We previously identified a nonsense mutation in the stromal interaction molecule-1 (Stim1) resulting in expression of a truncated STIM1 in the stroke-prone spontaneously hypertensive rat (SHRSP). In this study, we evaluated activity of the store-operated Ca(2+)-entry (SOCE) regulated by STIM1 to clarify putative functional abnormalities of the truncated STIM1. As a result, reduced SOCE activity resulting in suppression of cyclooxygenase-2 expression induced by SOCE was found in cultured astrocytes with the truncated STIM1 when compared with those with the wild-type. Our results indicated that the truncated STIM1 impaired Ca(2+) signaling regulated by SOCE and that the impaired SOCE activity might be responsible for pathological phenotypes in SHRSP.
Keywords: Store-operated Ca(2+)-entry; Stroke-prone spontaneously hypertensive rat; Stromal interaction molecule-1.
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