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Stromal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum Ca 2+  sensor, has been shown to control a Ca 2+ -dependent signal that promotes cardiac hypertrophy. However, whether STIM1 has adaptive role that helps to protect against cardiac overload stress remains unknown. We hypothesized that STIM1 deficiency causes a maladaptive response to pressure overload stress. We investigated STIM1 heterozygous KO ( STIM1  +/– ) mice hearts, in which STIM1 protein levels decreased to 27% of wild-type (WT) with no compensatory increase in STIM2. Under stress-free conditions, no significant differences were observed in electrocardiographic and echocardiographic parameters or blood pressure between  STIM1  +/– and WT mice. However, when  STIM1   +/–  mice were subjected to transverse aortic constriction (TAC),  STIM1   +/–  mice had a higher mortality rate than WT mice. The TAC-induced increase in the heart weight to body weight ratio (mean mg/g ± standard error of the mean) was significantly inhibited in  STIM1  +/– mice (WT sham, 4.12 ± 0.14; WT TAC, 6.23 ± 0.40;  STIM1  +/– sham, 4.53 ± 0.16;  STIM1  +/– TAC, 4.63 ± 0.08). Reverse transcription-polymerase chain reaction analysis of the left ventricles of TAC-treated  STIM1  +/– mice showed inhibited induction of cardiac fetal genes, including those encoding brain and atrial natriuretic proteins. Western blot analysis showed upregulated expression of transient receptor potential channel 1 (TRPC1) in TAC-treated WT mice, but suppressed expression in TAC-treated  STIM1  +/– mice. Taken together, the hearts of STIM1 haploinsufficient mice had a superficial resemblance to the WT phenotype under stress-free conditions; however, STIM1 haploinsufficient mice showed a maladaptive response to cardiac pressure overload.

Stromal interaction molecule 1 haploinsufficiency causes maladaptive response to pressure overload