Systems biology approach to exploring the effect of cyclic stretching on cardiac cell physiology.
Cells, Cultured
Chemokine CCL2
/ genetics
Cholesterol
/ biosynthesis
Energy Metabolism
Gene Expression Profiling
Gene Expression Regulation
High-Throughput Nucleotide Sequencing
Humans
Inhibitor of Differentiation Protein 1
/ genetics
Inhibitor of Differentiation Proteins
/ genetics
Mechanotransduction, Cellular
/ genetics
Muscle Spindles
/ metabolism
Myocytes, Cardiac
/ metabolism
Neoplasm Proteins
/ genetics
Plasminogen Activator Inhibitor 1
/ genetics
Real-Time Polymerase Chain Reaction
Stress, Mechanical
Systems Biology
Time Factors
Transcriptome
cardiac cell
cyclic stretching
functional enrichment
next-generation sequencing
Journal
Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617
Informations de publication
Date de publication:
05 08 2020
05 08 2020
Historique:
received:
11
03
2020
accepted:
27
05
2020
pubmed:
8
8
2020
medline:
20
4
2021
entrez:
8
8
2020
Statut:
ppublish
Résumé
Although mechanical forces are involved in pressure-overloaded cardiomyopathy, their effects on gene transcription profiles are not fully understood. Here, we used next-generation sequencing (NGS) to investigate changes in genomic profiles after cyclic mechanical stretching of human cardiomyocytes. We found that 85, 87, 32, 29, and 28 genes were differentially expressed after 1, 4, 12, 24, and 48 hours of stretching. Furthermore, 10 of the 29 genes that were up-regulated and 11 of the 28 that were down-regulated after 24 h showed the same changes after 48 h. We then examined expression of the genes that encode serpin family E member 1 (SERPINE1), DNA-binding protein inhibitor 1 (ID1), DNA-binding protein inhibitor 3 (ID3), and CCL2, a cytokine that acts as chemotactic factor in monocytes, in an RT-PCR experiment. The same changes were observed for all four genes after all cyclic stretching durations, confirming the NGS results. Taken together, these findings suggest that cyclical stretching can alter cardiac cell physiology by activating cardiac cell metabolism and impacting cholesterol biosynthesis signaling.
Identifiants
pubmed: 32759460
pii: 103465
doi: 10.18632/aging.103465
pmc: PMC7485730
doi:
Substances chimiques
CCL2 protein, human
0
Chemokine CCL2
0
ID1 protein, human
0
Inhibitor of Differentiation Protein 1
0
Inhibitor of Differentiation Proteins
0
Neoplasm Proteins
0
Plasminogen Activator Inhibitor 1
0
SERPINE1 protein, human
0
ID3 protein, human
147785-34-0
Cholesterol
97C5T2UQ7J
Types de publication
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
16035-16045Références
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