High-Fat Diet during Mouse Pregnancy Impairs Fetal Heart Development.

Maternal overnutrition correlates with detrimental outcomes in offspring. However, the specific effects of gestational exposure to a high-fat diet (HFD) on fetal development remain unclear. This study aimed to elucidate the developmental phenotypes of neonatal organs and cardiomyocytes of mice exposed to gestational HFD, revealing growth retardation and a notable reduction in cardiomyocyte cell cycle activity.

Activation of Imprinted Gene Promotes Cardiac Fibrosis After Ischemic Injury.

Background: Cardiac fibrosis, characterized by excessive extracellular matrix (ECM) deposition in the myocardium, is an important target for heart disease treatments. (paternally expressed gene 3) is an imprinted gene expressed from the paternal allele, and de novo purine biosynthesis (DNPB) is a crucial pathway for nucleotide synthesis. However, the roles of PW1 and DNPB in ECM production by cardiac fibroblasts during myocardial ischemia are not yet understood.

Genetic lineage tracing identifies cardiac mesenchymal-to-adipose transition in an arrhythmogenic cardiomyopathy model.

Arrhythmogenic cardiomyopathy (ACM) is one of the most common inherited cardiomyopathies, characterized by progressive fibrofatty replacement in the myocardium. However, the cellular origin of cardiac adipocytes in ACM remains largely unknown. Unraveling the cellular source of cardiac adipocytes in ACM would elucidate the underlying pathological process and provide a potential target for therapy.

Tumor Necrosis Factor-Alpha Disrupts Cx43-Mediated Corneal Endothelial Gap Junction Intercellular Communication.

Connexin43 (Cx43)-mediated gap junctions are vital in maintaining corneal endothelium homeostasis. Tumor necrosis factor-alpha (TNF-) is among the most important inflammatory factors which cause corneal endothelial dysfunction in various eye diseases. However, the effect of TNF- on Cx43-mediated gap junctions of the corneal endothelium remains undefined.

A Bi-Layer Hydrogel Cardiac Patch Made of Recombinant Functional Proteins.

The development of minimally invasive cardiac patches, either as hemostatic dressing or treating myocardial infarction, is of clinical significance but remains a major challenge. Designing such patches often requires simultaneous consideration of several material attributes, including bioabsorption, non-toxicity, matching the mechanic properties of heart tissues, and working efficiently in wet and dynamic environments. Using genetically engineered multi-domain proteins, a printed bi-layer proteinaceous hydrogel patch for heart failure treatments is reported.

Generation and characterization of a Myh6-driven Cre knockin mouse line.

Gene deletion by the Cre-Loxp system has facilitated functional studies of many critical genes in mice, offering important insights and allowing deeper understanding on the mechanisms underlying organ development and diseases, such as heart development and diseases. In this study, we generated a Myh6-Cre knockin mouse model by inserting the IRES-Cre-wpre-polyA cassette between the translational stop codon and the 3' untranslated region of the endogenous Myh6 gene. By crossing knockin mice with the Rosa26 reporter lines, we found that Myh6-Cre targeted cardiomyocytes at the embryonic and postnatal stages.

PDGFRb mesenchymal cells, but not NG2 mural cells, contribute to cardiac fat.

Understanding cellular origins of cardiac adipocytes (CAs) can offer important implications for the treatment of fat-associated cardiovascular diseases. Here, we perform lineage tracing studies by using various genetic models and find that cardiac mesenchymal cells (MCs) contribute to CAs in postnatal development and adult homeostasis. Although PDGFRa and PDGFRb MCs both give rise to intramyocardial adipocytes, PDGFRb MCs are demonstrated to be the major source of intramyocardial adipocytes.

No Evidence for Erythro-Myeloid Progenitor-Derived Vascular Endothelial Cells in Multiple Organs.

Rationale: Endothelial cells are thought to emerge de novo from the mesoderm to form the entire circulatory system. Recently, erythro-myeloid progenitors (EMPs) have been proposed to be another remarkable developmental origin for blood vessels in multiple organs, including the hindbrain, liver, lung, and heart, as demonstrated by lineage tracing studies using different genetic tools. These observations challenge the current consensus that intraembryonic vessels are thought to expand solely by the proliferation of preexisting endothelial cells.

Dual lineage tracing identifies intermediate mesenchymal stage for endocardial contribution to fibroblasts, coronary mural cells, and adipocytes.

Early embryonic endocardium undergoes endothelial-to-mesenchymal transition to form cardiac cushion mesenchymal cells (MCs). Embryonic endocardium also gives rise to fibroblasts, intramyocardial adipocytes, and coronary mural cells, including smooth muscle cells and pericytes, in development. Whether endocardial cells directly differentiate into fibroblasts, coronary mural cells, and adipocytes or indirectly via an intermediate stage of endocardial-derived cushion MCs remains unknown.

Acute ocular hypertension disrupts barrier integrity and pump function in rat corneal endothelial cells.

Acute ocular hypertension (AOH) frequently compromises corneal endothelial cell (CEC) function in clinical practice. This type of stress induces corneal oedema and a decrease in the corneal endothelial cell density (ECD). The anterior chamber of the right eye of Sprague-Dawley rats was irrigated with Balanced Salt Solution (BSS) for two hours, and the left eye served as a control to determine the time-dependent effects of AOH on endothelial cell morphology and function.