Journal of Cellular Physiology最新文献

The aging process often leads to immune-related diseases, including infections, tumors, and autoimmune disorders. Recently, researchers identified a special subpopulation of B cells in elderly female mice that increases with age and accumulates prematurely in mouse models of autoimmune diseases or viral infections; these B cells are known as age-related B cells (ABCs). These cells possess distinctive cell surface phenotypes and transcriptional characteristics, and the cell population is widely recognized as CD11c⁺CD11b⁺T-bet⁺CD21^-CD23^- cells. Research has shown that ABCs are a heterogeneous group of B cells that originate independently of the germinal center and are insensitive to B-cell receptor (BCR) and CD40 stimulation, differentiating and proliferating in response to toll-like receptor 7 (TLR7) and IL-21 stimulation. Additionally, they secrete self-antibodies and cytokines to regulate the immune response. These issues have aroused widespread interest among researchers in this field. This review summarizes recent research progress on ABCs, including the functions and regulation of ABCs in aging, viral infection, autoimmune diseases, and organ transplantation.

Neural precursor cells (NPCs) are a group of cells with self-renewal and multi-differentiation potential. MicroRNAs are required for neurogenesis in the central nervous system (CNS). Recent reports suggest that miR-1224 is important in human CNS diseases. However, its function in neurogenesis of brain development is unclear. The current study demonstrated the essential while developing the neocortex. The results showed that miR-1224 facilitated more NPCs to differentiate into neurons and oligodendrocytes while suppressing astrocyte differentiation. Conversely, inhibition of miR-1224 enhances the self-renewal ability and apoptosis of NPCs. The role of miR-1224 in the developing neocortex was examined by performing in-utero electroporation in vivo. It was observed that depletion impeded upper-layer Cux1⁺ neuronal generation while transforming radial glial cells into IPCs. However, miR-1224 promoted NPC proliferation in the ventricular zone. Moreover, miR-1224 negatively regulated the expression of Dlx1 in NPCs by directly targeting the mRNA 3’-UTR region. These findings indicated that miR-1224 is a crucial NPC neurogenesis regulator during cortical development.

Primary cilia, functioning as crucial hubs for signal sensing and transduction, are integral to the development and maintenance of homeostasis across various organs. However, their roles in tooth homeostasis and repair remain inadequately understood. In this study, we reveal an indispensable role for primary cilia in regulating the homeostasis and regeneration of teeth, primarily through the regulation of cell proliferation. Using cilium-deficient mice, we demonstrate that disruption of ciliary homeostasis leads to abnormal tooth morphology, stunted growth and notably impaired tooth repair. RNA sequencing reveals a dysregulation in genes associated with various biological processes such as cell proliferation, differentiation, and cycle regulation. Furthermore, we show that cilium-deficient mice display reduced cell proliferation. Our findings highlight a critical function for primary cilia in the regulation of tooth homeostasis and regeneration and have important implications for the development of tooth regeneration therapies.

Incorporating autologous patient-derived products has become imperative to enhance the continually improving outcomes in bone tissue engineering. With this objective in mind, this study aimed to evaluate the osteogenic potential of 3D-printed allograft-alginate-gelatin scaffolds coated with stromal vascular fraction (SVF) and platelet-rich fibrin (PRF). The primary goal was to develop a tissue-engineered construct capable of facilitating efficient bone regeneration through the utilization of biomaterials with advantageous properties and patient-derived products. To achieve this goal, 3D-printed gelatin, allograft, and alginate scaffolds were utilized, along with stem cells derived from the buccal fat pad and human-derived components (PRF, SVF). Cells were seeded onto scaffolds, both with and without SVF/PRF, and subjected to comprehensive assessments including adhesion, proliferation, differentiation (gene expression and protein secretion levels), penetration, and gene expression analysis over 14 days. The data was reported as mean ± standard deviation (SD). Two-way or one-way analysis of variance (ANOVA) was performed, followed by a Tukey post hoc test for multiple comparisons. Statistical significance was determined as a p value below 0.05. The scaffolds demonstrated structural integrity, and the addition of PRF coatings significantly enhanced cellular adhesion, proliferation, and differentiation compared to other groups. Gene expression analysis showed increased expression of osteogenic and angiogenic markers in the PRF-coated scaffolds. These findings highlight the promising role of PRF-coated scaffolds in promoting osteogenesis and facilitating bone tissue regeneration. This study emphasizes the development of patient-specific tissue-engineered constructs as a valuable approach for effective bone regeneration.

RUNX3 is a master developmental transcriptional factor that has been implicated as a tumor suppressor in many cancers. However, the exact role of RUNX3 in cancer pathogenesis remains to be completely elucidated. Recently, it has emerged that RUNX3 is involved in the DNA damage response. Here, we demonstrate that heterodimerization of RUNX3 with CBFβ is necessary for its stability by protecting RUNX3 from RUNX3 ADP-ribosylation-dependent ubiquitination and degradation. We further identify new amino acid residues that are targets for PARylation and demonstrate that RUNX3 PARylation at these residues is necessary for localization of RUNX3 to DNA double strand break sites (DBSs). We also demonstrate that both RUNX3 PARylation and CBFβ heterodimerization with RUNX3 positively regulates homologous recombination (HR) repair, in part by promoting the recruitment of CtIP and phospho-RPA2 to the DBSs to mediate HR repair. In summary, we provide evidence that RUNX3 regulates HR repair activity in a PARylation-dependent manner.

Cardiac fibrosis represents the terminal pathological manifestation of various heart diseases, with the formation of fibroblasts playing a pivotal role in this process. Consequently, targeting the formation and function of fibroblasts holds significant potential for improving outcomes in heart disease. Recent research reveals the considerable potential of fibroblasts in ameliorating cardiac conditions, demonstrating different functional characteristics at various time points and spatial locations. Therefore, precise modulation of fibroblast activity may offer an effective approach for treating cardiac fibrosis and achieving targeted therapeutic outcomes. In this review, we focus on the fate and inhibition of fibroblasts, analyze their dynamic changes in cardiac diseases, and propose a framework for identifying markers of fibroblast activation mechanisms and selecting optimal time windows for therapeutic intervention. By synthesizing research findings in these areas, we aim to provide new strategies and directions for the precise treatment of fibroblasts in cardiac diseases.