A promoter that drives gene expression preferentially in male transgenic rats
Male
0301 basic medicine
Injections, Subcutaneous
Ovariectomy
Blotting, Western
Enzyme-Linked Immunosorbent Assay
Estrogens
Real-Time Polymerase Chain Reaction
Rats
Animals, Genetically Modified
Mice
03 medical and health sciences
C-Reactive Protein
Gene Expression Regulation
Liver
Albumins
Animals
Humans
Female
Promoter Regions, Genetic
Orchiectomy
DNA Primers
DOI:
10.1007/s11248-013-9773-9
Publication Date:
2013-12-14T15:46:47Z
AUTHORS (13)
ABSTRACT
Gender-preferential gene expression is a widespread phenomenon in humans. It is important to study how gender differences influence the pathogenesis of various diseases and response to specific drugs. The aim of this study is to determine if the mouse albumin enhancer/promoter may serve as the promoter to introduce gender-preferential gene expression in transgenic animals. We created four independent transgenic rat lines in which the human C-reactive protein transgene was under the control of mouse albumin enhancer/promoter. Quantitative real time RT-PCR analysis showed that transgene expression in the liver of male rats was significantly higher than transgene expression in the female rats (P < 0.05).There was a 5.3-fold (male/female) difference in line-519, and a 12.2-fold (male/female) difference in line-488. Enzyme-linked immunosorbent assay showed that the serum of male transgenic rats had a 13- to 679-fold difference at the protein level on transgene production compared with female transgenic rats. The male-to-female difference in gene expression was 10- to 17-fold in the liver of transgenic rats. Orchiectomy dramatically reduced protein production from the transgene in the liver. Testosterone administration into female rats did not increase the transgene expression, but estrogen administration into the male rats reduced transgene expression. This study provides a valuable tool for investigating the pathological roles of genes that are expressed in a gender-preferential manner in human disease.
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CITATIONS (10)
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