Biomaterials Advances
·
2025
·
IF 6
Bo Li,Chengwei Wang,Junbo Jiang,Miaomiao Zhang,Shixin Xu,Jinxin Zhang,Zhiyi Gao,Jierui Li,Li Xie,Wen Zhao
Wound healing is a complex and critical physiological process. Traditional cell transplantation strategies often fail to ensure long-term cell survival owing to the detrimental effects of the wound microenvironment, such as acidity, hypoxia, and nutrient deficiency. Therefore, encapsulating cells within microcapsules before transplantation to the wound site is highly desirable. In this work, a core–shell conductive nanofiber membrane with favorable mechanical properties was integrated with conductive microcapsules loaded with adipose-derived mesenchymal stem cells (ADSCs) to create an ADSCs delivery system, resulting in a microencapsulated ADSCs/conductive nanofiber composite dressing. Both the conductive nanofibers and microcapsule materials exhibited a porous, breathable structure. The core–shell conductive nanofibers showed excellent porosity, hydrophilicity, and in vitro degradation properties. Furthermore, the composite dressing exhibited good biocompatibility and antibacterial properties. Electrical stimulation in vitro effectively promoted the paracrine activity of the ADSCs within the microcapsules, preserving their viability and stemness. In vivo experiments revealed that the composite dressing group exhibited a significantly enhanced wound contraction compared to the control group, with the neoepidermis at the wound site more closely resembling the normal skin structure, displaying an increased and well-organized collagen deposition. Moreover, the expression of pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) was reduced while microvessel formation increased, thereby accelerating wound healing. In conclusion, the microencapsulated ADSCs/conductive nanofiber composite dressing possessed excellent conductivity, antibacterial properties, biocompatibility, and inflammation-modulating capabilities, endowing it with significant research value in tissue engineering as an innovative wound repair system.
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DOI
PubMed
高影响因子
ACS Nano
·
2025
·
IF 16
Yinghua Tao,Tao Liu,Fengya Jing,Xin Tan,Xiaocong Zhao,Katrien V. Bernaerts,Ruipeng Jia,Jun Zhao,Yi Yin,Tianzhu Zhang
Repairing tissue, especially in chronic wounds, is a major clinical challenge. Traditional treatments often lead to slow recovery and poor biocompatibility. Adipose-derived stem cell exosomes (ADSC-exo) offer a promising solution for tissue regeneration due to their anti-inflammatory and immunomodulatory effects. However, directly injecting stem cells results in a low survival and function loss. This study introduces a Janus G-Avs patch that promotes tissue repair by releasing ADSC-exo and prevents postoperative tissue adhesion. The patch’s top layer, created via coaxial electrospinning, acts as an ADSC-exo delivery system with a core–shell structure by incorporating ADSC-exo and hyaluronic acid (HA) into methacrylate gelatin (GelMA) to prolong exosome release. The bottom layer consists of a 4arm-PLGA(4aPLGA)-Glu/PCL electrospun membrane, offering a lubricated antifouling surface that prevents protein adsorption and provides mechanical support. In rat models, the G-Avs patch has demonstrated its ability to enhance cell proliferation, promote angiogenesis, and encourage macrophage polarization toward the M2 phenotype, thereby mitigating inflammatory responses and promoting tissue repair. Transcriptomic analysis indicates that the G-Avs patch augments cellular energy metabolism by upregulating metabolic pathways and downregulating immune-inflammatory pathways, collectively supporting tissue repair. In summary, the Janus G-Avs patch has a strong clinical potential.
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PubMed
高影响因子
INTERNATIONAL OPHTHALMOLOGY
·
2026
·Vol. 46
·期 1
·80
·
IF 1.4
Hang Zhongci,Li Yingxian,Ren Weijie,Du Hongwu
Purpose Human umbilical cord mesenchymal stem cell lysates (UCML) have crucial bioactivities, including tissue regeneration, wound healing, and immune regulation, showing great potential for treating eye diseases. This study investigates the therapeutic efficacy of UCML loaded in artificial tears (AT@UCML) on dry eye syndrome (DES) and retinal injury. Methods This study first evaluated the safety, antioxidant properties, and tissue-repairing effects of AT@UCML in disease-relevant ocular cells. Then, we treated DES and ischemia/reperfusion (I/R) retinal injury mouse models by AT@UCML. To assess the effects in DES mice, we measured tear secretion, corneal damage, and goblet cell numbers. For I/R mice, we examined retinal ganglion cell numbers and retinal thickness. Results Experiments showed that AT@UCML reduced oxidative stress and protected ocular cells. In DES mice, it increased tear secretion, repaired corneal damage, and restored goblet cell counts. In I/R mice, it reduced retinal ganglion cell loss and restored retinal thickness. Conclusions AT@UCML effectively treated DES and I/R injuries by protecting key ocular cells. This study expands the application of stem cell therapy in ophthalmology and provides a basis for developing related treatments.
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高影响因子
Biochemistry and Cell Biology
·
2024
·
IF 2.4
Wei Yan,Ruolan Wu,Yingying Lee,Liqun Xu,Xiao Li,Junwei Li,Ronghao Deng,Xing Fan,Yilang Wu,Haibao Zhu,Aihua Mao,Jianxin Shen,Chi-ju Wei
Enucleated cells, also known as cytoplasts, are valuable tools with a wide range of applications. However, their potential for bio-engineering is greatly restricted by the short lifespan. We postulated that the enucleation process damages the integrity of the plasma membrane and thus activates a cell death program(s). The results showed that a tiny hole was generated transiently on the plasma membrane when the nucleus was spun off, while force-gated ion channels were activated in response to the pulling by the nucleus. Influx of extracellular calcium stimulated the opening of calcium channels and the release of calcium from endoplasmic reticulum and mitochondria. Long lasting calcium transient increased protein phosphorylation and activated caspase 9 and calpain proteinase activities. Subsequently, mitochondria membrane permeability and Reactive Oxygen Species (ROS) levels were significantly elevated, which eventually led to eryptosis-like cell death. When extracellular calcium was maintained at optimal concentration, the lifespan of enucleated cells was extended; however, huge amounts of vacuoles appeared in the cytoplasm, possibly derived from enlarged autophagosomes. Inhibition of vacuolation by inhibitors of autophagy or in co-culture with primary muscle cells did not rescue cells dying from the paraptosis-like pathway. These results offer valuable insights for further investigation into the intricate mechanisms underlying enucleated cell death.
研究领域:
细胞生物学
·
干细胞研究
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分子生物学
·
钙信号传导
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高影响因子
CELLULAR & MOLECULAR BIOLOGY LETTERS
·
2024
·
IF 9.2
Zeying Zhang,Di Yang,Xiaoyuan Yan,Qiujing Qiu,Jiajie Guo,Lihong Qiu
Background Differentiating dental pulp stem cells (DPSCs) into odontoblasts is a critical process for tooth self-repair and dentine‒pulp engineering strategies in the clinic. However, the mechanism underlying the regulation of DPSC odontoblastic differentiation remains largely unknown. Here, we demonstrated that BCL-2 interacting protein 3 (BNIP3)-dependent mitophagy is associated with importin subunit beta-1 (KPNB1)-activating transcription factor 4 (ATF4), which promotes DPSC odontoblastic differentiation. Methods The key genes involved in DPSC odontogenic differentiation were identified via bioinformatics. Stable silencing or overexpression of BNIP3 was performed to investigate its impact on DPSC differentiation in vitro ( n ≥ 3). To explore the role of BNIP3 in vivo, tooth root fragments loaded with the hydrogel-transfected DPSC complex were implanted into nude mice ( n ≥ 6). Dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP) polymerase chain reaction (PCR) were conducted to explore the binding site of ATF4 to the BNIP3 promoter ( n ≥ 3). Mitochondrial function experiments were performed to investigate the impact of ATF4-BNIP3 on mitochondria ( n ≥ 3). Immunoprecipitation (IP) mass spectrometry (MS) was used to investigate the interaction between ATF4 and its binding protein, KPNB1. Plasmids containing wild-type (WT)/mutant (MUT)-nuclear localization signal (NLS) forms of ATF4 were constructed to determine the specific amino acid residues recognized by KPNB1 and their effects on DPSC odontoblastic differentiation ( n ≥ 3). Results Compared with those in the control group, the levels of autophagy and mitophagy, especially BNIP3-dependent mitophagy, were greater in the DPSC odontoblastic differentiation group ( P < 0.05). Genetic silencing or overexpression of BNIP3 demonstrated that BNIP3 expression was positively correlated with the transition of DPSCs into odontoblasts both in vitro and in vivo ( P < 0.05). ATF4 regulates the expression of BNIP3 by directly binding to approximately −1292 to −1279 bp and approximately −1185 to −1172 bp within the BNIP3 promoter region, which is associated with mitophagy and mitochondrial reactive oxygen species (mtROS) levels ( P < 0.05). Moreover, ATF4 increased mitophagy, mitochondrial function, and cell differentiation potential via BNIP3 ( P < 0.05). Mechanistically, KPNB1 is a novel interacting protein of ATF4 that specifically recognizes amino acids (aa) 280–299 within ATF4 to control its translocation into the nucleus and subsequent transcription and differentiation processes ( P < 0.05). Conclusions We reported that the critical role of KPNB1/ATF4/BNIP3 axis-dependent mitophagy could provide new cues for the regeneration of the dental pulp‒dentin complex in DPSCs. Graphical Abstract Supplementary Information The online version contains supplementary material available at 10.1186/s11658-024-00664-9.
研究领域:
牙科学
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干细胞生物学
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分子生物学
·
细胞生物学
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高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2026
·
IF 13.2
Yujia Li,Sijia Liu,Zimai Liu,Zixian Wu,Jiao Lu,Yuanyuan Wei,Qianxi Lu,Xiaoman Guo,Xinmeng Zhang,Yaxin Yang,Yilin Wang,Yingying Zhao,Yiyuan Guo,Yongchao Wang,Zhenzhen Chen
Cancer stem cells (CSCs) are pivotal drivers of therapeutic resistance, tumor recurrence, and metastasis due to their self-renewal capacity and localization in poorly vascularized, hypoxic tumor niches. These characteristics limit the efficacy of conventional therapies and underscore the need for CSC-targeted strategies. In this study, we propose a novel in situ cancer vaccine strategy specifically targeting CSCs to overcome these limitations. Using phage display screening, we identified a CD133-targeting peptide and constructed a CD133-functionalized PLGA nanoparticle (CD133-PLGA@DOX) for the selective delivery of doxorubicin to CD133 + CSCs. This nanoplatform achieved precise CSC targeting and induced effective cytotoxicity, particularly against CSCs enriched post-radiotherapy. Importantly, targeted CSC destruction led to the local release of CSC antigens, which served as an endogenous antigen reservoir and triggered a potent in situ vaccine-like immune response. Treatment with CD133-PLGA@DOX significantly promoted dendritic cell maturation, enhanced antigen-specific cytotoxic T cell infiltration, and established long-term immune memory. This strategy—simultaneous CSC eradication and in situ CSC antigen release—demonstrates strong therapeutic efficacy and holds promise for preventing tumor recurrence and overcoming resistance in solid tumors.
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高影响因子
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
·
2025
·Vol. 122
·期 44
·e2513015122
·
IF 9.1
Anqi Li,Dong Tong,Benjamin Ohlstein,Zheng Guo
Recent work suggests that asymmetric segregation of preexisting and newly synthesized canonical histone 3.1 (H3.1), but not variant histone 3.3A (H3.3A), plays an important role in the asymmetric outcome of Drosophila germline stem cell (GSC) and intestinal stem cell (ISC) divisions. However, this finding relied on the Gal4/UAS system and Flp-out technology to swap expression of exogenous fluorescent proteins—an approach that decouples H3.1 expression from the cell cycle and may be prone to artifacts. Here, by photoswitching photoconvertible H3-Dendra2 proteins expressed under their native controls in living flies, we find that preexisting and newly synthesized H3.1 and H3.3A are symmetrically segregated in dividing ISCs and somatic cyst stem cells (CySCs) in male testes. While H3.3A was found to be symmetrically segregated during GSC divisions, analysis of the H3.1 segregation in GSCs was complicated by our unexpected finding that H3.1-Dendra2 expressed under its normal control within the context of a histone transgene is not detectable in GSCs, owing to regulatory elements in the 3’UTR that mediate translational repression by the RNA-binding proteins Nanos and Pumilio. Nevertheless, when this repression is obviated by using a 3’UTR devoid of such elements, H3.1-Dendra2 is expressed in GSCs and symmetrically segregated without affecting lineage outcomes. We obtained similar results when the coding sequence of H3.3A was edited to encode H3.1 in the context of an H3.3A-Dendra2 knock-in allele. Our findings thus challenge the prevailing model of asymmetric histone segregation and reveal an unexpected molecular mechanism of posttranscriptional repression of H3.1 in GSCs.
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高影响因子
Biomaterials Science
·
2021
·Vol. 9
·期 22
·7603-7616
·
IF 6.843
Wei Yu,Bin Hu,Kofi Oti Boakye-Yiadom,William Ho,Qijing Chen,Xiaoyang Xu,Xue-Qing Zhang
Osteoarthritis (OA), a chronic and degenerative joint disease, remains a challenge in treatment due to the lack of disease-modifying therapies. As a promising therapeutic agent, adipose-derived stem cells (ADSCs) have an effective anti-inflammatory and chondroprotective paracrine effect that can be enhanced by genetic modification. Unfortunately, direct cell delivery without matrix support often results in poor viability of therapeutic cells. Herein, a hydrogel implant approach that enabled intra-articular delivery of gene-engineered ADSCs was developed for improved therapeutic outcomes in a surgically induced rat OA model. An injectable extracellular matrix (ECM)-mimicking hydrogel was prepared as the carrier for cell delivery, providing a favorable microenvironment for ADSC spreading and proliferation. The ECM-mimicking hydrogel could reduce cell death during and post injection. Additionally, ADSCs were genetically modified to overexpress transforming growth factor-β1 (TGF-β1), one of the paracrine factors that exert an anti-inflammatory and pro-anabolic effect. The gene-engineered ADSCs overexpressing TGF-β1 (T-ADSCs) had an enhanced paracrine effect on OA-like chondrocytes, which effectively decreased the expression of tumor necrosis factor-alpha and increased the expression of collagen II and aggrecan. In a surgically induced rat OA model, intra-articular injection of the T-ADSC-loaded hydrogel markedly reduced cartilage degeneration, joint inflammation, and the loss of the subchondral bone. Taken together, this study provides a potential biomaterial strategy for enhanced OA treatment by delivering the gene-engineered ADSCs within an ECM-mimicking hydrogel.
研究领域:
再生医学
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干细胞治疗
·
骨科
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高影响因子
JOURNAL OF BONE AND MINERAL RESEARCH
·
2023
·Vol. 38
·期 4
·556-567
·
IF 6.2
Ruiye Bi,Xueting Luo,Qianli Li,Peiran Li,Haohan Li,Yi Fan,Binbin Ying,Songsong Zhu
Temporomandibular joint (TMJ) growth requires orchestrated interactions between various cell types. Recent studies revealed that fibrocartilage stem cells (FCSCs) in the TMJ cartilage play critical roles as cell resources for joint development and repair. However, the detailed molecular network that influences FCSC fate during TMJ cartilage development remains to be elucidated. Here, we investigate the functional role of Igf1 in FCSCs for TMJ cartilage growth and homeostasis by lineage tracing using Gli1-CreER + ; Tm flfl mice and conditional Igf1 deletion using Gli1-/Col2-CreER + ; Igf1 fl/fl mice. In Gli1-CreER + ; Tm flfl mice, red fluorescence + (RFP + ) FCSCs show a favorable proliferative capacity. Igf1 deletion in Gli1 + / Col2 + cell lineages leads to distinct pathological changes in TMJ cartilage. More serious cartilage thickness and cell density reductions are found in the superficial layers in Gli1-CreER + ; Igf1 fl/fl mice. After long-term Igf1 deletion, a severe disordered cell arrangement is found in both groups. When Igf1 is conditionally deleted in vivo, the red fluorescent protein-labeled Gli1 + FCSC shows a significant disruption of chondrogenic differentiation, cell proliferation, and apoptosis leading to TMJ cartilage disarrangement and subchondral bone loss. Immunostaining shows that pAkt signaling is blocked in all cartilage layers after the Gli1 + -specific deletion of Igf1 . In vitro, Igf1 deletion disrupts FCSC capacities, including proliferation and chondrogenesis. Moreover, the deletion of Igf1 in FCSCs significantly aggravates the joint osteoarthritis phenotype in the unilateral anterior crossbite mouse model, characterized by decreased cartilage thickness and cell numbers as well as a loss of extracellular matrix secretions. These findings uncover Igf1 as a regulator of TMJ cartilage growth and repair. The deletion of Igf1 disrupts the progenitor capacity of FCSCs, leading to a disordered cell distribution and exaggerating TMJ cartilage dysfunction. © 2023 American Society for Bone and Mineral Research (ASBMR).
研究领域:
发育生物学
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干细胞生物学
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骨科
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分子生物学
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病理学
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PubMed
高影响因子
Journal of Biomaterials and Tissue Engineering
·
2017
·Vol. 7
·期 4
·283-290
·
IF 1.383
Meng Zengdong,Liu Wei,Zhang Yuqin,Zhang Lei,Tang Xu,Lian XingYe,Xie Hui,Li Lei,Wang Chengjian
Hydroxyapatite bioceramics as a kind of bone defect repair and replacement material has been in clinical application for years. In order to further clarify the role of the addition of Sr on the physicochemical properties of these materials, a series of Sr-substituted hydroxyapatites
(Sr-HA) were synthesized by high temperature solid state methods and characterized extensively. The proliferation and osteogenesis reactivity of these materials in BMSCs was evaluated, and the behavior towards MG-63 osteoblast cells (in terms of cytotoxicity, proliferation and differentiation
assays) was studied. Our results indicated that the addition of Sr does influence the structure of HA, and the crystallinity degree of the materials decreased with Sr addition. The increasing amounts of Sr in the HA composition causes a decrease in the specific surface area and an enrichment
of Sr-apatite phase at the surface of the samples. Bioactivity tests show that the presence of Sr did not produce any cytotoxic effect. Moreover, Sr-HA increased the proliferation of BMSCs and MG-63 osteoblast cells and enhanced BMSCs differentiation to osteoblast cells. Thus the Sr-HA is
an optimal scaffold material for bone tissue engineering, which can be potentially applied in clinical practice for bone defect repair by compounding with osteoblasts.
研究领域:
材料科学
·
生物材料
·
组织工程
·
细胞生物学
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高影响因子
INORGANIC CHEMISTRY COMMUNICATIONS
·
2019
·
IF 1.795
Junchao Qian,Yaping Wang,Zhigang Chen,Chengbao Liu,Yuyang Zhou,Yue Yang,Yenan Song,Biao Kong
Mn 3 O 4 -CeO 2 /holey-graphene nano-composite was fabricated by hydrothermal reaction on the honeycomb-like porous graphene structure. The hybrid materials displayed enhanced capacitive performance (310 F·g −1 at 2 A·g −1 ). After 1000 cycles, the initial capacitance of the composite still has 92.4% retained. The improved electrochemical performance might be ascribed to the intimate combination of the pesudocapacitance from nanoparticles well-dispersed on graphene sheets and double layer capacitance from excellent conductive graphene scaffold. The investigation presents a promising application of nanoparticles/graphene composites as electrode materials for energy storage.
研究领域:
材料科学
·
电化学
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DOI
高影响因子
ANALYTICAL CHEMISTRY
·
2020
·
IF 6.785
Jiafeng Wang,Guohua Qi,Xiaozhang Qu,Xiaoxu Ling,Zhimin Zhang,Yongdong Jin
Dental pulp stem cells (DPSCs) are considered one of the key cells in tooth regeneration engineering. Understanding molecular biological information on DPSCs during differentiation is of great significance for the construction of tissue-engineered teeth. In this study, we investigated the differentiation process of DPSCs stimulated by drugs and gained molecular insights in the process. By using label-free and noninvasive surface enhanced Raman spectroscopy (SERS) to monitor molecular change profiling in the cell nucleus of single DPSCs during the differentiation process, we found that two pivotal differentiation biomarkers, alkaline phosphatase (ALP) and dentin sialophosphoprotein (DSPP), were overexpressed during the process. Continuous and intermittent monitoring of SERS spectra from the nuclear region indicated that the expression of proteins and related amino acids of tryptophan were markedly increased until peak period of differentiation (on day 14). Meanwhile corresponding transformation of DNA/RNA backbone vibrational modes was also observed during the differentiation process, indicating the occurrence of replication or transcription of DNA. The method provides a useful tool for the molecular biology studies of DPSCs differentiation, and the finding will broaden our understanding of DPSCs differentiation.
研究领域:
干细胞生物学
·
组织工程
·
分子生物学
·
拉曼光谱
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PubMed
高影响因子
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