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.
(Less)
- author
- 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
- organization
- publishing date
- 2022
- 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
-
- scopus:85129672120
- pmid:35563680
- 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
- 2024-12-13 05:55:47
@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}},
}