Neoeriocitrin Targeting Beclin1 Deubiquitination and Autophagy in Osteogenic Differentiation of Human Dental Pulp Stem Cells.

Adv Sci (Weinh)

Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, 210008, China.

Published: August 2025


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Human dental pulp stem cells (hDPSCs) are dental-derived mesenchymal stem cells with robust multipotent differentiation potentials, rendering them promising for bone tissue engineering. However, their differentiation relies on expensive, hard-to-control growth factors. Neoeriocitrin (Neo), a natural flavonoid, promotes cell proliferation and regulates alkaline phosphatase activities. However, Neo's effect on hDPSCs osteogenesis and bone regeneration is unknown. This study investigated Neo's impact on hDPSCs osteogenic differentiation and its mechanisms for bone regeneration. Neo effectively boosted hDPSCs osteogenic differentiation in vitro and facilitated bone regeneration in rat calvarial defects in vivo. Thermal proteome profiling revealed Neo directly binds Beclin1, validated by cellular thermal shift assay, molecular docking, and molecular dynamics. Neo stabilized Beclin1 by inhibiting ubiquitination-mediated degradation, increasing autophagy in Neo-treated hDPSCs. Furthermore, Neo-enhanced osteogenic differentiation is activated by the Beclin1 network, pivotal for bone regeneration. Elucidating the Neo-Beclin1 interaction provides insights into regulating hDPSCs differentiation and opens new avenues for enhancing bone regeneration strategies.

Download full-text PDF

Source
http://dx.doi.org/10.1002/advs.202504378DOI Listing

Publication Analysis

Top Keywords

bone regeneration
20
osteogenic differentiation
16
stem cells
12
human dental
8
dental pulp
8
pulp stem
8
hdpscs osteogenic
8
differentiation
7
hdpscs
6
bone
6

Similar Publications

Aim: To investigate the functional significance of mitophagy in age-related osteogenic decline and the underlying mechanisms using in vivo and in vitro models.

Materials And Methods: An alveolar bone defect model in aged mice and a serial passaging-induced ageing model of human periodontal ligament stem cells (PDLSCs) were established. Osteogenic potential in mice was assessed by micro-CT, immunofluorescence, immunohistochemical analyses and histological staining.

View Article and Find Full Text PDF

Aim: Prickle planar cell polarity (PCP) protein 2 (Prickle2) encodes a homologue of Drosophila prickle and is involved in the non-canonical Wnt/PCP signalling pathway. However, its exact role in dentinogenesis remains unclear. Dentinogenesis, a key process in tooth morphogenesis, involves the patterned arrangement of odontoblasts and the formation of dentine matrix along the pulp cavity.

View Article and Find Full Text PDF

Objectives: Demineralised dentin matrix (DDM) is an effective scaffold material for bone tissue engineering. However, the osteoimmunological mechanism of DDM remains unexplored. Th17/Treg cell balance has been noticed as a crucial factor in bone regeneration.

View Article and Find Full Text PDF

Senescence-regulating agents remodel mesenchymal stem cell-schwann cell circuitry for diabetic bone regeneration.

Biomaterials

August 2025

Department of Oral and Cranio-maxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laborator

Bone healing requires Schwann cells (SCs) paracrine factors for mesenchymal stem cell function. Diabetes mellitus (DM) patients are susceptible to developing SCs dysfunction and impairing bone healing. Rare research considered reconstructing mesenchymal stem cell-schwann cell circuitry in diabetic bone regeneration.

View Article and Find Full Text PDF

In situ articular cartilage (AC) regeneration is a meticulously coordinated process. Microfracture has been the most extensive clinical approach in AC repair, but it faces challenges such as matrix degradation, generation, and remodeling within a local inflammatory microenvironment. So far, it remains a challenge to establish a multistage regulatory framework for coordinating these cellular events, particularly the immune response and chondrocyte proliferation in microfracture-mediated AC repair microenvironments, which is crucial for promoting AC regeneration quality.

View Article and Find Full Text PDF