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Short‐Term Blockade of Pro‐Inflammatory Alarmin S100A9 Favorably Modulates Left Ventricle Proteome and Related Signaling Pathways Involved in Post‐Myocardial Infarction Recovery

Boteanu, Raluca Maria ; Suica, Viorel Iulian ; Uyy, Elena ; Ivan, Luminita ; Cerveanu‐hogas, Aurel ; Mares, Razvan Gheorghita LU ; Simionescu, Maya ; Schiopu, Alexandru LU and Antohe, Felicia (2022) In International Journal of Molecular Sciences 23(9).
Abstract

Prognosis after myocardial infarction (MI) varies greatly depending on the extent of dam-aged area and the management of biological processes during recovery. Reportedly, the inhibition of the pro‐inflammatory S100A9 reduces myocardial damage after MI. We hypothesize that a S100A9 blockade induces changes of major signaling pathways implicated in post‐MI healing. Mass spectrometry‐based proteomics and gene analyses of infarcted mice left ventricle were performed. The S100A9 blocker (ABR‐23890) was given for 3 days after coronary ligation. At 3 and 7 days post‐ MI, ventricle samples were analyzed versus control and Sham‐operated mice. Blockade of S100A9 modulated the expressed proteins involved in five biological processes: leukocyte... (More)

Prognosis after myocardial infarction (MI) varies greatly depending on the extent of dam-aged area and the management of biological processes during recovery. Reportedly, the inhibition of the pro‐inflammatory S100A9 reduces myocardial damage after MI. We hypothesize that a S100A9 blockade induces changes of major signaling pathways implicated in post‐MI healing. Mass spectrometry‐based proteomics and gene analyses of infarcted mice left ventricle were performed. The S100A9 blocker (ABR‐23890) was given for 3 days after coronary ligation. At 3 and 7 days post‐ MI, ventricle samples were analyzed versus control and Sham‐operated mice. Blockade of S100A9 modulated the expressed proteins involved in five biological processes: leukocyte cell–cell adhesion, regulation of the muscle cell apoptotic process, regulation of the intrinsic apoptotic signaling pathway, sarco-mere organization and cardiac muscle hypertrophy. The blocker induced regulation of 36 proteins inter-acting with or targeted by the cellular tumor antigen p53, prevented myocardial compensatory hy-pertrophy, and reduced cardiac markers of post‐ischemic stress. The blockade effect was prominent at day 7 post‐MI when the quantitative features of the ventricle proteome were closer to controls. Blockade of S100A9 restores key biological processes altered post‐MI. These processes could be val-uable new pharmacological targets for the treatment of ischemic heart. Mass spectrometry data are available via ProteomeXchange with identifier PXD033683.

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author
; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
apoptosis, cardiac repair, hypertrophy, myocardial infarction, S100A9
in
International Journal of Molecular Sciences
volume
23
issue
9
article number
5289
publisher
MDPI AG
external identifiers
  • pmid:35563680
  • scopus:85129672120
ISSN
1661-6596
DOI
10.3390/ijms23095289
language
English
LU publication?
yes
id
b9a8031d-cf07-4f69-92a2-adba57fab9cf
date added to LUP
2022-07-06 15:07:59
date last changed
2024-11-01 00:25:47
@article{b9a8031d-cf07-4f69-92a2-adba57fab9cf,
  abstract     = {{<p>Prognosis after myocardial infarction (MI) varies greatly depending on the extent of dam-aged area and the management of biological processes during recovery. Reportedly, the inhibition of the pro‐inflammatory S100A9 reduces myocardial damage after MI. We hypothesize that a S100A9 blockade induces changes of major signaling pathways implicated in post‐MI healing. Mass spectrometry‐based proteomics and gene analyses of infarcted mice left ventricle were performed. The S100A9 blocker (ABR‐23890) was given for 3 days after coronary ligation. At 3 and 7 days post‐ MI, ventricle samples were analyzed versus control and Sham‐operated mice. Blockade of S100A9 modulated the expressed proteins involved in five biological processes: leukocyte cell–cell adhesion, regulation of the muscle cell apoptotic process, regulation of the intrinsic apoptotic signaling pathway, sarco-mere organization and cardiac muscle hypertrophy. The blocker induced regulation of 36 proteins inter-acting with or targeted by the cellular tumor antigen p53, prevented myocardial compensatory hy-pertrophy, and reduced cardiac markers of post‐ischemic stress. The blockade effect was prominent at day 7 post‐MI when the quantitative features of the ventricle proteome were closer to controls. Blockade of S100A9 restores key biological processes altered post‐MI. These processes could be val-uable new pharmacological targets for the treatment of ischemic heart. Mass spectrometry data are available via ProteomeXchange with identifier PXD033683.</p>}},
  author       = {{Boteanu, Raluca Maria and Suica, Viorel Iulian and Uyy, Elena and Ivan, Luminita and Cerveanu‐hogas, Aurel and Mares, Razvan Gheorghita and Simionescu, Maya and Schiopu, Alexandru and Antohe, Felicia}},
  issn         = {{1661-6596}},
  keywords     = {{apoptosis; cardiac repair; hypertrophy; myocardial infarction; S100A9}},
  language     = {{eng}},
  number       = {{9}},
  publisher    = {{MDPI AG}},
  series       = {{International Journal of Molecular Sciences}},
  title        = {{Short‐Term Blockade of Pro‐Inflammatory Alarmin S100A9 Favorably Modulates Left Ventricle Proteome and Related Signaling Pathways Involved in Post‐Myocardial Infarction Recovery}},
  url          = {{http://dx.doi.org/10.3390/ijms23095289}},
  doi          = {{10.3390/ijms23095289}},
  volume       = {{23}},
  year         = {{2022}},
}