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Ca 2 Control of Transcription Can We Extrapolate Signaling Cascades From Neurons to Vascular Smooth Muscle Cells ?

The Ca 2 hypothesis of transcription suggests that increments in the cytosolic Ca concentration [Ca ]c can activate transcription. The Ca hypothesis has emerged in the field of neurosciences1,2 and was translated to vascular smooth muscle cells (VSMC) by the Burlington group.3–5 The article by Pulver et al in this issue6 demonstrates a close correlation between the increase in [Ca ]c, phosphorylation of nuclear CREB, and the expression of c-fos. Pulver et al introduce the idea that transcriptional activation may be regulated by store-operated Ca entry (SOCE)7–9 as it is activated when thapsigargin blocks the Ca -ATPase SERCA, thereby depleting the SR Ca content. The authors demonstrate this thapsigargin effect not only in cultured VSMC but also in VSMC of intact arteries. They conclude that SOCE may activate transcription and may therefore control the differentiated (contractile) or proliferative (secretory) phenotype of VSMC.10