Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease
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 le...
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ftzenodo:oai:zenodo.org:4975877 2023-05-15T15:50:37+02:00 Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease Yang, Vicky K. Tai, Albert K. Huh, Terry P. Meola, Dawn M. Juhr, Christine M. Robinson, Nicholas A. Hoffman, Andrew M. 2018-11-15 https://zenodo.org/record/4975877 https://doi.org/10.5061/dryad.3274k unknown doi:10.1371/journal.pone.0188617 https://zenodo.org/communities/dryad https://zenodo.org/record/4975877 https://doi.org/10.5061/dryad.3274k oai:zenodo.org:4975877 info:eu-repo/semantics/openAccess https://creativecommons.org/publicdomain/zero/1.0/legalcode Canis lupus familiaris info:eu-repo/semantics/other dataset 2018 ftzenodo https://doi.org/10.5061/dryad.3274k10.1371/journal.pone.0188617 2023-03-10T14:10:51Z 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 Dataset Canis lupus Zenodo |
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Canis lupus familiaris Yang, Vicky K. Tai, Albert K. Huh, Terry P. Meola, Dawn M. Juhr, Christine M. Robinson, Nicholas A. Hoffman, Andrew M. Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease |
topic_facet |
Canis lupus familiaris |
description |
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 |
format |
Dataset |
author |
Yang, Vicky K. Tai, Albert K. Huh, Terry P. Meola, Dawn M. Juhr, Christine M. Robinson, Nicholas A. Hoffman, Andrew M. |
author_facet |
Yang, Vicky K. Tai, Albert K. Huh, Terry P. Meola, Dawn M. Juhr, Christine M. Robinson, Nicholas A. Hoffman, Andrew M. |
author_sort |
Yang, Vicky K. |
title |
Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease |
title_short |
Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease |
title_full |
Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease |
title_fullStr |
Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease |
title_full_unstemmed |
Data from: Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease |
title_sort |
data from: dysregulation of valvular interstitial cell let-7c, mir-17, mir-20a, and mir-30d in naturally occurring canine myxomatous mitral valve disease |
publishDate |
2018 |
url |
https://zenodo.org/record/4975877 https://doi.org/10.5061/dryad.3274k |
genre |
Canis lupus |
genre_facet |
Canis lupus |
op_relation |
doi:10.1371/journal.pone.0188617 https://zenodo.org/communities/dryad https://zenodo.org/record/4975877 https://doi.org/10.5061/dryad.3274k oai:zenodo.org:4975877 |
op_rights |
info:eu-repo/semantics/openAccess https://creativecommons.org/publicdomain/zero/1.0/legalcode |
op_doi |
https://doi.org/10.5061/dryad.3274k10.1371/journal.pone.0188617 |
_version_ |
1766385610753310720 |