Cross talk between glucose metabolism and immunosuppression in IFN-γ-primed mesenchymal stem cells.

The immunosuppressive function "licensed" by IFN-γ is a vital attribute of mesenchymal stem cells (MSCs) widely used in the treatment of inflammatory diseases. However, the mechanism and impact of metabolic reprogramming on MSC immunomodulatory plasticity remain unclear. Here, we explored the mechanism by which glucose metabolism affects the immunomodulatory reprogramming of MSCs "licensed" by IFN-γ.

Micromechanical Compatibility between Cells and Scaffolds Directs the Phenotypic Transition of Stem Cells.

This study experimentally substantiates that the micromechanical compatibility between cell and substrate is essential for cells to achieve energetically favorable mechanotransduction that directs phenotypic transitions. The argument for this compatibility is based on a thermodynamic model that suggests that the response of cells to their substrate mechanical environment is a consequence of the interchange between forms of energy governing the cell-substrate interaction. Experimental validation for the model has been carried out by investigating the osteogenic differentiation of dental follicle stem cells (DFSCs) seeded on electrospun fibrous scaffolds.

[Possibility of mesenchymal stem cell transplantation in the treatment of coronavirus disease 2019].

2019 Novel coronavirus (2019-nCoV) infection has caused a global pandemic. Although researchers have carried out a lot of research on 2019-nCoV, analyzed the molecular structure and conducted evolutionary tree analysis, there is still insufficient understanding of its specific pathogenic mechanism, resulting in the lack of specific and effective therapeutic drugs and method. 2019-nCoV infection can cause inflammation and may deteriorate to acute respiratory distress syndrome (ARDS) and sepsis, which have become the main complication of its death.

Specific protein 1, c-Abl and ERK1/2 form a regulatory loop.

The tyrosine kinase c-Abl participates in the regulation of various cellular functions including cell proliferation, adhesion, migration, smooth muscle contraction and cancer progression. However, knowledge regarding transcriptional regulation of c-Abl is surprisingly limited. Sp1 is a founding member of the Sp1 transcription factor family that has been implicated in housekeeping gene expression, tumor cell proliferation and differentiation.

Overexpression of soluble ADAM33 promotes a hypercontractile phenotype of the airway smooth muscle cell in rat.

A disintegrin and metalloproteinase 33 (ADAM33) has been identified as a susceptibility gene for asthma, but details of the causality are not fully understood. We hypothesize that soluble ADAM33 (sADAM33) overexpression can alter the mechanical behaviors of airway smooth muscle cells (ASMCs) via regulation of the cell's contractile phenotype, and thus contributes to airway hyperresponsiveness (AHR) in asthma. To test this hypothesis, we either overexpressed or knocked down the sADAM33 in rat ASMCs by transfecting the cells with sADAM33 coding sequence or a small interfering RNA (siRNA) that specifically targets the ADAM33 disintegrin domain, and subsequently assessed the cells for stiffness, contractility and traction force, together with the expression level of contractile and proliferative phenotype markers.

A novel peptide ADAM8 inhibitor attenuates bronchial hyperresponsiveness and Th2 cytokine mediated inflammation of murine asthmatic models.

A disintegrin and metalloproteinase 8 (ADAM8) has been identified as a signature gene associated with moderate and severe asthma. Studies in mice have demonstrated that the severity of asthma can be reduced by either transgenic knock-out or by antibodies blocking ADAM8 function, highlighting ADAM8 as potential drug target for asthma therapy. Here, we examined the therapeutic effect of an ADAM8 inhibitor peptide (BK-1361) that specifically blocks cellular ADAM8 activity in ovalbumin-sensitized and challenged Balb/c mice.

ADAM8 in asthma. Friend or foe to airway inflammation?

Airway inflammation has been suggested as the pathological basis in asthma pathogenesis. Recruitment of leukocytes from the vasculature into airway sites is essential for induction of airway inflammation, a process thought to be mediated by a disintegrin and metalloprotease 8 (ADAM8). However, there is an apparent controversy about whether ADAM8 helps or hampers transmigration of leukocytes through endothelium in airway inflammation of asthma.

Phylogenetic and molecular evolution of the ADAM (A Disintegrin And Metalloprotease) gene family from Xenopus tropicalis, to Mus musculus, Rattus norvegicus, and Homo sapiens.

ADAM (a disintegrin and metalloprotease) genes have been identified in various tissues and species, and recently associated with several important human diseases such as tumor and asthma. Although various biological processes have been known for the ADAM family in different species including fertilization, neurogenesis, infection and inflammation, little is known about its detailed phylogenetic and molecular evolutionary history. In this study, the ADAMs of Xenopus (Silurana) tropicalis, Mus musculus, Rattus norvegicus, and Homo sapiens were collected and analyzed by using the Bayesian analysis and gene synteny analysis to establish a comprehensive phylogenetic relationship and evolutionary drive of this gene family.