Characterization of early myocardial inflammation in ischemia-reperfusion injury

Abstract

BackgroundMyocardial injury may be caused by myocardial ischemia-reperfusion (IR), and salvaging such an injury is still a great challenge in clinical practice. This study comprehensively characterized the physiopathologic changes of myocardial injury after IR to explore the underlying mechanism in the early reperfusion phase with particular emphasis on early myocardial inflammation.Methods and ResultsThe experimental IR model was obtained by the left anterior descending artery’s transient ligation of C57BL/6 mice. T2W signals of all mice showed increased signal at different IR stages. It was positively correlated with inflammatory cytokines and cells. T2W imaging by 7.0 T MRI surprisingly detected signal enhancement, but histopathology and flow cytometry did not reveal any inflammatory cells infiltration within 3 h after IR. Cardiomyocyte swelling and increased vascular permeability were observed by WGA staining and ultrastructural analysis, respectively. The 3 h IR group showed that the cardiomyocytes were severely affected with disintegrating myofilaments and mitochondria. Both VEGF and phosphorylated Src protein were markedly expressed in the 3 h IR group in comparison with the sham group, and TUNEL staining displayed little positive cells. Cleaved caspase-3 apoptin also has similar expression levels with that of the sham group. Resident macrophages had notably become M1 phenotype. The T2W signal was still elevated, and we observed that collagen deposition occurred from 1 to 7 days.ConclusionsThe inflammation response during the first week after reperfusion injury gradually increase 3 h later, but the main manifestation before that was edema. This study indicated that the first 3 h may be crucial to the early rescue process for reperfusion-induced myocardial injury due to inflammatory cell infiltration absence and apoptosis.

Multilineage-Differentiating Stress-Enduring Cells: A Powerful Tool for Tissue Damage Repair

“…To date, Muse cells have been used in neurological diseases [63,66,[107][108][109][110][111][112], cardiac systemic diseases [39,49,55,75,[113][114][115][116], renal diseases [40,99,117], dermatological diseases [44,78,[118][119][120], liver diseases [29,41,67,101,121], and other diseases to demonstrate their desirable effects in treating and repairing damaged tissues. In these disease models, Muse cells can migrate to the lesion site and spontaneously differentiate into histocompatible cells such as neurons (ectoderm) [43,111,122], cardiomyocytes (mesoderm) [115,123], glomerulocytes (mesoderm) [40,117], vascular endothelial cells (mesoderm) [34,120]and hepatocytes (entoderm) [41,101,121].…”

High-resolution magnetic resonance vessel wall imaging in ischemic stroke and carotid artery atherosclerotic stenosis: A review

“…T2W and PD-weighted imaging provide additional information about the vessel wall. T2W imaging is sensitive to edema and inflammation within the vessel wall [ 52 ], while PD-weighted imaging is sensitive to plaque components such as lipid-rich cores and calcifications [ 45 ] ( Fig. 2 ).…”

“…In summary, HR-VWI requires the use of T1W BB, T2W and PD-weighted imaging, and 3D TOF-MRA. Complementary information provided by these contrast techniques about vessel walls, plaques, and blood flow enables a comprehensive assessment of carotid artery disease and aids in clinical management decisions [ 45 , 51 , 52 , 53 ]. According to the signal intensity of histology on different sequences, various pulse sequences in HR-VWI are associated with distinct advantages and disadvantages.…”

Multilineage-differentiating stress-enduring cells: a powerful tool for tissue damage repair

“…To date, Muse cells have been used in neurological diseases ( Uchida H. et al, 2017 ; Shimamura et al, 2017 ; Hori et al, 2020 ; Ozuru et al, 2020 ; Chen et al, 2021 ; Kajitani et al, 2021 ; Suzuki et al, 2021 ; Yin et al, 2023 ), cardiac systemic diseases ( Amin et al, 2018 ; Minatoguchi et al, 2018 ; Tanaka et al, 2018 ; Yamada et al, 2018 ; Yamada et al, 2022 ; Yamada et al, 2022 ; Castillo et al, 2023 ; Wu et al, 2023 ), renal diseases ( Batchelder et al, 2009 ; Uchida N. et al, 2017 ; Uchida et al, 2018 ), dermatological diseases ( Yamauchi et al, 2017 ; Yamauchi, 2018 ; Guo et al, 2020 ; Fei et al, 2021 ; Fujita et al, 2021 ; Fujita et al, 2021 ), liver diseases ( Iseki et al, 2017 ; Nishizuka, 2018 ; Hessheimer et al, 2021b ; Shono et al, 2021 ; Kikuchi et al, 2022 ), and other diseases to demonstrate their desirable effects in treating and repairing damaged tissues. In these disease models, Muse cells can migrate to the lesion site and spontaneously differentiate into histocompatible cells such as neurons (ectoderm) ( Zheng et al, 2018 ; Hori et al, 2020 ; Yamashita et al, 2021 ), cardiomyocytes (mesoderm) ( Noda et al, 2020 ; Yamada et al, 2022 ), glomerulocytes (mesoderm) ( Batchelder et al, 2009 ; Uchida N. et al, 2017 ), vascular endothelial cells (mesoderm) ( Kinoshita et al, 2015 ; Yamauchi, 2018 ) and hepatocytes (entoderm) ( Iseki et al, 2017 ; Hessheimer et al, 2021b ; Shono et al, 2021 ).…”