10.3389/fphar.2018.00868.s001
Martin Houde
Martin
Houde
Adel Schwertani
Adel
Schwertani
Hanène Touil
Hanène
Touil
Louisane Desbiens
Louisane
Desbiens
Otman Sarrhini
Otman
Sarrhini
Roger Lecomte
Roger
Lecomte
Martin Lepage
Martin
Lepage
Hugo Gagnon
Hugo
Gagnon
Shinji Takai
Shinji
Takai
Gunnar Pejler
Gunnar
Pejler
Danielle Jacques
Danielle
Jacques
Fernand Gobeil
Fernand
Gobeil
Robert Day
Robert
Day
Pedro D’Orléans-Juste
Pedro
D’Orléans-Juste
Data_Sheet_1_Mouse Mast Cell Protease 4 Deletion Protects Heart Function and Survival After Permanent Myocardial Infarction.pdf
Frontiers
2018
chymase
mouse mast cell protease 4
myocardial infarction
positron emission tomography
glycoproteomics
active caspase-3
collagen
2018-08-31 04:02:38
Dataset
https://frontiersin.figshare.com/articles/dataset/Data_Sheet_1_Mouse_Mast_Cell_Protease_4_Deletion_Protects_Heart_Function_and_Survival_After_Permanent_Myocardial_Infarction_pdf/7034069
<p>Chymase, a mast cell serine protease involved in the generation of multiple cardiovascular factors, such as angiotensin II and endothelin-1 (ET-1), is elevated and participates in tissue degeneration after permanent myocardial infarction (PMI). Anesthetized 4-month old male wild-type (WT) C57BL/6J mice and mouse mast cell protease-4 knockout (mMCP-4 KO) congeners were subjected to ligation of the left anterior descending (LAD) coronary artery. A group of mice was then subjected to Kaplan-Meier 28-day survival analysis. In another group of mice, <sup>18</sup>F-fluorodeoxyglucose positron emission tomography (PET) was performed to evaluate heart function and the infarcted zone 3 days post-PMI surgery. Cardiac morphology following PMI was evaluated on formalin-fixed heart slices and glycoproteomic analysis was performed using mass spectrometry. Finally, cardiac and lung tissue content of immunoreactive ET-1 was determined. PMI caused 60% mortality in WT mice, due to left ventricular wall rupture, and 7% in mMCP-4 KO mice. Cardiac PET analysis revealed a significant reduction in left ventricular volume (systolic and diastolic) and preserved the ejection fraction in mMCP-4 KO compared to WT animals. The infarcted area, apoptotic signaling and wall remodeling were significantly decreased in mMCP-4 KO mice compared to their WT congeners, while collagen deposition was increased. Glycoproteomic analysis showed an increase in apolipoprotein A1, an established chymase substrate in mMCP-4 KO mice compared to WT mice post-PMI. ET-1 levels were increased in the lungs of WT, but not mMCP-4 KO mice, 24 h post-PMI. Thus, the genetic deletion of mMCP-4 improved survival and heart function post-PMI.</p>