Anthropometric parameters of obesity can be alternative biomarkers for the potential cardiac dysfunction in obese children.

Childhood obesity, as one of the potential risk factors of cardiovascular diseases, is closely associated with the incidence of cardiovascular disease at a younger age and has become a public health concern worldwide. However, its potential effects on the cardiovascular system have still remained elusive. In this study, we systematically evaluated the cardiovascular characteristics of 79 obese children and 161 normal weight children in Guangzhou (China) using the potential biomarkers for cardiovascular disease.

Modulating Lysine Crotonylation in Cardiomyocytes Improves Myocardial Outcomes.

Background: Ischemic heart disease is a major global public health challenge, and its functional outcomes remain poor. Lysine crotonylation (Kcr) was recently identified as a post-translational histone modification that robustly indicates active promoters. However, the role of Kcr in myocardial injury is unknown.

Wnt4 is crucial for cardiac repair by regulating mesenchymal-endothelial transition via the phospho-JNK/JNK.

Wnt4 plays a critical role in development and is reactivated during fibrotic injury; however, the role of Wnt4 in cardiac repair remains unclear. In this study, our aim was to clarify the pathophysiological role and mechanisms of Wnt4 following acute cardiac ischemic reperfusion injury. We investigated the spatio-temporal expression of Wnt4 following acute cardiac ischemic reperfusion injury and found that Wnt4 was upregulated as an early injury response gene in cardiac fibroblasts near the injury border zone and associated with mesenchymal-endothelial transition (MEndoT), a beneficial process for revascularizing the damaged myocardium in cardiac repair.

Diverging targets mediate the pathological roleof miR-199a-5p and miR-199a-3p by promoting cardiac hypertrophy and fibrosis.

MicroRNA-199a-5p (miR-199a-5p) and -3p are enriched in the myocardium, but it is unknown whether miR-199a-5p and -3p are co-expressed in cardiac remodeling and what roles they have in cardiac hypertrophy and fibrosis. We show that miR-199a-5p and -3p are co-upregulated in the mouse and human myocardium with cardiac remodeling and in Ang-II-treated neonatal mouse ventricular cardiomyocytes (NMVCs) and cardiac fibroblasts (CFs). miR-199a-5p and -3p could aggravate cardiac hypertrophy and fibrosis and .

DDR2, a discoidin domain receptor, is a marker of periosteal osteoblast and osteoblast progenitors.

Introduction: The periosteum has a bilayered structure that surrounds cortical bone. The outer layer is rich in connective tissue and fibroblasts, while the inner layer in contact with the cortical surface of the bone predominantly consists of osteoblasts and osteoblast progenitors. The identification of cell-specific surface markers of the bilayered structure of the periosteum is important for the purpose of tissue regeneration.

Mesenchymal-endothelial transition-derived cells as a potential new regulatory target for cardiac hypertrophy.

The role of Mesenchymal-endothelial transition (MEndoT) in cardiac hypertrophy is unclear. To determine the difference between MEndoT-derived and coronary endothelial cells is essential for understanding the revascularizing strategy in cardiac repair. Using lineage tracing we demonstrated that MEndoT-derived cells exhibit highly heterogeneous which were characterized with highly expression of endothelial markers such as vascular endothelial cadherin(VECAD) and occludin but low expression of Tek receptor tyrosine kinase(Tek), isolectin B4, endothelial nitric oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardiac hypertrophy.

Infant cardiosphere-derived cells exhibit non-durable heart protection in dilated cardiomyopathy rats.

Stem cells provide a new strategy for the treatment of cardiac diseases; however, their effectiveness in dilated cardiomyopathy (DCM) has not been investigated. In this study, cardiosphere-derived cells (CDCs) were isolated from infants (≤ 24 months) and identified by the cell surface markers CD105, CD90, CD117 and CD45, which is consistent with a previous report, although increased CD34 expression was observed. The molecular expression profile of CDCs from infants was determined by RNA sequencing and compared with adult CDCs, showing that infant CDCs have almost completely altered gene expression patterns compared with adult CDCs.

Circular RNA circRNA_000203 aggravates cardiac hypertrophy via suppressing miR-26b-5p and miR-140-3p binding to Gata4.

Aims: Circular RNAs (circRNAs) are involved in gene regulation in a variety of physiological and pathological processes. The present study aimed to investigate the effect of circRNA_000203 on cardiac hypertrophy and the potential mechanisms involved.

Methods And Results: CircRNA_000203 was found to be up-regulated in the myocardium of Ang-II-infused mice and in the cytoplasma of Ang-II-treated neonatal mouse ventricular cardiomyocytes (NMVCs).

Mesenchymal-endothelial transition contributes to cardiac neovascularization.

Endothelial cells contribute to a subset of cardiac fibroblasts by undergoing endothelial-to-mesenchymal transition, but whether cardiac fibroblasts can adopt an endothelial cell fate and directly contribute to neovascularization after cardiac injury is not known. Here, using genetic fate map techniques, we demonstrate that cardiac fibroblasts rapidly adopt an endothelial-cell-like phenotype after acute ischaemic cardiac injury. Fibroblast-derived endothelial cells exhibit anatomical and functional characteristics of native endothelial cells.

Rib fractures and death from deletion of osteoblast βcatenin in adult mice is rescued by corticosteroids.

Ribs are primarily made of cortical bone and are necessary for chest expansion and ventilation. Rib fractures represent the most common type of non-traumatic fractures in the elderly yet few studies have focused on the biology of rib fragility. Here, we show that deletion of βcatenin in Col1a2 expressing osteoblasts of adult mice leads to aggressive osteoclastogenesis with increased serum levels of the osteoclastogenic cytokine RANKL, extensive rib resorption, multiple spontaneous rib fractures and chest wall deformities.

Wnt1/βcatenin injury response activates the epicardium and cardiac fibroblasts to promote cardiac repair.

Wnts are required for cardiogenesis but the role of specific Wnts in cardiac repair remains unknown. In this report, we show that a dynamic Wnt1/βcatenin injury response activates the epicardium and cardiac fibroblasts to promote cardiac repair. Acute ischaemic cardiac injury upregulates Wnt1 that is initially expressed in the epicardium and subsequently by cardiac fibroblasts in the region of injury.

Wnt1 is a proangiogenic molecule, enhances human endothelial progenitor function, and increases blood flow to ischemic limbs in a HGF-dependent manner.

Human endothelial progenitor cells (hEPCs) participate in neovascularization of ischemic tissues. Function and number of hEPCs decline in patients with cardiovascular disease, and therapeutic strategies to enhance hEPC function remain an important field of investigation. The Wnt signaling system, comprising 19 lipophilic proteins, regulates vascular patterning in the developing embryo.

Modulation of nucleobindin-1 and nucleobindin-2 by caspases.

Nucleobindin-1 (NUCB1) and nucleobindin-2 (NUCB2) are multifunctional proteins that interact with Ca(2+), nucleic acids and various regulatory proteins in different signaling pathways. So far, our understanding of the regulation of the biological functions of nucleobindins remains limited. In our proteome-wide selection for downstream caspase substrates, both NUCB1 and NUCB2 are found to be the downstream substrates of caspases.

Fibronectin type III domain based monobody with high avidity.

Significant efforts have been made to improve the target-binding strength of numerous affinity molecules that are widely used in biomedical research and clinical applications. While many antibody-like fragments have been successfully optimized through affinity maturation, the process is time-consuming and restricted by the stability, solubility, and expression level of the protein sequences. To generate a fibronectin type III domain (FN3) based monobody that binds to the tumor-related biomarkers with exceptional high strength and stability, we developed a multivalent strategy by fusing an alphavbeta3-binding FN3 monobody with a short COMP pentamerization domain through a linker that facilitates appropriate display of multivalent FN3 domains.

Investigation of interaction between two neutralizing monoclonal antibodies and SARS virus using biosensor based on imaging ellipsometry.

Two neutralizing human scFv, b1 and h12 were identified initially using ELISA,employing highly purified virus as the coating antigen. The biosensor technique based on imaging ellipsometry was employed directly to detect two neutralizing monoclonal antibodies and serial serum samples from 10 SARS patients and 12 volunteers who had not SARS. Further, the kinetic process of interaction between the antibodies and SARS-CoV was studied using the real-time function of the biosensor.

A human neutralizing antibody against a conformational epitope shared by oligomeric SARS S1 protein.

An antibody phage-display library was constructed from the B cells of convalescent severe acute respiratory syndrome (SARS) patients and screened using inactivated SARS coronavirus (CoV) virions as antigens. More than 80 positive clones were isolated from the library and one of them, scFv H12, was extensively characterized. scFv H12 bound to SARS-CoV with high affinity (equilibrium dissociation constant, Kd=73.

[Expression and renaturation of a novel human single-chain Fv antibody against SARS-CoV].

A novel human ScFv H12 against SARS-CoV has been selected from a SARS immune library. In order to produce a large amount of ScFv H12, pET28a-H12 expression vector was constructed and ScFv H12 was expressed at yield about 30% of total proteins in E. coli .

A human SARS-CoV neutralizing antibody against epitope on S2 protein.

An immune antibody phage-display library was constructed from B cells of SARS convalescent patients. More than 80 clones were selected from the library by using the whole inactivated SARS-CoV virions as target. One human scFv, B1, was characterized extensively.

Probing the structure of the SARS coronavirus using scanning electron microscopy.

A novel coronavirus, SARS-CoV, has been confirmed to be the aetiological agent of SARS. Transmission electron microscope (TEM) images played an important role in initial identification of the pathogen. In order to obtain greater morphological detail of SARS-CoV than could be obtained by TEM, we used ultra-high resolution scanning electron microscopy (SEM) to image the virus particles.