Repair Injured Heart by Regulating Cardiac Regenerative Signals

Cai, Wenfeng; Liu, Guansheng; Wang, Lei; Paul, Christian; Wen, Zhiyuan; Wang, Yigang

doi:10.1155/2016/6193419

Cited by 12 publications

(7 citation statements)

References 114 publications

(123 reference statements)

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“…Our results showing that the reverse changes in the BM and heart MSC content during AC progression, together with the evidence that BM cells actively contribute to heart remodeling in different disease conditions [30,31], guided the hypothesis that engraftment of BM-derived MSCs could play a role in myocardial remodeling in Dsg2 mut/mut mice. We thus set out to quantify myocardial infiltration by MSCs and to determine whether it was dependent on heart damage, or if the cell intrinsic properties of Dsg2 mut/mut MSCs could play a role.…”

Section: Intravenously Injected Bone Marrow-derived Dsg2 Mut/mut Mesenchymal Stromal Cells Have Increased Propensity To Migrate To the Acsupporting

confidence: 67%

“…The BM is one of the main sources of MSCs, and myocardial injury and cell death recruit BM-derived MSCs, which contribute to heart remodeling [ 30 , 31 ]. We thus assessed the expression of desmosomal genes in cardiac- and BM-MSCs, compared the levels of the different desmosomal proteins in the two cell populations, and assessed the effects of AC-linked Dsg2 variant on cardiac- and BM-MSC phenotypes and biology.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Arrhythmogenic Cardiomyopathy Is a Multicellular Disease Affecting Cardiac and Bone Marrow Mesenchymal Stromal Cells

Scalco

Liboni

Angioni

et al. 2021

JCM

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Arrhythmogenic cardiomyopathy (AC) is a familial cardiac disorder at high risk of arrhythmic sudden death in the young and athletes. AC is hallmarked by myocardial replacement with fibro-fatty tissue, favoring life-threatening cardiac arrhythmias and contractile dysfunction. The AC pathogenesis is unclear, and the disease urgently needs mechanism-driven therapies. Current AC research is mainly focused on ‘desmosome-carrying’ cardiomyocytes, but desmosomal proteins are also expressed by non-myocyte cells, which also harbor AC variants, including mesenchymal stromal cells (MSCs). Consistently, cardiac-MSCs contribute to adipose tissue in human AC hearts. We thus approached AC as a multicellular disorder, hypothesizing that it also affects extra-cardiac bone marrow (BM)-MSCs. Our results show changes in the desmosomal protein profile of both cardiac- and BM- MSCs, from desmoglein-2 (Dsg2)-mutant mice, accompanied with profound alterations in cytoskeletal organization, which are directly caused by AC-linked DSG2 downregulation. In addition, AC BM-MSCs display increased proliferation rate, both in vitro and in vivo, and, by using the principle of the competition homing assay, we demonstrated that mutant circulating BM-MSCs have increased propensity to migrate to the AC heart. Taken altogether, our results indicate that cardiac- and BM- MSCs are additional cell types affected in Dsg2-linked AC, warranting the novel classification of AC as a multicellular and multiorgan disease.

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Section: Intravenously Injected Bone Marrow-derived Dsg2 Mut/mut Mesenchymal Stromal Cells Have Increased Propensity To Migrate To the Acsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Arrhythmogenic Cardiomyopathy Is a Multicellular Disease Affecting Cardiac and Bone Marrow Mesenchymal Stromal Cells

Scalco

Liboni

Angioni

et al. 2021

JCM

View full text Add to dashboard Cite

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“…Zebrafish cardiac regeneration involves multiple signaling pathways [11][12][13]. BMP signaling is vital for vertebrate cardiovascular development [14,15], and its function in cardiac injury and repair has become more appreciated.…”

Section: Introductionmentioning

confidence: 99%

BMP and Notch Signaling Pathways differentially regulate Cardiomyocyte Proliferation during Ventricle Regeneration

Wang¹,

Hu²,

Pang³

et al. 2021

Int. J. Biol. Sci.

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Adult mammalian hearts show limited capacity to proliferate after injury, while zebrafish are capable to completely regenerate injured hearts through the proliferation of spared cardiomyocytes. BMP and Notch signaling pathways have been implicated in cardiomyocyte proliferation during zebrafish heart regeneration. However, the molecular mechanism underneath this process as well as the interaction between these two pathways remains to be further explored. In this study we showed BMP signaling was activated after ventricle ablation and acted epistatic downstream of Notch signaling. Inhibition of both signaling pathways differentially influenced ventricle regeneration and cardiomyocyte proliferation, as revealed by time-lapse analysis using a cardiomyocyte-specific FUCCI (fluorescent ubiquitylation-based cell cycle indicator) system. Further experiments revealed that inhibition of BMP and Notch signaling led to cell-cycle arrest at different phases. Overall, our results shed light on the interaction between BMP and Notch signaling pathways and their functions in cardiomyocyte proliferation during cardiac regeneration.

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“…NRG-1 activated during myocardial infarct and cardiomyocytes will proliferate after damage and through the regeneration helped by the intracellular and extracellular signal. NRG-1 regulates cardiogenesis and cardiac regeneration [9], [10].…”

Section: Discussionmentioning

confidence: 99%

Relationship between Plasma Neuregulin-1 and MDA Levels with Severity of CAD

Aliska¹,

Fadil²,

Ilhami³

et al. 2020

Open Access Maced J Med Sci

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BACKGROUND: Neuregulins (NRGs) are one of the epidermal growth factors (EGF) superfamily, which released in cellular injuries, such as neurons and myocardial cells. Neuregulin-1β (NRG-1β) could be activated when stress happens to myocardial cells, acting as a survival factor to repair the injury. Malondialdehyde (MDA) is also produced during oxidative stress in cardiac injury. In vivo study of myocardial cells in rats and dogs that got ischemic, dilated, and viral cardiomyopathy showed that NRG-1 could improve the injured cardiac performance, attenuated pathological changes, and prolonged survival of the cells. AIM: We aimed to observe NRG-1 levels in CAD patients in Indonesia, mainly focused in Minang ethnicity. This study also analyzes the relationship between NRG-1 and MDA with CAD’s severity. METHODS: We measured plasma NRG-1 in 61 nondiabetic patients within 38–82 years old range with STEMI, NSTEMI, and UAP. RESULTS: We found their plasma NRG1, respectively, was 10.3 (1.9–38.2) ng/ml, 14.3 ± 7.2 ng/ml, and 7.05 (4.5–0.4) ng/mL. Plasma NRG 1 increased in AMI patients. CONCLUSION: This study concludes that NRG1’s activated during cardiac cells injury, in any AMI.

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Repair Injured Heart by Regulating Cardiac Regenerative Signals

Cited by 12 publications

References 114 publications

Arrhythmogenic Cardiomyopathy Is a Multicellular Disease Affecting Cardiac and Bone Marrow Mesenchymal Stromal Cells

Arrhythmogenic Cardiomyopathy Is a Multicellular Disease Affecting Cardiac and Bone Marrow Mesenchymal Stromal Cells

BMP and Notch Signaling Pathways differentially regulate Cardiomyocyte Proliferation during Ventricle Regeneration

Relationship between Plasma Neuregulin-1 and MDA Levels with Severity of CAD

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