Fibrin Hydrogel Aided Cardiac Progenitor Cell Delivery Enhances Regenerative Tendency in Myocardial Infarct Model

2020 ◽  
Vol 04 (05) ◽  
Author(s):  
Subha S ◽  
Sachin J Shenoy ◽  
Arya Anil ◽  
Sabareeswaran A ◽  
Deepthi AN ◽  
...  
Keyword(s):  
Progenitor Cell ◽  
Myocardial Infarct ◽  
Cell Delivery ◽  
Cardiac Progenitor Cell ◽  
Myocardial Infarct Model

Heart Repair Induced by Cardiac Progenitor Cell Delivery within Polypyrrole-Loaded Cardiogel Post-ischemia

2021 ◽  
Author(s):  
Melika Parchehbaf-Kashani ◽  
Hassan Ansari ◽  
Elena Mahmoudi ◽  
Maryam Barekat ◽  
Mohammadmajid Sepantafar ◽  
...  
Keyword(s):  
Progenitor Cell ◽  
Cell Delivery ◽  
Cardiac Progenitor Cell ◽  
Heart Repair

scholarly journals Human Cardiac Progenitor Cell Grafts as Unrestricted Source of Supernumerary Cardiac Cells in Healthy Murine Hearts

Stem Cells ◽  
2011 ◽  
Vol 29 (12) ◽  
pp. 2051-2061 ◽  
Author(s):  
Giancarlo Forte ◽  
Stefano Pietronave ◽  
Giorgia Nardone ◽  
Andrea Zamperone ◽  
Eugenio Magnani ◽  
...  
Keyword(s):  
Progenitor Cell ◽  
Cardiac Cells ◽  
Cardiac Progenitor Cell

scholarly journals Accumulation of mitochondrial DNA mutations disrupts cardiac progenitor cell function and reduces survival

2017 ◽  
Vol 292 (27) ◽  
pp. 11348-11348
Author(s):  
Amabel M. Orogo ◽  
Eileen R. Gonzalez ◽  
Dieter A. Kubli ◽  
Igor L. Baptista ◽  
Sang-Bing Ong ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Progenitor Cell ◽  
Cell Function ◽  
Cardiac Progenitor Cell ◽  
Mitochondrial Dna Mutations ◽  
Dna Mutations

Abstract 340: Short Telomeres Induce Autophagy and Modulate Cardiac Progenitor Cell Fate

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Nirmala Hariharan ◽  
Collin Matsumoto ◽  
Jacqueline Emathinger ◽  
Saba Daneshpooy ◽  
Minyoung Shin ◽  
...  
Keyword(s):  
Cell Fate ◽  
Progenitor Cell ◽  
Smooth Muscle Actin ◽  
Wild Mouse ◽  
Degradation Process ◽  
Mouse Strains ◽  
Therapeutic Effects ◽  
Cardiac Progenitor Cell ◽  
Altered Cell ◽  
The Impact

Aging severely limits myocardial regeneration. Delineating the impact of age-associated factors such as short telomeres is critical to enhance the regenerative potential of cardiac progenitor cells (CPCs). We hypothesize that short telomeres induce autophagy and elicit the age-associated change in cardiac progenitor cell fate. We compared mouse strains with different telomere lengths (TL) for phenotypic characteristics of aging and also isolated CPCs from them. Naturally occurring wild mouse strain Mus musculus castaneus (CAST) possessing short telomeres (TL:18Kb) exhibits early cardiac aging with diastolic dysfunction, hypertrophy, fibrosis and increase in senescence markers p53 and p16, as compared to common lab strains FVB (TL:75Kb) and C57 (TL:50Kb). CAST CPCs with short TLs have altered cell fate as characterized by slower proliferation (p<0.01); increased senescence identified by beta-galactosidase activity (p<0.05); increased basal commitment as determined by expression of lineage markers smooth muscle actin, Tie2, and sarcomeric actinin (16.6, 1.7 and 1.75, p<0.05); as well as loss of quiescence marker expression. Consistent findings of altered cell fate are also evident in old CPCs isolated from aged mice with significantly shorter TLs. Cell fate changes occurring downstream from short TL are at least partially p53 dependent, as p53 inhibition rescues the irreversible cell cycle arrest observed in CAST CPCs. Mechanistically, short TLs induce autophagy, a catabolic protein degradation process. Autophagy flux is increased in CAST CPCs as evidenced by increased LC3 (p<0.05), reduced p62 expression (-52%, p<0.05) and increased accumulation of autophagic puncta. Pharmacological inhibition of autophagosome formation, but not autolysosome formation reverses the cell fate to a more youthful phenotype. Overall the data suggests that short TLs activate autophagy to accommodate cell fate changes that tip the equilibrium away from quiescence and proliferation into differentiation and senescence, leading to age-associated exhaustion of CPCs. The study provides the mechanistic basis underlying age-associated cell fate changes that will enable identification of molecular strategies to enhance the therapeutic effects of aged CPCs.

Abstract 297: Nkx2–5 Transcriptionally Activates C-kit-ligand And Regulates Cardiac Progenitor Cell Populations

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rebecca L Scotland ◽  
Xiaozhong Shi ◽  
Anwarul Ferdous ◽  
Michael Kyba ◽  
Daniel J Garry
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Progenitor Cell ◽  
Transcriptional Regulator ◽  
Luciferase Reporter ◽  
Transcriptional Networks ◽  
Cell Populations ◽  
Cardiac Progenitor Cell ◽  
Downstream Target ◽  
Kit Ligand

C-kit-ligand, also known as stem cell factor, is expressed broadly and has a functional role during hematopoesis, gametogenesis, melanogenesis, mast cell growth and differentiation. Although the receptor for c-kit-ligand, c-kit, has been utilized as a marker to identify cardiac stem cell and progenitor cell populations, the transcriptional regulation and biological function of c-kit-ligand during cardiogenesis has not been defined. Here we demonstrate that c-kit-ligand is a novel downstream target of Nkx2–5. The homeodomain transcription factor, Nkx2–5, is one of the earliest markers of the cardiac lineage and mice lacking this transcription factor are nonviable. To identify potential Nkx2–5 downstream target genes, we utilized ES/EBs that were engineered to overexpress Nkx2–5 and undertook transcriptome analysis of embyroid bodies with and without Nkx2–5 induction. We observed a significant increase in c-kit-ligand expression following Nkx2–5 induction suggesting a role for Nkx2–5 in the activation of c-kit-ligand. Furthermore, analysis of the c-kit-ligand promoter revealed three evolutionarily conserved Nkx2–5 response elements, supporting the notion that Nkx2–5 is a transcriptional regulator of gene expression. We undertook transcriptional assays and transfected the c-kit-ligand promoter-luciferase reporter in the absence and presence of increasing amounts of Nkx2–5. We observed that Nkx2–5, in a dose dependent fashion, was a potent transcriptional activator of c-kit-ligand. These studies enhance our understanding of Nkx2–5 mediated transcriptional networks and further emphasize that Nkx2–5 is an important transcriptional regulator of cardiac progenitor cell populations.

Tunable, Injectable Hydrogels Based on Peptide-Cross-Linked, Cyclized Polymer Nanoparticles for Neural Progenitor Cell Delivery

2017 ◽  
Vol 18 (9) ◽  
pp. 2723-2731 ◽  
Author(s):  
Tianyu Zhao ◽  
Drew L. Sellers ◽  
Yilong Cheng ◽  
Philip J. Horner ◽  
Suzie H. Pun
Keyword(s):  
Progenitor Cell ◽  
Neural Progenitor Cell ◽  
Neural Progenitor ◽  
Polymer Nanoparticles ◽  
Cell Delivery ◽  
Injectable Hydrogels
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