Effect of vitamin A deficiency and retinoic acid repletion on intestinal and hepatic apolipoprotein A-I mRNA levels of adult rats

R. Zolfaghari, A. Catharine Ross

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Abstract

Apolipoprotein A-I (apoA-I) gene expression is known to be regulated by nutritional and hormonal factors. Experiments were conducted to determine the effects of vitamin A deficiency and retinoic acid repletion on the in vivo expression of apoA-I in rat intestine and liver. The relative abundance of apoA-I mRNA (apoA-I/β-actin ratio) in the intestine did not differ significantly between vitamin A-deficient and -sufficient rats. However, the relative abundance of hepatic apoA-I mRNA of vitamin A-deficient rats was 2.2- to 6-times that of sufficient rats. Even marginal vitamin A status resulted in a significant increase in hepatic apoA-I mRNA expression. Treatment of vitamin A-deficient rats with a single dose of retinoic acid (20 μg, 20 h before tissues were collected) reduced the hepatic apoA-I mRNA/β actin ratio by about 40%, while further reduction (about 60-65%) was observed after two treatments with retinoic acid. By nuclear run-on assay, the increase in hepatic apoA-I mRNA in vitamin A-deficient rats was attributable to increased transcription of the apoA-I gene. However, immunoblot analysis showed no apparent differences in apoA-I protein in either liver homogenates or plasma of vitamin A-deficient and -sufficient rats. These data indicate that apoA-I gene expression in vivo is sensitive to retinoid status and suggest that there is additional regulation of post-transcriptional events.

Original languageEnglish (US)
Pages (from-to)1985-1992
Number of pages8
JournalJournal of Lipid Research
Volume35
Issue number11
StatePublished - 1994

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Vitamin A Deficiency
Apolipoprotein A-I
Tretinoin
Vitamin A
Rats
Messenger RNA
Liver
Gene expression
Intestines
Actins
Gene Expression
Retinoids
Transcription
Assays
Genes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Endocrinology
  • Cell Biology

Cite this

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title = "Effect of vitamin A deficiency and retinoic acid repletion on intestinal and hepatic apolipoprotein A-I mRNA levels of adult rats",
abstract = "Apolipoprotein A-I (apoA-I) gene expression is known to be regulated by nutritional and hormonal factors. Experiments were conducted to determine the effects of vitamin A deficiency and retinoic acid repletion on the in vivo expression of apoA-I in rat intestine and liver. The relative abundance of apoA-I mRNA (apoA-I/β-actin ratio) in the intestine did not differ significantly between vitamin A-deficient and -sufficient rats. However, the relative abundance of hepatic apoA-I mRNA of vitamin A-deficient rats was 2.2- to 6-times that of sufficient rats. Even marginal vitamin A status resulted in a significant increase in hepatic apoA-I mRNA expression. Treatment of vitamin A-deficient rats with a single dose of retinoic acid (20 μg, 20 h before tissues were collected) reduced the hepatic apoA-I mRNA/β actin ratio by about 40{\%}, while further reduction (about 60-65{\%}) was observed after two treatments with retinoic acid. By nuclear run-on assay, the increase in hepatic apoA-I mRNA in vitamin A-deficient rats was attributable to increased transcription of the apoA-I gene. However, immunoblot analysis showed no apparent differences in apoA-I protein in either liver homogenates or plasma of vitamin A-deficient and -sufficient rats. These data indicate that apoA-I gene expression in vivo is sensitive to retinoid status and suggest that there is additional regulation of post-transcriptional events.",
author = "R. Zolfaghari and Ross, {A. Catharine}",
year = "1994",
language = "English (US)",
volume = "35",
pages = "1985--1992",
journal = "Journal of Lipid Research",
issn = "0022-2275",
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T1 - Effect of vitamin A deficiency and retinoic acid repletion on intestinal and hepatic apolipoprotein A-I mRNA levels of adult rats

AU - Zolfaghari, R.

AU - Ross, A. Catharine

PY - 1994

Y1 - 1994

N2 - Apolipoprotein A-I (apoA-I) gene expression is known to be regulated by nutritional and hormonal factors. Experiments were conducted to determine the effects of vitamin A deficiency and retinoic acid repletion on the in vivo expression of apoA-I in rat intestine and liver. The relative abundance of apoA-I mRNA (apoA-I/β-actin ratio) in the intestine did not differ significantly between vitamin A-deficient and -sufficient rats. However, the relative abundance of hepatic apoA-I mRNA of vitamin A-deficient rats was 2.2- to 6-times that of sufficient rats. Even marginal vitamin A status resulted in a significant increase in hepatic apoA-I mRNA expression. Treatment of vitamin A-deficient rats with a single dose of retinoic acid (20 μg, 20 h before tissues were collected) reduced the hepatic apoA-I mRNA/β actin ratio by about 40%, while further reduction (about 60-65%) was observed after two treatments with retinoic acid. By nuclear run-on assay, the increase in hepatic apoA-I mRNA in vitamin A-deficient rats was attributable to increased transcription of the apoA-I gene. However, immunoblot analysis showed no apparent differences in apoA-I protein in either liver homogenates or plasma of vitamin A-deficient and -sufficient rats. These data indicate that apoA-I gene expression in vivo is sensitive to retinoid status and suggest that there is additional regulation of post-transcriptional events.

AB - Apolipoprotein A-I (apoA-I) gene expression is known to be regulated by nutritional and hormonal factors. Experiments were conducted to determine the effects of vitamin A deficiency and retinoic acid repletion on the in vivo expression of apoA-I in rat intestine and liver. The relative abundance of apoA-I mRNA (apoA-I/β-actin ratio) in the intestine did not differ significantly between vitamin A-deficient and -sufficient rats. However, the relative abundance of hepatic apoA-I mRNA of vitamin A-deficient rats was 2.2- to 6-times that of sufficient rats. Even marginal vitamin A status resulted in a significant increase in hepatic apoA-I mRNA expression. Treatment of vitamin A-deficient rats with a single dose of retinoic acid (20 μg, 20 h before tissues were collected) reduced the hepatic apoA-I mRNA/β actin ratio by about 40%, while further reduction (about 60-65%) was observed after two treatments with retinoic acid. By nuclear run-on assay, the increase in hepatic apoA-I mRNA in vitamin A-deficient rats was attributable to increased transcription of the apoA-I gene. However, immunoblot analysis showed no apparent differences in apoA-I protein in either liver homogenates or plasma of vitamin A-deficient and -sufficient rats. These data indicate that apoA-I gene expression in vivo is sensitive to retinoid status and suggest that there is additional regulation of post-transcriptional events.

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