Micro-/nano-structured zirconia surface promotes osteogenic differentiation of human bone marrow mesenchymal stem cells by reducing pyroptosis under inflammatory conditions.

Background/purpose: Promoting osteogenesis under inflammatory conditions holds promise for preventing and mitigating peri-implantitis. Cell pyroptosis inhibits osteoblast-mediated bone formation. Although the surface topography of implant materials influences both osteogenesis and inflammatory responses, its effects on pyroptosis and osteogenesis under inflammatory conditions have not been thoroughly investigated.

Digitally designed occlusion of an implant-supported crown considering physiological tooth displacement under occlusal loading.

Physiological natural tooth displacement under occlusal loading can influence intraoral occlusal contacts. However, gypsum casts and digital scans cannot simulate the physiological tooth displacement under occlusal loading. The occlusal design of the implant-supported crowns has been based mainly on the experience of dental laboratory technicians, lacking accuracy and individualization.

Caspase-3/GSDME-mediated pyroptosis leads to osteogenic dysfunction of osteoblast-like cells.

Objective: Cell pyroptosis is implicated in progressive bone loss in dental inflammatory diseases. We induced caspase-3/Gasdermin E (GSDME)-mediated pyroptosis in osteoblast-like cells and evaluated the effects on osteogenesis.

Materials And Methods: Osteoblast-like cells were treated with various concentrations of sodium butyrate (NaB) to identify the most appropriate for inducing caspase-3/GSDME-mediated pyroptosis.

LUBAC assembles a ubiquitin signaling platform at mitochondria for signal amplification and transport of NF-κB to the nucleus.

Mitochondria are increasingly recognized as cellular hubs to orchestrate signaling pathways that regulate metabolism, redox homeostasis, and cell fate decisions. Recent research revealed a role of mitochondria also in innate immune signaling; however, the mechanisms of how mitochondria affect signal transduction are poorly understood. Here, we show that the NF-κB pathway activated by TNF employs mitochondria as a platform for signal amplification and shuttling of activated NF-κB to the nucleus.

An in vitro vesicle formation assay reveals cargo clients and factors that mediate vesicular trafficking.

The fidelity of protein transport in the secretory pathway relies on the accurate sorting of proteins to their correct destinations. To deepen our understanding of the underlying molecular mechanisms, it is important to develop a robust approach to systematically reveal cargo proteins that depend on specific sorting machinery to be enriched into transport vesicles. Here, we used an in vitro assay that reconstitutes packaging of human cargo proteins into vesicles to quantify cargo capture.

Protein quality control by the proteasome and autophagy: A regulatory role of ubiquitin and liquid-liquid phase separation.

Degradation of dysfunctional, damaged, or misfolded proteins is a crucial component of the protein quality control network to maintain cellular proteostasis. Dysfunction in proteostasis regulation due to imbalances in protein synthesis, folding, and degradation challenges the integrity of the cellular proteome and favors the accumulation of aggregated proteins that can damage cells by a loss of their functions and/or a gain of adverse functions. Ubiquitination is an essential player in proteostasis regulation but also in orchestrating signaling pathways in response to various stress conditions.