Cardiac transcriptome analysis of BBLN-transgenic mice by NGS
The study applied NGS to determine the cardiac transcriptomes of BBLN-transgenic mice with FVB/N background in comparison to those of non-transgenic FVB/N mice at an age of 8 months. The BBLN (Bublin coiled-coil protein) is the chromosome 9 open reading frame, C9orf16, with largely unknown function. To investigate the cardiac phenotype of increased cardiac BBLN transcript levels we generated BBLN-transgenic (Tg-BBLN) mice. Echocardiography documented that Tg-BBLN mice developed features of heart failure at an age of 8 months. To elucidate pathomechanisms of heart failure induced by BBLN, we performed NGS of the cardiac transcriptomes of eight-month-old, male, BBLN-transgenic mice with cardiac-specific expression of BBLN under control of the myocardium-specific, alpha-MHC promoter. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic BBLN expression. Overall design: Cardiac transcriptomes were determined by NGS of total hearts isolated from four male BBLN-transgenic (Tg-BBLN) mice at an age of 8 months. Tg-BBLN mice have an FVB/N background. Therefore,  four, age-matched, non-transgenic, male FVB/N mice were used as the non-transgenic control group. Hearts were isolated from male mice at the end of the observation period at an age of 8 months. The group size was n=4 male mice at an age of 8 months per group. Tg-BBLN mice showed symptoms of heart failure. NGS data of the cardiac transcriptome confirmed the heart heart failure phenotype induced by an increased cardiac BBLN transcript level. All the mice of the study were weaned at an age of 3 to 4 weeks. The mice were housed under SPF conditions in groups of 2-4 mice in individually ventilated cages  with a 12h dark cycle, and had free access to food and water until the end of the observation period at an age of 8 months.