Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease

• Main Authors: Yang, Vicky K., Tai, Albert K., Huh, Terry P., Meola, Dawn M., Juhr, Christine M., Robinson, Nicholas A., Hoffman, Andrew M.
• Format: Dataset
• Language: unknown
• Published: Data Archiving and Networked Services (DANS) 2017
• Subjects: Life sciences; medicine and health care; Canis lupus familiaris; socio; envir; Canis lupus
• Online Access: https://doi.org/10.5061/dryad.3274k

Canine myxomatous mitral valve disease (MMVD) resembles the early stages of myxomatous pathology seen in human non-syndromic mitral valve prolapse, a common valvular heart disease in the adult human population. Canine MMVD is seen in older subjects, suggesting age-related epigenetic dysregulation leading to derangements in valvular cell populations and matrix synthesis or degradation. We hypothesized that valvular interstitial cells (VICs) undergo disease-relevant changes in miRNA expression. In primary VIC lines from diseased and control valves, miRNA expression was profiled using RT-qPCR and next generation sequencing. VICs from diseased valves showed phenotypic changes consistent with myofibroblastic differentiation (vimentinlow+, a-SMAhigh+), increases in senescence markers (p21, SA-b-gal), and decreased cell viability and proliferation potential. RT-qPCR and miRNA sequencing analyses both showed significant (p<0.05) downregulation of let-7c, miR-17, miR-20a, and miR-30d in VICs from diseased valves compared to controls. Decreased let-7c, miR-17, and miR-20a may contribute to myofibroblastic differentiation in addition to cell senescence, and decreased miR-30d may disinhibit cell apoptosis. These data support the hypothesis that epigenetic dysregulation plays an important role in age-related canine MMVD. RNAseq dataExcel data file with RNAseq count dataDESeq2_normalized_data.xlsxRT-qPCR DataPCR data with Ct numbersVICs PCR Data.xlsx