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Introduction: Injectable scaffolds are emerging as a promising strategy in the field of myocardial tissue engineering. Among injectable scaffolds, microparticles have been poorly investigated. The goal of this study was the development of novel gelatin/gellan microparticles that could be used as an injectable scaffold to repair the infarcted myocardium. In particular, the effect of particle size on cardiac progenitor cell response was investigated.
Methods: Particles were produced by a water-in-oil emulsion method. Phosphatidylcholine was used as a surfactant. Particles with different diameter ranges (125-300 µm and 350-450 µm) were fabricated using two different surfactant concentrations. Morphological, physicochemical, and functional characterizations were carried out. Cardiac progenitor cell adhesion and growth on microparticles were tested both in static and dynamic suspension culture conditions.
Results: Morphological analysis of the produced particles showed a spherical shape and porous surface. The hydrophilicity of particle matrix and the presence of intermolecular interactions between gellan and gelatin were pointed out by the physicochemical characterization. A weight loss of 75 ± 5 % after 90 days of hydrolytic degradation was observed. Injectability through a narrow needle (26 G) and persistence of the microparticles at the injection site were preliminarily verified by ex vivo test. In vitro cell culture tests showed a preservation of rat cardiac progenitor biologic properties and indicated a preferential cell adherence to microparticles with a smaller size.
Conclusion: Overall, the obtained results indicate that the produced gelatin/gellan microparticles could be potentially employed as injectable scaffolds for myocardial regeneration.
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http://dx.doi.org/10.1177/2280800018782844 | DOI Listing |
Dev Biol
September 2025
Department of Orthopedics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Electronic address:
Thrombocytopenia-Absent Radius (TAR) syndrome is a rare congenital condition with reduced platelets, forelimb anomalies, and variable heart and kidney defects. TAR syndrome is caused by mutations in RBM8A/Y14, a component of the exon junction complex. How perturbing a general mRNA-processing factor causes the selective TAR Syndrome phenotypes remains unknown.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Cardiogenesis relies on the integrated interplay between cardiac transcription factors and signaling pathways. Here, we uncover a role for type IIA procollagen (IIA), an extracellular matrix (ECM) protein encoded by an alternatively spliced transcript, encoding a N-terminal cysteine-rich domain, as a critical regulator in a cardiac gene regulatory feedback loop. The cysteine-rich domain of IIA protein was previously reported to interact with bone morphogenetic proteins (BMPs) and transforming growth factors-beta (TGFβ) in in vitro binding assays and acts as a BMP antagonist in amphibian embryo assays.
View Article and Find Full Text PDFCard Fail Rev
August 2025
Unit of Internal Medicine "G.Baccelli", Department of Precision and Regenerative Medicine and Ionian Area (DiMePRe-J), University of Bari, University Hospital Policlinico di Bari Bari, Italy.
Heart failure (HF) is closely linked to endothelial dysfunction, which contributes significantly to its progression. Endothelial dysfunction in HF is marked by reduced nitric oxide bioavailability, increased oxidative stress and inflammation, all of which impair vascular function. Endothelial progenitor cells (EPCs) - vital for vascular repair - are particularly affected, with their dysfunction further exacerbating HF outcomes.
View Article and Find Full Text PDFFront Pediatr
August 2025
Fetal Medicine Unit, St George's University Hospitals NHS Foundation Trust, University of London, London, United Kingdom.
Emerging evidence suggests a potential link between maternal SARS-CoV-2 infection during early pregnancy and the development of congenital heart defects (CHD) in offspring. Although vertical transmission of SARS-CoV-2 is rare, the virus has been associated with placental complications and increased maternal morbidity. Recent studies from China report increased rates of CHD and anomalies such as situs inversus when infection occurs during gestational weeks 4-6, a critical window for cardiac development.
View Article and Find Full Text PDFCirc Res
September 2025
Department of Cell Biology and Anatomy, Cardiovascular Translational Research Center, School of Medicine Columbia, University of South Carolina. (L.P., E.W.W., T.J.C., M.T.F., C.G.M., C.F.W.).
Background: Small artery remodeling and endothelial dysfunction are hallmarks of hypertension. Evidence supports a likely causal association between cardiovascular diseases and endothelial-to-mesenchymal transition, a cellular transdifferentiation process in which endothelial cells (ECs) partially lose their identity and acquire mesenchymal phenotypes. EC reprogramming represents an innovative strategy in regenerative medicine to prevent deleterious effects induced by cardiovascular diseases.
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