Follistatin‐like 1: A dual regulator that promotes cardiomyocyte proliferation and fibrosis

2020 ◽  
Vol 235 (9) ◽  
pp. 5893-5902 ◽  
Author(s):  
Siyuan Hu ◽  
Hua Liu ◽  
Zhixi Hu ◽  
Lin Li ◽  
Yi Yang
Keyword(s):  
Cardiomyocyte Proliferation ◽  
Dual Regulator

scholarly journals Cardiac regeneration: epicardial mediated repair

2015 ◽  
Vol 282 (1821) ◽  
pp. 20152147 ◽  
Author(s):  
Teresa Kennedy-Lydon ◽  
Nadia Rosenthal
Keyword(s):  
Stem Cells ◽  
Endothelial Cells ◽  
Cardiac Fibroblasts ◽  
Cardiac Regeneration ◽  
Repair Process ◽  
Regenerative Process ◽  
Cardiac Stem Cell ◽  
Cardiomyocyte Proliferation ◽  
Lower Vertebrates

The hearts of lower vertebrates such as fish and salamanders display scarless regeneration following injury, although this feature is lost in adult mammals. The remarkable capacity of the neonatal mammalian heart to regenerate suggests that the underlying machinery required for the regenerative process is evolutionarily retained. Recent studies highlight the epicardial covering of the heart as an important source of the signalling factors required for the repair process. The developing epicardium is also a major source of cardiac fibroblasts, smooth muscle, endothelial cells and stem cells. Here, we examine animal models that are capable of scarless regeneration, the role of the epicardium as a source of cells, signalling mechanisms implicated in the regenerative process and how these mechanisms influence cardiomyocyte proliferation. We also discuss recent advances in cardiac stem cell research and potential therapeutic targets arising from these studies.

The impact of glucocorticoids on Neuregulin-1/ERBB2 signaling in cardiomyocyte proliferation and heart regeneration

2020 ◽  
Vol 140 ◽  
pp. 30
Author(s):  
Nicola Pianca ◽  
Francesca Pontis ◽  
Alla Aharonov ◽  
Chiara Bongiovanni ◽  
Martina Mazzeschi ◽  
...  
Keyword(s):  
Heart Regeneration ◽  
Cardiomyocyte Proliferation ◽  
Neuregulin 1 ◽  
The Impact ◽  
Erbb2 Signaling

scholarly journals A Systematic Exposition of Methods used for Quantification of Heart Regeneration after Apex Resection in Zebrafish

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 548 ◽  
Author(s):  
Helene Juul Belling ◽  
Wolfgang Hofmeister ◽  
Ditte Caroline Andersen
Keyword(s):  
Human Heart ◽  
Quantitative Methods ◽  
Heart Function ◽  
Heart Regeneration ◽  
Cardiomyocyte Proliferation ◽  
Ability To Regenerate ◽  
Specific Proteins ◽  
Heart Injury ◽  
Whole Heart ◽  
Study Designs

Myocardial infarction (MI) is a worldwide condition that affects millions of people. This is mainly caused by the adult human heart lacking the ability to regenerate upon injury, whereas zebrafish have the capacity through cardiomyocyte proliferation to fully regenerate the heart following injury such as apex resection (AR). But a systematic overview of the methods used to evidence heart regrowth and regeneration in the zebrafish is lacking. Herein, we conducted a systematical search in Embase and Pubmed for studies on heart regeneration in the zebrafish following injury and identified 47 AR studies meeting the inclusion criteria. Overall, three different methods were used to assess heart regeneration in zebrafish AR hearts. 45 out of 47 studies performed qualitative (37) and quantitative (8) histology, whereas immunohistochemistry for various cell cycle markers combined with cardiomyocyte specific proteins was used in 34 out of 47 studies to determine cardiomyocyte proliferation qualitatively (6 studies) or quantitatively (28 studies). For both methods, analysis was based on selected heart sections and not the whole heart, which may bias interpretations. Likewise, interstudy comparison of reported cardiomyocyte proliferation indexes seems complicated by distinct study designs and reporting manners. Finally, six studies performed functional analysis to determine heart function, a hallmark of human heart injury after MI. In conclusion, our data implies that future studies should consider more quantitative methods eventually taking the 3D of the zebrafish heart into consideration when evidencing myocardial regrowth after AR. Furthermore, standardized guidelines for reporting cardiomyocyte proliferation and sham surgery details may be considered to enable inter study comparisons and robustly determine the effect of given genes on the process of heart regeneration.

Possible role of a dual regulator of neuroinflammation and autophagy in a simulated space environment

2021 ◽  
Author(s):  
Shicong Zhao ◽  
Sizhu Pei ◽  
Ailu Wang ◽  
Yu Chen ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Space Environment ◽  
Dual Regulator

scholarly journals Deletion of Akt1 causes heart defects and abnormal cardiomyocyte proliferation

2010 ◽  
Vol 347 (2) ◽  
pp. 384-391 ◽  
Author(s):  
Zai Chang ◽  
Qin Zhang ◽  
Qiuting Feng ◽  
Jie Xu ◽  
Teng Teng ◽  
...  
Keyword(s):  
Heart Defects ◽  
Cardiomyocyte Proliferation

scholarly journals CDK9 and its repressor LARP7 modulate cardiomyocyte proliferation and response to injury in the zebrafish heart

2015 ◽  
Vol 128 (24) ◽  
pp. 4560-4571 ◽  
Author(s):  
G. Matrone ◽  
K. S. Wilson ◽  
S. Maqsood ◽  
J. J. Mullins ◽  
C. S. Tucker ◽  
...  
Keyword(s):  
Cardiomyocyte Proliferation ◽  
Zebrafish Heart

Bone Marrow-Derived Mesenchymal Stem Cells (BMSCs)-Exosome Carrying MiRNA-312 Inhibits Sevoflurane-Induced Cardiomyocyte Apoptosis Through Activation of Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) Pathway

2022 ◽  
Vol 12 (5) ◽  
pp. 947-952
Author(s):  
Jun Zhang ◽  
Yuying Gao ◽  
Peng Chen ◽  
Yu Zhou ◽  
Sheng Guo ◽  
...  
Keyword(s):  
Protein Kinase B ◽  
Cardiomyocyte Apoptosis ◽  
Erk Signaling ◽  
Akt Pathway ◽  
Cardiomyocyte Proliferation ◽  
Akt Signaling Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Dmso Treatment ◽  
Induced Apoptosis ◽  
Related Proteins

This study was to explore the mechanism by how exosomes (exo) derived from BMSCs affects cardiomyocyte apoptosis. BMSCs were isolated and incubated with cardiomyocytes while the cardiomyocytes were exposed to sevoflurane or DMSO treatment. Apoptotic cells were calculated and level of apoptosis related proteins was detected by Western blot. Through transfection with microRNA-(miRNA)-312 inhibitor, we evaluated the effect of BMSC-exo on the sevoflurane-induced apoptosis. Sevoflurane significantly inhibited the viability of cardiomyocytes and induced cardiomyocyte apoptosis. Besides, sevoflurane decreased the expression of miR-312 and enhanced Bax expression in cardiomyocytes through restraining the phosphorylation of MAPK/ERK. Treatment with BMSC-exo, however, activated MAPK/ERK signaling by up-regulating miR-312, thereby inhibiting cardiomyocyte apoptosis, promoting cardiomyocyte proliferation, and elevating the level of Bcl-2. In conclusion, BMSC-exo-derived miR-312 inhibits sevoflurane-induced cardiomyocyte apoptosis by activating PI3K/AKT signaling pathway.

Abstract 124: Function of the Cytoskeletal Proteins Alpha-catenins in Myocardial Growth Control

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Jifen Li ◽  
Sarah Carrante ◽  
Roslyn Yi ◽  
Frans van Roy ◽  
Glenn L. Radice
Keyword(s):  
Heart Development ◽  
Growth Control ◽  
Cytoskeletal Proteins ◽  
Neonatal Rat ◽  
Nuclear Accumulation ◽  
Mouse Heart ◽  
Cardiomyocyte Proliferation ◽  
Rat Cardiomyocytes ◽  
Neonatal Cardiomyocytes

Introduction: Mammalian heart possesses regenerative potential immediately after birth and lost by one week of age. The mechanisms that govern neonatal cardiomyocyte proliferation and regenerative capacity are poorly understood. Recent reports indicate that Yap-Tead transcriptional complex is necessary and sufficient for cardiomyocyte proliferation. During postnatal development, N-cadherin/catenin adhesion complex becomes concentrated at termini of cardiomyocytes facilitating maturation of a specialized intercellular junction structure, the intercalated disc (ICD). This process coincides with the time cardiomyocytes exit cell cycle soon after birth. Hypothesis: We hypothesize that coincident with maturation of ICD α-catenins sequester transcriptional coactivator Yap in cytosol thus preventing activation of genes critical for cardiomyocyte proliferation. Methods: We deleted αE-catenin / αT-catenin genes (α-cat DKO) in perinatal mouse heart and knockdown (KD) α-catenins in neonatal rat cardiomyocytes to study functional impact of α-catenins ablation on ICD maturation. Results: We previously demonstrated that adult α-cat DKO mice exhibited decrease in scar size and improved function post myocardial infarction. In present study, we investigated function of α-catenins during postnatal heart development. We found increase in the number of Yap-positive nuclei (58.7% in DKO vs. 35.8 % in WT, n=13, p<0.001) and PCNA (53.9% in DKO vs. 47.8%, n=8, p<0.05) at postnatal day 1 and day 7 of α-cat DKO heart, respectively. Loss of α-catenins resulted in reduction in N-cadherin at ICD at day 14. We observed an increase number of mononucleated myocytes and decrease number of binucleated myocytes in α-cat DKO compared to controls. Using siRNA KD, we were able to replicate α-cat DKO proliferative phenotype in vitro. The number of BrdU-positive cells was decreased in α-cat KD after interfering with Yap expression (2.91% in α-cat KD vs. 2.02% in α-cat/Yap KD, n>2500 cells, p<0.05), suggesting α-catenins regulate cell proliferation through Yap in neonatal cardiomyocytes. Conclusion: Our results suggest that maturation of ICD regulates α-catenin-Yap interactions in cytosol, thus preventing Yap nuclear accumulation and cardiomyocyte proliferation.

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