Tissue and Cell, Journal Year: 2023, Volume and Issue: 83, P. 102155 - 102155
Published: July 8, 2023
Language: Английский
Bioactive Materials, Journal Year: 2024, Volume and Issue: 38, P. 137 - 153
Published: April 27, 2024
Language: Английский
Citations
15
Advanced Healthcare Materials, Journal Year: 2024, Volume and Issue: 13(9)
Published: Jan. 23, 2024
Abstract Partial‐thickness cartilage defect (PTCD) is a common and formidable clinical challenge without effective therapeutic approaches. The inherent anti‐adhesive characteristics of the extracellular matrix within pose significant impediment to integration cells or biomaterials with native during repair. Here, an injectable photocrosslinked bioadhesive hydrogel, consisting gelatin methacryloyl (GM), acryloyl‐6‐aminocaproic acid‐ g ‐N‐hydroxysuccinimide (AN), poly(lactic‐ co ‐glycolic acid) microspheres loaded kartogenin (KGN) (abbreviated as GM/AN/KGN hydrogel), designed enhance interfacial repair PTCD. After injected in situ at irregular defect, stable robust hydrogel network rapidly formed by ultraviolet irradiation, it can be quickly tightly adhered through amide bonds. exhibits good adhesion strength up 27.25 ± 1.22 kPa lap shear experiments. demonstrates adhesion, low swelling, resistance fatigue, biocompatibility, chondrogenesis properties vitro. A rat model PTCD restoration smoother surface, seamless integration, abundant aggrecan type II collagen production. adhesive long‐term chondrogenic differentiation capacity shows great potential facilitate
Language: Английский
Citations
9
Journal of Orthopaedic Translation, Journal Year: 2024, Volume and Issue: 49, P. 156 - 166
Published: Oct. 11, 2024
Language: Английский
Citations
6
Nano Letters, Journal Year: 2023, Volume and Issue: 23(17), P. 7950 - 7960
Published: July 7, 2023
It is a big challenge to design biomimetic physical microenvironment with greater similarity in vivo tissue observe real cell behaviors. We established novel culture platform based on patterned equidistant micropillars stiff and soft stiffnesses mimic the changes that happened transition from normal osteoporotic disease. first demonstrated micropillar substrate decreased osteocyte synaptogenesis through synaptogyrin 1 this decrease was accompanied by impairment of mechanoperception cellular cytoskeletal rearrangement. then found reduced mainly via inactivation Erk/MAPK signaling. finally substrate-mediated impacted cell-to-cell communication matrix mineralization osteocytes. Taken together, study provides evidence mechanical responses are much more similar those osteocytes at bone level.
Language: Английский
Citations
11
Advanced Science, Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 30, 2024
Abstract The virulent bacteria‐induced host immune response dominates the occurrence and progression of periodontal diseases because roles individual virulence factors from these pathogens in initiation spread inflammation. Outer membrane vesicles (OMVs) as a pathogenic entity have recently attracted great attention messenger bridges between bacteria tissues. Herein, novel role OMVs derived Fusobacterium nucleatum periodontitis is dissected. In rat model, it found that F. caused deterioration by enhancing inflammation periodontium absorption alveolar bone, which almost equivalent to effect itself. Furthermore, can independently induce shown. pathogenicity attributed multiple components identified omics. After entering human ligament stem cells (hPDLSCs) endocytosis, activated NLRP3 inflammasomes impaired mineralization hPDLSCs through NF‐κB (p65) signaling, leading final injury damage bone periodontitis. These results provide new understanding cues for prevention
Language: Английский
Citations
4
Life Sciences, Journal Year: 2023, Volume and Issue: 334, P. 122233 - 122233
Published: Oct. 31, 2023
Language: Английский
Citations
10
Advanced Healthcare Materials, Journal Year: 2023, Volume and Issue: 12(30)
Published: Aug. 19, 2023
It is recognized that the changes in physical properties of extracellular matrix (ECM) result fine-tuned cell responses including morphology, proliferation and differentiation. In this study, a novel patterned equidistant micropillar substrate based on polydimethylsiloxane (PDMS) designed to mimic collagen fiber-like network cartilage matrix. By changing component curing agent an oligomeric base, substrates with same topology but different stiffnesses are obtained it found chondrocytes seeded onto soft maintain their phenotype by gathering type II aggrecan more effectively than those stiff substrate. Moreover, sense respond altering ECM-cytoskeleton-focal adhesion axis. Further, substrate-preserved chondrocyte dependent activation Wnt/β-catenin signaling. Finally, indicated osteoid-like region formation loss stiffened sclerotic area osteoarthritis validate triggered stiffnesses. This study provides behavior similar real at tissue level during transition from normal state osteoarthritis.
Language: Английский
Citations
9
International Endodontic Journal, Journal Year: 2024, Volume and Issue: 57(5), P. 549 - 565
Published: Feb. 9, 2024
Abstract Aim To explore the influence of PDGF‐AA on cell communication between human dental pulp stem cells (DPSCs) by characterizing gap junction intercellular (GJIC) and its potential biomechanical mechanism. Methodology Quantitative real‐time PCR was used to measure connexin family member expression in DPSCs. Cell migration CCK‐8 assays were utilized examine DPSC proliferation. A scrape loading/dye transfer assay applied evaluate GJIC triggered PDGF‐AA, a PI3K/Akt signalling pathway blocker (LY294002) PDGFR‐α (AG1296). Western blotting immunofluorescence test distribution Cx43 p‐Akt proteins Scanning electron microscopy (SEM) observe morphology Results promoted formation cells. upregulates enhance communication. binds activates regulate Conclusions This research demonstrated that can Cx43‐mediated DPSCs via PDGFR‐α/PI3K/Akt axis, which provides new cues for regeneration from perspective
Language: Английский
Citations
2
Cell Proliferation, Journal Year: 2023, Volume and Issue: 57(5)
Published: Nov. 27, 2023
Abstract It is well recognized that mitochondrial dynamics plays a vital role in cartilage physiology. Any perturbation could cause disorders metabolism and even lead to the occurrence of diseases such as osteoarthritis (OA). TGF‐β3, an important growth factor appears joints OA disease, shows its great potential chondrocyte metabolism. Nevertheless, TGF‐β3 on still not understood. Here we aimed investigate effect chondrocytes reveal underlying bio‐mechanism. By using transmission electron microscopy (TEM) for number morphology mitochondria, western blotting protein expressions, immunofluorescence cytoplasmic distributions proteins, RNA sequencing transcriptome changes related dynamics. We found increase mitochondria chondrocytes. TGF‐β3‐enhanced was via promoting fission. The fission induced by mediated AMPK signaling. activated canonical p‐Smad3 signaling resultantly AMPK‐induced Taken together, these results elucidate understanding provide cues therapeutic strategies injury disease terms energy
Language: Английский
Citations
6
Cell Death Discovery, Journal Year: 2023, Volume and Issue: 9(1)
Published: July 15, 2023
Fibroblast growth factor 19 (FGF19) has appeared as a new possible avenue in the treatment of skeletal metabolic disorders. However, role FGF19 on cell cycle progression system is poorly understood. Here we demonstrated that had ability to reduce proliferation chondrocytes and cause G2 phase arrest through its interaction with β-Klotho (KLB), an important accessory protein helps link receptor. FGF19-mediated by regulating expressions cdk1/cylinb1, chk1 gadd45a. We then confirmed binding membrane receptor FGFR4 was necessary for arrest, further proved via activation p38/MAPK signaling. Through inhibitor experiments, discovered inhibition led down-regulation p38 signaling even presence FGF19. Meanwhile, inhibiting reduced induced Furthermore, blocking facilitated retain expression cdk1 cyclinb1 been decreased gadd45a enhanced chondrocytes. Taking together, this study first demonstrate induces at FGFR4-p38/MAPK axis enlarges our understanding about
Language: Английский
Citations
5