Expression and Regulatory Mechanisms of SNAP25 and Syntaxin 1A in H9c2 Cells

Two SNARE proteins, SNAP25 and STX1A, are widely expressed in neurons and neuroendocrine cells, and more recently, shown to be expressed in the heart, but their underlying mechanisms remain unknown. This study examined the regulation of SNAP25 and STX1A gene promoters in the cardiac cell line, H9c2. The cells were treated with the HDAC inhibitor, trichostatin A (TSA), forskolin to activate PKA, or retinoic acid to induce differentiation to a more cardiac phenotype. The data showed greater activity of the -292 bp SNAP25 promoter compared to the -1517 bp full-length construct. Similarly, the -204 bp promoter constructs of STX1A were higher than the full-length -1931 bp promoter. Neither treatment with TSA, forskolin nor retinoic acid induced expression of SNAP25 or STX1A in H9c2 cells. The results demonstrate SNARE protein expression cannot be induced in H9c2 cells. Further studies are required to determine the regulation of SNARE proteins in the heart.