In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 310, No. 1 ( 2016-01-01), p. H92-H103
Abstract:
Sarcolipin (SLN) is a small proteolipid and a regulator of sarco(endo)plasmic reticulum Ca 2+ -ATPase. In heart tissue, SLN is exclusively expressed in the atrium. Previously, we inserted Cre recombinase into the endogenous SLN locus by homologous recombination and succeeded in generating SLN-Cre knockin (Sln Cre/+ ) mice. This Sln Cre/+ mouse can be used to generate an atrium-specific gene-targeting mutant, and it is based on the Cre-loxP system. In the present study, we used adult Sln Cre/+ mice atria and analyzed the effects of heterozygous SLN deletion by Cre knockin before use as the gene targeting mouse. Both SLN mRNA and protein levels were decreased in Sln Cre/+ mouse atria, but there were no morphological, physiological, or molecular biological abnormalities. The properties of contractility and Ca 2+ handling were similar to wild-type (WT) mice, and expression levels of several stress markers and sarcoplasmic reticulum-related protein levels were not different between Sln Cre/+ and WT mice. Moreover, there was no significant difference in sarco(endo)plasmic reticulum Ca 2+ -ATPase activity between the two groups. We showed that Sln Cre/+ mice were not significantly different from WT mice in all aspects that were examined. The present study provides basic characteristics of Sln Cre/+ mice and possibly information on the usefulness of Sln Cre/+ mice as an atrium-specific gene-targeting model.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.00411.2015
Language:
English
Publisher:
American Physiological Society
Publication Date:
2016
detail.hit.zdb_id:
1477308-9
SSG:
12
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