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

Abstract 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+, α-SMAhigh+), increases in senescence markers (p21, SA-β-gαl), 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.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 29315310
OWN - NLM
STAT- In-Process
LR  - 20180117
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 13
IP  - 1
DP  - 2018
TI  - Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d 
      in naturally occurring canine myxomatous mitral valve disease.
PG  - e0188617
LID - 10.1371/journal.pone.0188617 [doi]
AB  - 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+, alpha-SMAhigh+), increases in
      senescence markers (p21, SA-beta-galphal), and decreased cell viability and
      proliferation potential. RT-qPCR and miRNA sequencing analyses both showed
      significant (p&lt;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.
FAU - Yang, Vicky K
AU  - Yang VK
AUID- ORCID: 0000-0002-1281-4250
AD  - Department of Clinical Sciences, Tufts University Cummings School of Veterinary
      Medicine, North Grafton, Massachusetts, United States of America.
FAU - Tai, Albert K
AU  - Tai AK
AD  - Department of Integrative Physiology and Pathobiology, Tufts University School of
      Medicine, Boston, Massachusetts, United States of America.
FAU - Huh, Terry P
AU  - Huh TP
AD  - Department of Clinical Sciences, Tufts University Cummings School of Veterinary
      Medicine, North Grafton, Massachusetts, United States of America.
FAU - Meola, Dawn M
AU  - Meola DM
AD  - Department of Clinical Sciences, Tufts University Cummings School of Veterinary
      Medicine, North Grafton, Massachusetts, United States of America.
FAU - Juhr, Christine M
AU  - Juhr CM
AD  - Department of Clinical Sciences, Tufts University Cummings School of Veterinary
      Medicine, North Grafton, Massachusetts, United States of America.
FAU - Robinson, Nicholas A
AU  - Robinson NA
AD  - Department of Biomedical Sciences, Tufts University Cummings School of Veterinary
      Medicine, North Grafton, Massachusetts, United States of America.
FAU - Hoffman, Andrew M
AU  - Hoffman AM
AD  - Department of Clinical Sciences, Tufts University Cummings School of Veterinary
      Medicine, North Grafton, Massachusetts, United States of America.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180109
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
EDAT- 2018/01/10 06:00
MHDA- 2018/01/10 06:00
CRDT- 2018/01/10 06:00
PHST- 2017/07/24 00:00 [received]
PHST- 2017/11/10 00:00 [accepted]
PHST- 2018/01/10 06:00 [entrez]
PHST- 2018/01/10 06:00 [pubmed]
PHST- 2018/01/10 06:00 [medline]
AID - 10.1371/journal.pone.0188617 [doi]
AID - PONE-D-17-27669 [pii]
PST - epublish
SO  - PLoS One. 2018 Jan 9;13(1):e0188617. doi: 10.1371/journal.pone.0188617.
      eCollection 2018.