease

Pradhan‐Sundd¹,

Kosar²,

Saggi³

et al. 2019

Hepatology

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BaCKgRoUND aND aIMS:The Wnt/β-catenin signaling pathway has a well-described role in liver pathobiology. Its suppression was recently shown to decrease bile acid (BA) synthesis, thus preventing the development of cholestatic liver injury and fibrosis after bile duct ligation (BDL). appRoaCH aND ReSUltS: To generalize these observations, we suppressed β-catenin in Mdr2 knockout (KO) mice, which develop sclerosing cholangitis due to regurgitation of BA from leaky ducts. When β-catenin was knocked down (KD) in KO for 2 weeks, hepatic and biliary injury were exacerbated in comparison to KO given placebo, as shown by serum biochemistry, ductular reaction, inflammation, and fibrosis. Simultaneously, KO/KD livers displayed increased oxidative stress and senescence and an impaired regenerative response. Although the total liver BA levels were similar between KO/ KD and KO, there was significant dysregulation of BA transporters and BA detoxification/synthesis enzymes in KO/KD compared with KO alone. Multiphoton intravital microscopy revealed a mixing of blood and bile in the sinusoids, and validated the presence of increased serum BA in KO/KD mice. Although hepatocyte junctions were intact, KO/KD livers had significant canalicular defects, which resulted from loss of hepatocyte polarity. Thus, in contrast to the protective effect of β-catenin KD in BDL model, β-catenin KD in Mdr2 KO aggravated rather than alleviated injury by interfering with expression of BA transporters, hepatocyte polarity, canalicular structure, and the regenerative response. CoNClUSIoNS:The resulting imbalance between ongoing injury and restitution led to worsening of the Mdr2 KO phenotype, suggesting caution in targeting β-catenin globally for all cholestatic conditions. (Hepatology 2020;71:1732-1749).

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CD10 immunostaining of bile canaliculi in liver biopsies: change of staining pattern with the development of cirrhosis

Cited by 34 publications

References 9 publications

Lack of hepatocellular CD10 along bile canaliculi is physiologic in early childhood and persistent in Alagille syndrome

Lack of hepatocellular CD10 along bile canaliculi is physiologic in early childhood and persistent in Alagille syndrome

Availability of CD10 as a Histopathological Diagnostic Marker

Wnt/β‐Catenin Signaling Plays a Protective Role in the Mdr2 Knockout Murine Model of Cholestatic Liver Disease

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