Hepatic angiomyolipoma and hepatic stellate cells share a similar gene expression profile

Rajesh Kannangai, Anna Mae Diehl, Jason Sicklick, Marcus Rojkind, David L Thomas, Michael Torbenson

Research output: Contribution to journalArticle

Abstract

Background and Aims: Angiomyolipomas (AMLs) of the liver are rare neoplasms composed of large epithelioid cells with intermixed fat and blood vessels. Hepatic AMLs have no clear normal-cell counterpart in the liver. However, AMLs and stellate cells both are positive for neural crest-derived markers including HMB-45 antigen. Methods: To further explore the similarities between hepatic AMLs and stellate cells, gene expression of a hepatic AML was studied by cDNA microarray. Real-time polymerase chain reaction was used to confirm gene expression. Hepatic stellate cells can be quiescent, activated, or have a myofibroblastic phenotype depending on their state of activation. Expression of known markers of activated stellate cells was compared between the AML, activated primary mouse stellate cells, and stellate cell lines with activated and myofibroblastic phenotypes. Next, 5 novel genes from the AML were selected because they were not previously known to be markers of stellate cells and mRNA expression measured in the activated mouse stellate cells and in myofibroblastic stellate cell lines. Finally, expression levels of 10 novel genes were determined in 5 cirrhotic and 5 noncirrhotic human livers. Results: Overexpression of known markers of activated stellate cells including transforming growth factor β (TGF-β), smooth muscle actin, and collagen was found in the hepatic AML. Three of 5 novel markers that were identified in the AML, RRAD (Ras-related associated with diabetes), CTSK (cathepsin K), and NIBAN were also found to be overexpressed in activated stellate cells compared with quiescent or myofibroblastic stellate cells. In addition, 9 of 10 novel genes overexpressed in AML were also overexpressed in cirrhotic human livers versus noncirrhotic livers. Conclusions: Hepatic AMLs share a similar gene expression profile and may differentiate toward activated stellate cells.

Original languageEnglish (US)
Pages (from-to)341-347
Number of pages7
JournalHuman Pathology
Volume36
Issue number4
DOIs
StatePublished - Apr 2005

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Angiomyolipoma
Hepatic Stellate Cells
Transcriptome
Liver
Cathepsin K
Genes
Phenotype
Gene Expression
Cell Line
Epithelioid Cells
Neural Crest
Transforming Growth Factors
Liver Neoplasms
Oligonucleotide Array Sequence Analysis
Smooth Muscle
Blood Vessels
Actins
Real-Time Polymerase Chain Reaction
Collagen
Fats

Keywords

  • Hepatic angiomyolipoma
  • Stellate cell

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Hepatic angiomyolipoma and hepatic stellate cells share a similar gene expression profile. / Kannangai, Rajesh; Diehl, Anna Mae; Sicklick, Jason; Rojkind, Marcus; Thomas, David L; Torbenson, Michael.

In: Human Pathology, Vol. 36, No. 4, 04.2005, p. 341-347.

Research output: Contribution to journalArticle

Kannangai, Rajesh ; Diehl, Anna Mae ; Sicklick, Jason ; Rojkind, Marcus ; Thomas, David L ; Torbenson, Michael. / Hepatic angiomyolipoma and hepatic stellate cells share a similar gene expression profile. In: Human Pathology. 2005 ; Vol. 36, No. 4. pp. 341-347.
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abstract = "Background and Aims: Angiomyolipomas (AMLs) of the liver are rare neoplasms composed of large epithelioid cells with intermixed fat and blood vessels. Hepatic AMLs have no clear normal-cell counterpart in the liver. However, AMLs and stellate cells both are positive for neural crest-derived markers including HMB-45 antigen. Methods: To further explore the similarities between hepatic AMLs and stellate cells, gene expression of a hepatic AML was studied by cDNA microarray. Real-time polymerase chain reaction was used to confirm gene expression. Hepatic stellate cells can be quiescent, activated, or have a myofibroblastic phenotype depending on their state of activation. Expression of known markers of activated stellate cells was compared between the AML, activated primary mouse stellate cells, and stellate cell lines with activated and myofibroblastic phenotypes. Next, 5 novel genes from the AML were selected because they were not previously known to be markers of stellate cells and mRNA expression measured in the activated mouse stellate cells and in myofibroblastic stellate cell lines. Finally, expression levels of 10 novel genes were determined in 5 cirrhotic and 5 noncirrhotic human livers. Results: Overexpression of known markers of activated stellate cells including transforming growth factor β (TGF-β), smooth muscle actin, and collagen was found in the hepatic AML. Three of 5 novel markers that were identified in the AML, RRAD (Ras-related associated with diabetes), CTSK (cathepsin K), and NIBAN were also found to be overexpressed in activated stellate cells compared with quiescent or myofibroblastic stellate cells. In addition, 9 of 10 novel genes overexpressed in AML were also overexpressed in cirrhotic human livers versus noncirrhotic livers. Conclusions: Hepatic AMLs share a similar gene expression profile and may differentiate toward activated stellate cells.",
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AB - Background and Aims: Angiomyolipomas (AMLs) of the liver are rare neoplasms composed of large epithelioid cells with intermixed fat and blood vessels. Hepatic AMLs have no clear normal-cell counterpart in the liver. However, AMLs and stellate cells both are positive for neural crest-derived markers including HMB-45 antigen. Methods: To further explore the similarities between hepatic AMLs and stellate cells, gene expression of a hepatic AML was studied by cDNA microarray. Real-time polymerase chain reaction was used to confirm gene expression. Hepatic stellate cells can be quiescent, activated, or have a myofibroblastic phenotype depending on their state of activation. Expression of known markers of activated stellate cells was compared between the AML, activated primary mouse stellate cells, and stellate cell lines with activated and myofibroblastic phenotypes. Next, 5 novel genes from the AML were selected because they were not previously known to be markers of stellate cells and mRNA expression measured in the activated mouse stellate cells and in myofibroblastic stellate cell lines. Finally, expression levels of 10 novel genes were determined in 5 cirrhotic and 5 noncirrhotic human livers. Results: Overexpression of known markers of activated stellate cells including transforming growth factor β (TGF-β), smooth muscle actin, and collagen was found in the hepatic AML. Three of 5 novel markers that were identified in the AML, RRAD (Ras-related associated with diabetes), CTSK (cathepsin K), and NIBAN were also found to be overexpressed in activated stellate cells compared with quiescent or myofibroblastic stellate cells. In addition, 9 of 10 novel genes overexpressed in AML were also overexpressed in cirrhotic human livers versus noncirrhotic livers. Conclusions: Hepatic AMLs share a similar gene expression profile and may differentiate toward activated stellate cells.

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