Small Structures
·
2026
·Vol. 7
·期 4
·e202500875
·
IF 8.9
Hao Wang,Wenjun Zou,Kelv Shen,Yin Zhu,Baihan Sun,Feiyun Xia,Zeyu Han,Zhengfeng Lu
Early local inflammatory response following spinal cord injury (SCI) hinders achievement of satisfactory clinical outcomes because of surrounding bone marrow-derived mesenchymal stem cells (BMSCs) dysfunction and endogenous repair mechanisms inhibition. In this study, we develop a liposome-anchored hydrogel microsphere composite with dual functionality: modulating inflammation and promoting neural repair. Cationic liposomes modified with aldehyde groups (R-L), encapsulating traditional Chinese medicine monomer Rg1, are fabricated using thin-film dispersion method. These liposomes are subsequently combined with gelatin methacrylate (GelMA) microspheres loaded with stem cell chemoattractant SDF1α via a spontaneous Schiff base reaction and electrostatic adsorption, forming the composite R-L@S-GMs. Release assays reveal that Rg1 reaches a cumulative release of 74.8% by day 7, while SDF1α releases more gradually, reaching a comparable level by day 28. In vitro, R-L@S-GMs effectively induce macrophage polarization toward M2 phenotype, significantly enhance anti-inflammatory cytokine IL-10 secretion, and promote neuronal differentiation of recruited BMSCs. In vivo, local injection of R-L@S-GMs effectively suppresses local and systemic acute inflammatory responses, reduces scar formation, promotes angiogenesis and neuronal regeneration, and consequently improve hindlimb motor function. In conclusion, R-L@S-GMs developed in this study successfully reconcile early-phase inflammation control with late-stage neural repair, offering promising potential for minimally invasive therapies in SCI.
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Journal of Functional Biomaterials
·
2026
·Vol. 17
·期 3
·119
·
IF 5.9
Xu Li,Ziqi Huo,Zeyu Wang,Haoyuan Deng,Hongwei Shao,Ye Li,Chunyan Jiang
Achilles tendon rupture often leads to poor functional recovery due to limited self-healing, with mitochondrial dysfunction in tendon stromal cells (TSCs) being a key factor in disease progression. Here, we developed adipose-derived stromal cell (ADSC) membrane-coated mitochondria (Mito-NPs) to target this dysfunction and evaluate their therapeutic potential for tendon repair. Mito-NPs exhibited uniform size, stable surface charge, and effective membrane coating. In lipopolysaccharide-induced inflammatory TSCs, Mito-NPs enhanced oxidative phosphorylation, improved mitochondrial metabolic homeostasis, and reshaped gene expression profiles to normalize TSC functional phenotypes, including inflammation, migration, and collagen synthesis. When encapsulated in a reactive oxygen species (ROS)-responsive hydrogel (Mito-NPs@HG) and implanted into rat Achilles tendon injuries, Mito-NPs@HG improved gait function, decreased local inflammation, and promoted histological repair of damaged tendons by enhancing collagen organization and reducing inflammation. Our findings demonstrate that ADSC membrane-coated mitochondria effectively rescue TSC dysfunction and facilitate tendon regeneration, providing a promising translational strategy for treating tendon injuries.
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高影响因子
BMC MUSCULOSKELETAL DISORDERS
·
2026
·Vol. 27
·期 1
·134
·
IF 2.8
He Yinhao,Li Xiaosheng,Tu Zhixing,Chen Hongwen,Zeng Hui,Peng Qiang,Chen Tiezhu
Objective Developmental Dysplasia of the Hip (DDH) is an acetabular deformity caused by stress concentration or abnormal stress during weight-bearing, and it constitutes a significant etiological factor for secondary hip osteoarthritis. Currently, there remains controversy surrounding the selection of treatment protocols for DDH. This study aims to systematically evaluate the osteogenic and chondrogenic differentiation capacities of adipose-derived stem cells (ADSCs) seeded on 3D-printed porous polycaprolactone (PCL) scaffolds in vitro, thereby opening up a new avenue for addressing osteochondral tissue defects and providing a more effective and safe therapeutic approach for patients with developmental dysplasia of the hip. Methods Rat ADSCs were seeded onto fabricated 3DPPCL scaffolds. The scaffolds' biocompatibility and support for cell adhesion were confirmed. ADSCs were then cultured under osteogenic or chondrogenic conditions. Differentiation was assessed using Alizarin Red and Alcian Blue staining for mineralization and glycosaminoglycan (GAG) deposition, respectively, RT-qPCR for key gene markers (e.g., RUNX-2, COL-II), and immunofluorescence for protein expression. Experimental groups included scaffolds modified with different concentrations of dopamine or chondroitin sulfate. Results The 3DPPCL scaffolds supported robust ADSC adhesion and proliferation. Osteogenic induction significantly enhanced calcium deposition and upregulated osteogenic markers (RUNX-2, ALP). Notably, 3DPPCL/DA groups showed a concentration-dependent increase in mineralization. Conversely, chondrogenic induction markedly promoted GAG synthesis and the expression of cartilage-specific genes (SOX-9, COL-II), with the 300 mg/L 3DPPCL/CS group demonstrating the most pronounced effect. Conclusion This study demonstrates that 3DPPCL scaffolds effectively support the osteogenic and chondrogenic differentiation of ADSCs in vitro. The findings underscore the scaffold's potential as a promising platform for osteochondral tissue engineering, offering a novel and promising basis for developing combined bone-cartilage repair strategies relevant to conditions like DDH.
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PLoS One
·
2025
·Vol. 20
·期 6
·e0326978
·
IF 2.6
Chang Chen,Qiqi Yun,Juanli Ran,Ziyao Zhou,Pengxiang Zhang,Rong Li
Objective
This study investigated the interplay between Hippo-YAP and β-catenin signaling in regulating odontogenic differentiation of human dental pulp stem cells (DPSCs) and explored its potential implications for dentin-pulp regeneration.
Methods
Using lentivirus-mediated YAP overexpression/silencing, β-catenin siRNA knockdown, and pharmacological Wnt inhibition (via WIF-1), we assessed DPSC proliferation, migration, mineralization, and molecular markers (via qRT-PCR, immunofluorescence). In vivo validation employed subcutaneous transplantation of DPSC-seeded scaffolds in immunocompromised mice.
Results
YAP activation enhanced DPSC proliferation (1.44-fold), migration (1.39-fold), invasion (1.54-fold), and differentiation, as evidenced by elevated ALP activity (1.46-fold) and mineralization (1.36-fold). We observed transcriptional upregulation of odontogenic markers (RUNX2, DSPP, DMP1, OCN, ALP) and Wnt pathway components (β-catenin, Cyclin D1, c-Myc). Immunofluorescence revealed coordinated YAP and β-catenin expression patterns during differentiation. β-catenin silencing or Wnt inhibition abolished YAP-mediated functional enhancements and simultaneously suppressed YAP expression, partially confirming bidirectional regulation. In vivo , YAP-overexpressing DPSCs exhibited 1.27- to 1.62-fold induction of dentin-specific markers and β-catenin, whereas YAP silencing impaired these markers expression.
Conclusions
Our findings demonstrate that coordinated YAP and β-catenin signaling drives DPSC odontogenesis, with potential implications for dentin regeneration. Although reciprocal regulation is evident, direct molecular interactions require further validation.
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高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2025
·Vol. 26
·期 5
·2027
·
IF 4.9
Shuangliu Chen,Jiřimutu Xiao,Shijie Zhou,Taxi Wumiti,Zitong Zhao,Ruihua Zhao,Yalan Pan,Qing Wang,Yong Ma,Lan Wu,Yang Guo
Dysregulated iron metabolism-induced ferroptosis is considered a key pathological mechanism in the development of osteoporosis (OP). G protein-coupled receptor 30 (GPR30, also known as Gper1) is an estrogen-binding receptor that has shown therapeutic benefits in patients with certain degenerative diseases. Moreover, several studies have demonstrated the anti-ferroptotic effects of estrogen receptor activation. However, its role in the prevention and treatment of OP remains unclear, and there are currently no reports on the anti-ferroptotic function of GPR30 in OP. Therefore, this study aimed to investigate the ferroptosis-related effects and mechanisms of GPR30 in the context of OP. In vivo and in vitro experiments were conducted using wild-type (WT)C57BL/6female mice and GPR30-knockout (GPR30-KO)C57BL/6Jfemale mice. The microarchitecture of the distal femur was assessed using micro-computed tomography (micro-CT), and histomorphological changes were analyzed via hematoxylin and eosin (H&E) staining. Bone marrow mesenchymal stem cells (BMSCs) were isolated and cultured to establish an iron overload model using ferric ammonium citrate (FAC). Interventions included GPR30 overexpression via transfection and BMP-6 inhibition using LDN-214117. Cell viability was evaluated with the CCK-8 assay, while osteogenic differentiation and mineralization levels were assessed using ALP and Alizarin Red S (ARS) staining. Iron accumulation was detected via Prussian blue staining, oxidative stress levels were evaluated using ROS staining, and mitochondrial membrane potential changes were analyzed using JC-1 staining. Transmission electron microscopy (TEM) was employed to observe mitochondrial ultrastructural changes. Additionally, key gene and protein expression levels were measured using immunofluorescence and Western blotting. The micro-CT analysis revealed significant bone microarchitecture deterioration and bone loss in the GPR30-KO mouse model. At the cellular level, GPR30 overexpression markedly reduced iron accumulation and oxidative stress in BMSCs, restored the mitochondrial membrane potential, and improved the mitochondrial ultrastructure. Furthermore, GPR30 enhanced osteogenic differentiation in BMSCs by promoting the activation of the BMP-6/HEP/FPN signaling pathway, leading to increased expression of osteogenic markers. The protective effects of GPR30 were reversed by the BMP-6 inhibitor LDN-214117, indicating that BMP-6 is a critical mediator in GPR30-regulated iron metabolism and ferroptosis inhibition. GPR30 inhibits ferroptosis in BMSCs and enhances osteogenic differentiation by activating the BMP-6/HEP/FPN signaling pathway. This provides new insights and potential therapeutic targets for the treatment of osteoporosis OP.
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高影响因子
International Heart Journal
·
2026
·Vol. 67
·期 1
·87-97
·
IF 1.3
Zhuyuan Liu,Yanru He,Chunshu Hao
Myocardial ischemia-reperfusion injury (MI/RI) refers to the deterioration of cardiac function after restoring ischemic myocardium perfusion. Stem cell exosomes have produced unique advantages in treating MI/RI. However, the roles of exosomal microRNA-223-3p (miR-223-3p) from adipose-derived stem cells (ADSCs) on MI/RI are still unclear. This study aimed to investigate the effects of exosomal miR-223-3p from ADSCs on hypoxia/reoxygenation (H/R)-induced H9c2 cell injuries. Our findings indicated that the separated ADSC-derived exosomes (ADSC-Exo) were spherical, with a complete cell membrane, an average diameter of 110 nm, and CD9 and CD63 expression. ADSC-Exo increased the cell viability, proliferation, glutathione (GSH) level, and glutathione peroxidase 4 (GPX4) and miR-223-3p expression and decreased the apoptosis, reactive oxygen species (ROS), malondialdehyde (MDA), and Fe2+ levels and acyl-CoA synthetase long chain family member 4 (ACSL4) and transferrin receptor (TFRC) expression of H9c2 cells. Overexpressing exosomal miR-223-3p from ADSCs further strengthened the effects of ADSC-Exo on H9c2 cells. Overexpressing TFRC in H9c2 cells effectively reversed the effects of miR-223-3p overexpressed ADSC-Exo on H9c2 cells. In addition, miR-223-3p targeted and negatively regulated TFRC. This study confirmed that exosomal miR-223-3p from ADSCs alleviated H/R-induced ferroptosis of H9c2 cells by inhibiting TFRC, providing a novel target and pathway for the clinical treatment of MI/RI.
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BMC Oral Health
·
2024
·Vol. 24
·期 1
·1-17
·
IF 2.6
Li Yaoyao,Huang Xinhui,Fu Weihao,Zhang Zonghao,Xiao Kuancheng,Lv Hongbing
Reduced graphene oxide (rGO) is an graphene oxide (GO) derivative of graphene, which has a large specific surface area and exhibited satisfactory physicochemical characteristics. In this experiment, GO was reduced by PDA to generate PDA-GO complex, and then PDA-GO was combined with Chitosan (CS) to synthesize PDA-GO/CS composite scaffold. PDA-GO was added to CS to improve the degradation rate of CS, and it was hoped that PDA-GO/CS composite scaffolds could be used in bone tissue engineering. Physicochemical and antimicrobial properties of the different composite scaffolds were examined to find the optimal mass fraction. Besides, we examined the scaffold’s biocompatibility by Phalloidin staining and Live and Dead fluorescent staining. Finally, we applied ALP staining, RT-qPCR, and Alizarin red S staining to detect the effect of PDA-GO/CS on the osteogenic differentiation of human dental pulp stem cells (hDPSCs). The results showed that PDA-GO composite was successfully prepared and PDA-GO/CS composite scaffold was synthesized by combining PDA-GO with CS. Among them, 0.3%PDA-GO/CS scaffolds improves the antibacterial activity and hydrophilicity of CS, while reducing the degradation rate. In vitro, PDA-GO/CS has superior biocompatibility and enhances the early proliferation, migration and osteogenic differentiation of hDPSCs. In conclusion, PDA-GO/CS is a new scaffold materialsuitable for cell culture and has promising application prospect as scaffold for bone tissue engineering.
研究领域:
生物材料学
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组织工程学
·
细胞生物学
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PLoS Neglected Tropical Diseases
·
2024
·Vol. 18
·期 12
·e0012714
·
IF 3.4
Xuanyin Cui,Yi Cheng,Hongyan Wang,Xiaomao Li,Jinfu Li,Ke Zhang,Rong Mou
Ulcerative colitis (UC) is a chronic inflammatory bowel disease with an unknown etiology and is difficult to treat. Studies have shown that some helminths and their associated products have therapeutic potential in controlling or preventing inflammatory diseases. This study is to investigate the mitigation effects of Hymenolepis nana antigens (HnAg) on the UC model. HnAg significantly improved the disease activity index, colon length, and colonic pathological damage in mice with dextran sulfate sodium (DSS)-induced colitis. HnAg intervention could protect the number of goblet cells and enhance the expression of tight junction proteins and mucins, thereby improving intestinal barrier integrity. HnAg attenuated small intestinal organoid damage and stimulated intestinal stem cells proliferation in a DSS-induced mouse organoid inflammation model. The protective mechanism of HnAg might be related to the activation of the aryl hydrocarbon receptor (AhR)/IL-22 signaling pathway, which regulates intestinal barrier function and promotes the proliferation and differentiation of intestinal stem cells. In conclusion, HnAg has a therapeutic effect on UC mice. Our study provides a new approach for alleviating UC by Hymenolepis nana and its associated products.
Ulcerative colitis (UC) is an immune-mediated chronic inflammatory disease. Currently, commonly used drugs such as aminosalicylates and glucocorticosteroids are difficult to treat and have many adverse effects. In recent years, there has been a growing interest in utilizing the immunomodulatory abilities of worms to develop new therapies for the treatment of inflammatory and allergic diseases. Hymenolepis nana is a zoonotic parasitic worm that parasitizes the small intestines of humans and rodents and generally does not cause serious pathologic damage to their hosts, making it a potential class of intestinal parasites in helminthic therapy. In this study, we investigated the mitigating effect of Hymenolepis nana antigens (HnAg) on UC in mice from the perspective of maintaining intestinal mucosal barrier integrity. The results showed that HnAg alleviated UC in mice by activating the aryl hydrocarbon receptor (AhR)/IL-22 signaling pathway, promoting the proliferation and differentiation of intestinal stem cells, and modulating the integrity of the intestinal mucosal barrier. Meanwhile, HnAg attenuated DSS-induced inflammatory damage in mouse small intestinal organoid tissues and promoted intestinal stem cells proliferation. Suggesting that Hymenolepis nana and its related products may become a new option for alleviating UC.
研究领域:
免疫学
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胃肠病学
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药理学
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炎症性肠病
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高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2026
·
IF 5.6
Kerong Yang,Xi Yue,Jinliang Wu,Guanhao Chen,Shumin Yang,Haojun Ma,Hongyu Tan
Bone repair following large defects remains a significant clinical challenge due to limited osteogenic capacity. F-box only protein 6 (FBXO6), an E3 ubiquitin ligase known to promote degradation of downstream proteins, was highly expressed after osteogenic differentiation. Herein, the role of FBXO6 in osteoblastic differentiation and bone remodeling was explored. Rat bone marrow mesenchymal stem cells (BMSCs) were first isolated and characterized. Following 14 days of osteogenic induction, FBXO6 was significantly upregulated (approximately 4-fold increase). BMSCs overexpressing FBXO6 demonstrated enhanced osteogenic potential, evidenced by increased mRNA expression of osteogenic markers (runt-related transcription factor 2, osteocalcin, COL1A1), elevated alkaline phosphatase (ALP) activity, and greater formation of calcium nodules. Conversely, FBXO6-silenced BMSCs exhibited the opposite effects. FBXO6 overexpression activated the Wnt/β-catenin signaling pathway, a known mediator of osteogenic differentiation. This effect was reversed by treatment with the Wnt/β-catenin inhibitor DKK1. Furthermore, β-catenin overexpression rescued the impaired osteogenesis caused by FBXO6 silencing. Label-Free Quantitative Proteomics analysis identified 439 differentially expressed proteins in FBXO6-overexpressing cells (245 upregulated, 194 downregulated). STARD3 N-terminal like protein (STARD3NL) was prioritized for further investigation (log2FC = −0.97, p = 0.02). FBXO6 interacted with STARD3NL and promoted its destabilization. STARD3NL knockdown attenuated the effects of FBXO6 silencing on osteogenesis. In a 3-mm-diameter critical-size femoral defect model, implantation of collagen scaffolds seeded with FBXO6-downregulated BMSCs significantly suppressed osteogenesis. These findings demonstrate that FBXO6-modified BMSC implantation represents a promising therapeutic strategy for bone defect repair.
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CHINESE MEDICAL JOURNAL
·
2025
·
IF 7.3
Jia Pengyu,Wang Kui,Cheng Yiqin,Zhang Yan,Lu Yuying,Sun Haodong,Zhang Shuyue,Fan Pei,Zhang Yuanyuan,Yang Liufei,Wang Ning,Lu Haixia,Chen Xinlin,Liu Yong,Wei Haidong,Zhang Pengbo
Plain Language Summary Background: Sevoflurane impairs neurogenesis and cognitive function in the developing brain; however, the underlying mechanisms remain unclear. This study aimed to investigate the role of fatty acid β-oxidation (FAO) in neural stem/progenitor cells (NSPCs) as a potential factor in sevoflurane-induced neurogenesis inhibition and cognitive deficits. Methods: NSPCs, NE-4C cells, and postnatal day 7 (PND 7) rats were exposed to sevoflurane. Cell viability was measured using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. Neurogenesis was assessed by immunohistochemistry. Apoptosis was detected via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Cognitive function was tested with the Morris water maze. Lipid metabolism profiles were analyzed through lipidomics. Message RNA (mRNA) expression levels of key FAO enzymes and the major carnitine transporter were quantified by real-time reverse transcription polymerase chain reaction (RT-qPCR). Protein expression of carnitine palmitoyltransferase 1a (CPT1a) and nuclear peroxisome proliferator-activated receptor α (PPARα) was examined by Western blotting. CPT1a enzymatic activity was determined using a biochemical assay. FAO activity was measured with the FAOBlue assay. Results: Sevoflurane exposure impaired neurogenesis and cognitive function. In NSPCs, sevoflurane exposure induced extensive alterations in lipid metabolism intermediates, inhibited the mRNA expression of acyl-CoA oxidase 1 ( ACOX1 ), acyl-CoA oxidase 3 ( ACOX3 ), hydroxyacyl-CoA dehydrogenase beta subunit ( HADHB ), CPT1a , carnitine palmitoyltransferase 2 ( CPT2 ), acyl-CoA dehydrogenase short-chain ( ACADS ), and solute carrier family 22 member 5 ( SLC22A5 ), suppressed FAO activity, reduced CPT1a expression and activity, and decreased PPARα levels in the nucleus. Enhancing FAO activity in NSPCs ameliorated the negative effects of sevoflurane on neurogenesis. Overexpression of CPT1a rescued the sevoflurane-induced inhibition of FAO activity and neurogenesis in NE-4C cells. Pretreatment with palmitoylethanolamide (PEA), a PPAPα agonist, increased both the nuclear content of PPARα protein and the expression of CPT1a in NSPCs and rat hippocampus after sevoflurane exposure. Furthermore, pretreatment with PEA or the CPT1a substrate carnitine rescued sevoflurane-induced damage to FAO activity in NSPCs, neurogenesis, and cognitive function. Conclusion: Sevoflurane impairs neurogenesis and cognitive function by suppressing FAO in NSPCs of the developing brain. Boosting FAO activity in NSPCs could be a potential strategy to prevent sevoflurane-induced cognitive deficits. Plain Language Summary This study explored how sevoflurane, an anesthetic, affects brain development by impairing neurogenesis and cognitive function. Researchers found that sevoflurane disrupts fatty acid β-oxidation (FAO) in neural stem/progenitor cells (NSPCs), leading to changes in lipid metabolism and reduced expression of key enzymes. Enhancing FAO activity, either by overexpressing certain proteins or using compounds like palmitoylethanolamide (PEA) and carnitine, helped mitigate these negative effects. This suggests that targeting FAO in NSPCs could be a promising approach to counteract sevoflurane-induced cognitive deficits in the developing brain. Text is machine generated and may contain inaccuracies. FAQ
研究领域:
神经科学
·
发育生物学
·
麻醉学
·
代谢学
·
干细胞研究
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高影响因子
Advanced Healthcare Materials
·
2026
·
IF 11
Zongbin Sun,Qiuxia Zheng,Chongyang Bai,Desheng Liu,Yue Zhang,Ping Yang,Fanghong Wang,Rui Li,Jia Yao,Xun Li
Mesenchymal stem cell-derived exosomes represent a promising therapeutic avenue for tissue regeneration, yet their clinical translation is hindered by rapid clearance following systemic administration and the lack of optimized, sustained-release delivery strategies. To address these challenges, we crafted a biomimetic hydrogel to carry and gently release MSC-derived exosomes. We engineered a biocompatible, dextran-based composite hydrogel (carboxymethyl chitosan-oxidized dextran/tannic acid-iron complex, CMC-OD/TA-Fe(III)) for the encapsulation and sustained release of human umbilical cord MSC-derived exosomes. We systematically compared the organ biodistribution of exosomes delivered via this hydrogel platform using three distinct local routes: intraperitoneal injection, oral (intragastric) administration, and rectal administration, employing in vivo imaging and tissue immunofluorescence analyses in C57BL/6J mice. Following a single intraperitoneal dose, released exosomes accumulated primarily in the liver and spleen, with minimal brain enrichment. Notably, both oral and rectal administration—non-invasive alternatives to injection—facilitated considerable exosome dissemination to multiple organs. The significant distribution observed via the oral route specifically challenges the prevailing assumption regarding the inefficacy of gastrointestinal delivery for exosome-based therapeutics. This study provides critical insights into administration-route-dependent biodistribution patterns and proposes novel, non-invasive delivery strategies to enhance the therapeutic efficacy and application scenarios of exosomes.
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Science China-Chemistry
·
2020
·Vol. 63
·期 8
·1100-1111
·
IF 6.356
Rong Yan,Zhang Zhen,He Chaoliang,Chen Xuesi
Cell-material and cell-cell interactions represent two crucial aspects of the regulation of cell behavior. In the present study, poly (L-glutamic acid) (PLG) hydrogels were prepared by catalyst-free click crosslinking via a strain-promoted azide-alkyne cycloaddition (SPAAC) reaction between azido-grafted PLG (PLG-N 3 ) and azadibenzocyclooctyne-grafted PLG (PLG-ADIBO). The bioactive peptides c(RGDfK) and N-cadherin mimetic peptide (N-Cad) were both conjugated to the PLG hydrogel (denoted PLG+RGD/N-Cad) in order to regulate cell-material and cell-cell interactions. Gelation time and storage modulus of the hydrogels were tunable through variations in the concentration of polypeptide precursors. The hydrogels degraded gradually in the presence of proteinases. The viability of bone marrow mesenchymal stem cells (BMSCs) was maintained when cultured with extracts of the hydrogels or encapsulated within the hydrogels. Degradation was observed within 10 weeks following the subcutaneous injection of hydrogel solution in rats, displaying excellent histocompatibility in vivo . The introduction of RGD into the PLG hydrogel promoted the adhesion of BMSCs onto the hydrogels. Moreover, when encapsulated within the PLG+RGD/N-Cad hydrogel, BMSCs secreted cartilage-specific matrix, in addition to chondrogenic gene and protein expression being significantly enhanced in comparison with BMSCs encapsulated in hydrogels without N-Cad modification. These findings suggest that these biodegradable, bioactive polypeptide hydrogels have great potential for use in 3D cell culture and in cartilage tissue engineering.
研究领域:
生物材料
·
干细胞生物学
·
组织工程
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高影响因子
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