Zhouhale3588

After screening the titles, abstracts, and full texts, 13 articles were included in the review; 9 of these were in vitro, 3 were in vivo, and 1 included both in vitro and in vivo experiments.

At low concentrations, Zn

promoted cell proliferation and osteogenic differentiation, while high-dose Zn

resulted in cytotoxicity and inhibition of osteogenic differentiation. Additionally, one study showed that Zn

reduced apatite formation in simulated body fluid. In all of the in vivo experiments, Zn-containing materials enhanced bone formation.

At appropriate concentrations, Zn-doped synthetic polymer materials are better able to promote bone regeneration than materials without Zn.

At appropriate concentrations, Zn-doped synthetic polymer materials are better able to promote bone regeneration than materials without Zn.

Diabetic osteoporosis (DOP) is a systemic metabolic bone disease caused by diabetes mellitus (DM). Adipose-derived stem cells (ASCs) play an important role in bone regeneration. Our previous study confirmed that ASCs from DOP mice (DOP-ASCs) have a lower osteogenesis potential compared with control ASCs (CON-ASCs). However, the cause of this poor osteogenesis has not been elucidated. Therefore, this study investigated the underlying mechanism of the decline in the osteogenic potential of DOP-ASCs from the perspective of epigenetics and explored methods to enhance their osteogenic capacity.

The expression level of JNK1-associated membrane protein (JKAMP) and degree of DNA methylation in CON-ASCs and DOP-ASCs were measured by mRNA expression profiling and MeDIP sequencing, respectively. JKAMP small interfering RNA (siRNA) and a Jkamp overexpression plasmid were used to assess the role of JKAMP in osteogenic differentiation of CON-ASCs and DOP-ASCs. Immunofluorescence, qPCR, and western blotting were used toic target to prevent and treat osteoporosis.

Intragenic DNA methylation inhibits the osteogenic ability of DOP-ASCs by suppressing expression of JKAMP and the Wnt signaling pathway. This study shows an epigenetic explanation for the reduced osteogenic ability of DOP-ASCs and provides a potential therapeutic target to prevent and treat osteoporosis.Riemerella anatipestifer causes epizootic infectious disease in poultry resulting in serious economic losses especially to the duck industry. In our previous study, R. anatipestifer was found to lyse duck erythrocytes in vitro. In the present study, a random Tn4351 mutagenesis library of hemolytic R. anatipestifer strain SX containing 4000 mutants was constructed to investigate the genetic basis of hemolytic activity. Thirty mutants with reduced hemolytic activity and one with increased hemolytic activity were screened and insertions in 24 genes were identified. Of these genes, four were predicted to encode outer membrane proteins, one encoded a cytoplasmic membrane protein, 11 encoded cytoplasmic proteins, and eight encoded proteins with unknown locations. find more Based on current annotations of the R. anatipestifer genomes, of the 24 genes, 7 (29.17%) were involved in iron utilization. The hemolytic activities of the complemented strains M2 (pRES-Riean_0790) and M18 (pRES-Riean_0653) were restored, indicating that both Riean_0653 and Riean_0790 are involved in the hemolytic activity of strain SX. However, the recombinant proteins rRiean_0317, rRiean_0790, rRiean_0653, rRiean_1027, rRiean_1143, and rRiean_1561 had no hemolytic activity, suggesting that none were hemolysins.

The repair of large-scale full-thickness skin defects represents a challenging obstacle in skin tissue engineering. To address the most important problem in skin defect repair, namely insufficient blood supply, this study aimed to find a method that could promote the formation of vascularized skin tissue.

The phenotypes of ASCs and EPCs were identified respectively, and ASCs/EPCs were co-cultured in vitro to detect the expression of dermal and angiogenic genes. Furthermore, the co-culture system combined with dermal extracellular matrix hydrogel was used to repair the full-scale skin defects in rats.

The co-culture of ASCs/EPCs could increase skin- and angiogenesis-related gene expression in vitro. The results of in vivo animal experiments demonstrated that the ASCs/EPCs group could significantly accelerate the repair of skin defects by promoting the regeneration of vascularized skin.

It is feasible to replace traditional single-seed cells with the ASC/EPC co-culture system for vascularized skin regeneration. This system could ultimately enable clinicians to better repair the full-thickness skin defects and avoid donor site morbidity.

It is feasible to replace traditional single-seed cells with the ASC/EPC co-culture system for vascularized skin regeneration. This system could ultimately enable clinicians to better repair the full-thickness skin defects and avoid donor site morbidity.

Mesenchymal stromal cells (MSCs) constitute one of the cell types most frequently used in cell therapy. Although several studies have shown the efficacy of these cells to modulate inflammation in different animal models, the results obtained in human clinical trials have been more modest. Here, we aimed at improving the therapeutic properties of MSCs by inducing a transient expression of two molecules that could enhance two different properties of these cells. With the purpose of improving MSC migration towards inflamed sites, we induced a transient expression of the C-X-C chemokine receptor type 4 (CXCR4). Additionally, to augment the anti-inflammatory properties of MSCs, a transient expression of the anti-inflammatory cytokine, interleukin 10 (IL10), was also induced.

Human adipose tissue-derived MSCs were transfected with messenger RNAs carrying the codon-optimized versions of CXCR4 and/or IL10. mRNA-transfected MSCs were then studied, first to evaluate whether the characteristic phenotype of MSCs was of more efficient cell therapies for the treatment of inflammatory diseases.

Our results demonstrate that the transient co-expression of CXCR4 and IL10 enhances the therapeutic potential of MSCs in a local inflammation mouse model, suggesting that these mRNA-modified cells may constitute a new step in the development of more efficient cell therapies for the treatment of inflammatory diseases.