Heterozygous deletion of sarcolipin maintains normal cardiac function

Sarcolipin (SLN) is a small proteolipid and a regulator of sarco(endo)plasmic reticulum Ca²⁺-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 Ca²⁺ 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 Ca²⁺-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.