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Gene Expression of Endothelin Isoforms and Receptors in Endothelin-1 Knockout Mice

Authors: K, Maemura; H, Kurihara; Y, Kurihara; T, Kuwaki; M, Kumada; Y, Yazaki;

Gene Expression of Endothelin Isoforms and Receptors in Endothelin-1 Knockout Mice

Abstract

Gene expression of endothelin (ET) isoforms and receptors was examined in ET-1 knockout mice and compared with that of wild-type mice. ET-1 mRNA and peptide levels were in parallel with the number of Edn1 authentic alleles. ET-2 mRNA levels in intestine and ET-3 mRNA and/or peptide levels in lung, brain, and intestine were not different among Edn1+/+ wild-type, Edn1+/- heterozygous, and Edn1-/- homozygous mice. ET(A) and ETB receptor mRNA levels in several organs also were not different among Edn1+/+ wild-type, Edn1+/- heterozygous, and Edn1-/- homozygous mice. These results suggest that gene expression of ET-2, ET-3, and ET(A/B) receptors is not affected by levels of ET-1 production and is regulated independently. Neither compensation by redundant expression of other ET isoforms nor upregulation of ET receptors could explain the elevated blood pressure in Edn1+/- heterozygous mice.

Related Organizations
Keywords

Mice, Knockout, Mice, Mice, Inbred ICR, Receptors, Endothelin, Endothelins, Hypertension, Animals, Gene Expression, RNA, Messenger

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Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
20
Average
Top 10%
Top 10%