Transdifferentiation of rat hepatic stellate cells results in leptin expression

James John Potter, Lawrence Womack, Esteban Mezey, Frank A. Anania

Research output: Contribution to journalArticle

Abstract

Leptin is a peptide hormone that appears critical in regulating Fat metabolism. Recently, circulating leptin levels were reported higher in patients with alcoholic cirrhosis. In health, hepatic stellate cells store retinoids, but following liver injury they transdifferentiate into myofibroblast-like cells with loss of the retinoid stores. Leptin expression was demonstrated by detection of leptin mRNA by RT-PCR analysis and by immunohistochemistry viewed with confocal microscopy in transdifferentiated stellate cells after 14 days, or more, of culture. Leptin expression was not found in freshly isolated quiescent stellate cells. Leptin expression was not demonstrated in freshly isolated or cultured Kupffer cells. Treatment of activated stellate cells with either 1 μM retionic acid or 10 μM retinol acetate resulted in the inhibition of leptin mRNA expression. The observation that activated stellate cells in culture can express leptin has implications for understanding adipocyte biology in liver disease and treatment of malnutrition in cirrhotics.

Original languageEnglish (US)
Pages (from-to)178-182
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume244
Issue number1
DOIs
StatePublished - Mar 6 1998

Fingerprint

Hepatic Stellate Cells
Leptin
Rats
Retinoids
Liver
Alcoholic Liver Cirrhosis
Messenger RNA
Kupffer Cells
Myofibroblasts
Peptide Hormones
Confocal microscopy
Adipocytes
Metabolism
Confocal Microscopy
Malnutrition
Liver Diseases
Cultured Cells
Cell Culture Techniques
Immunohistochemistry
Fats

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Transdifferentiation of rat hepatic stellate cells results in leptin expression. / Potter, James John; Womack, Lawrence; Mezey, Esteban; Anania, Frank A.

In: Biochemical and Biophysical Research Communications, Vol. 244, No. 1, 06.03.1998, p. 178-182.

Research output: Contribution to journalArticle

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