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Mo, Q., Zheng, H., Liu, C., Sun, Y., Cao, Z., Sheng, R., . . . Chen, J. (2025). An all-silk-based functional system promotes tendon regeneration by regulating the cell fate of TSPCs in an inflammatory microenvironment. Acta Biomaterialia
Open this publication in new window or tab >>An all-silk-based functional system promotes tendon regeneration by regulating the cell fate of TSPCs in an inflammatory microenvironment
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2025 (English)In: Acta Biomaterialia, ISSN 1742-7061, E-ISSN 1878-7568Article in journal (Refereed) Epub ahead of print
Abstract [en]

The dysregulation of the inflammatory microenvironment following tendon injury significantly hinders regeneration. In this study, we developed an all-silk-derived functional scaffold (rKL@MPs-ASF) by integrating silk fibroin (SF) microspheres (MPs) loaded with the anti-inflammatory protein recombinant α-Klotho (rKL) into a biomimetic aligned SF (ASF) scaffold. This scaffold is designed to regulate the inflammatory microenvironment and facilitate tendon regeneration. Proteomic analysis revealed that rKL preserves the tenogenic differentiation potential of tendon stem/progenitor cells (TSPCs) by mitigating the oxidative stress response in a tumor necrosis factor-alpha-induced inflammatory microenvironment in vitro. The rKL@MPs-ASF scaffold demonstrated good drug loading/release capabilities and biocompatibility in vitro. In a rat full-thickness Achilles tendon defect model, the rKL@MPs-ASF scaffold reduced inflammatory cells infiltration and promoted fibroblast infiltration compared to the PBS@MPs-ASF group at 4 weeks post-operation. At 8 weeks post-operation, rKL@MPs-ASF-treated tendons showed increased collagen fiber deposition and reduced heterogeneous ossification, facilitating tendon regeneration and functional recovery. In conclusion, this all-silk-derived functional system creates a conducive microenvironment for tendon regeneration. Statement of significance: Regulation of the inflammatory microenvironment plays a crucial role in modulating the differentiation of TSPCs, thereby promoting tendon tissue regeneration. In this study, we demonstrate that rKL effectively preserves the tenogenic differentiation potential of TSPCs by mitigating oxidative stress within an inflammatory microenvironment. We developed an innovative, all-silk-based functional system (rKL@MPs-ASF), which integrates rKL-loaded SF MPs into an aligned silk fibroin scaffold. This system enables the controlled release of rKL, thereby modulating inflammation, promoting collagen fiber deposition, inhibiting heterotopic ossification, and ultimately improving tendon regeneration and functional recovery. Our findings highlight the potential of the rKL@MPs-ASF system, which combines structural and biological properties with a versatile drug-delivery platform, as a promising strategy for enhancing tendon repair and regenerative outcomes.

Place, publisher, year, edition, pages
Elsevier, 2025
Keywords
Anti-inflammation, Biomimetic scaffold, Tendon differentiation, Tendon repair, α-Klotho
National Category
Cell and Molecular Biology Biomaterials Science
Identifiers
urn:nbn:se:umu:diva-239434 (URN)10.1016/j.actbio.2025.05.040 (DOI)2-s2.0-105005951208 (Scopus ID)
Available from: 2025-06-02 Created: 2025-06-02 Last updated: 2025-06-02
Chen, J., Sheng, R., Mo, Q., Backman, L. J., Lu, Z., Long, Q., . . . Zhang, W. (2025). Controlled TPCA-1 delivery engineers a pro-tenogenic niche to initiate tendon regeneration by targeting IKKβ/NF-κB signaling. Bioactive Materials, 44, 319-338
Open this publication in new window or tab >>Controlled TPCA-1 delivery engineers a pro-tenogenic niche to initiate tendon regeneration by targeting IKKβ/NF-κB signaling
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2025 (English)In: Bioactive Materials, ISSN 2452-199X, Vol. 44, p. 319-338Article in journal (Refereed) Published
Abstract [en]

Tendon repair remains challenging due to its poor intrinsic healing capacity, and stem cell therapy has emerged as a promising strategy to promote tendon regeneration. Nevertheless, the inflammatory environment following acute tendon injuries disrupts stem cell differentiation, leading to unsatisfied outcomes. Our study recognized the critical role of NF-κB signaling in activating inflammation and suppressing tenogenic differentiation of stem cells after acute tendon injury via multiomics analysis. TPCA-1, a selective inhibitor of IKKβ/NF-κB signaling, efficiently restored the impaired tenogenesis of stem cells in the inflammatory environment. By developing a microsphere-incorporated hydrogel system for stem cell delivery and controlled release of TPCA-1, we successfully engineered a pro-tenogenic niche to initiate tenogenesis for tendon regeneration. Collectively, we recognize NF-κB signaling as a critical target to tailor a pro-tenogenic niche and propose the combined delivery of stem cells and TPCA-1 as a potential strategy for acute tendon injuries.

Place, publisher, year, edition, pages
Elsevier, 2025
Keywords
Acute tendon injury, Multiomics, NF-κB signaling, Stem cell therapy, Tenogenic differentiation
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-231330 (URN)10.1016/j.bioactmat.2024.10.016 (DOI)001359052300001 ()2-s2.0-85206982446 (Scopus ID)
Available from: 2024-10-31 Created: 2024-10-31 Last updated: 2025-04-24Bibliographically approved
Long, Q., Liu, C., Zheng, H., Wang, M., Liu, H., Liu, Y., . . . Chen, J. (2025). Enhancing tendon regeneration: investigating the impact of topography on the secretome of adipose-derived stem cells. Advanced Science, Article ID 2417447.
Open this publication in new window or tab >>Enhancing tendon regeneration: investigating the impact of topography on the secretome of adipose-derived stem cells
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2025 (English)In: Advanced Science, E-ISSN 2198-3844, article id 2417447Article in journal (Refereed) Epub ahead of print
Abstract [en]

Tendons are vital for maintaining integrity and movement, but current treatment options are insufficient for their regeneration after injuries. Previous studies have shown that the secretome from mesenchymal stem cells (MSCs) promoted tendon regeneration. However, limited studies have explored the impact of the physical microenvironment on the secretome's efficacy of MSCs. In this study, it is shown that the topographic orientation regulates the secretome of human adipose-derived stem cells (ADSCs) and promotes tendon regeneration. Conditioned medium (CM) is collected from ADSCs cultured on the scaffolds with different topography. The results show that CM generated from aligned structure group has a potent effect in promoting cell migration and proliferation, tenogenic differentiation, macrophage polarization toward M2 phenotype, tendon structure and mechanical function recovery. Proteomic analysis revealed that the aligned structure can up-regulate the secretion of Extracellular matrix (ECM) proteins while down-regulate proinflammatory factors. This modulation activates the MAPK, GPCR and Integrin signaling pathways which may account for the enhanced effect on tendon regeneration. This study offers a promising and safer non-cell-based treatment option for tendon repair.

Place, publisher, year, edition, pages
Wiley-VCH Verlagsgesellschaft, 2025
Keywords
ADSCs, paracrine, proteomics, tendon regeneration, topology
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-237231 (URN)10.1002/advs.202417447 (DOI)001445627000001 ()40091553 (PubMedID)2-s2.0-105000299912 (Scopus ID)
Available from: 2025-04-03 Created: 2025-04-03 Last updated: 2025-04-03
Li, J., Zhou, X., Chen, J., Zhu, S., Mateus, A., Eliasson, P., . . . Backman, L. J. (2025). Impact of static myoblast loading on protein secretion linked to tenocyte migration. Journal of Proteome Research, 24(5), 2529-2541
Open this publication in new window or tab >>Impact of static myoblast loading on protein secretion linked to tenocyte migration
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2025 (English)In: Journal of Proteome Research, ISSN 1535-3893, E-ISSN 1535-3907, Vol. 24, no 5, p. 2529-2541Article in journal (Refereed) Published
Abstract [en]

Exercise has been shown to promote wound healing, including tendon repair. Myokines released from the exercised muscles are believed to play a significant role in this process. In our previous study, we used an in vitro coculture and loading model to demonstrate that 2% static loading of myoblasts increased the migration and proliferation of cocultured tenocytes─two crucial aspects of wound healing. IGF-1, released from myoblasts in response to 2% static loading, was identified as a contributor to the increased proliferation. However, the factors responsible for the enhanced migration remained unknown. In the current study, we subjected myoblasts in single culture conditions to 2, 5, and 10% static loading and performed proteomic analysis of the cell supernatants. Gene Ontology (GO) analysis revealed that 2% static loading induced the secretion of NBL1, C5, and EFEMP1, which is associated with cell migration and motility. Further investigation by adding exogenous recombinant proteins to human tenocytes showed that NBL1 increased tenocyte migration but not proliferation. This effect was not observed with treatments using C5 and EFEMP1.

Place, publisher, year, edition, pages
American Chemical Society (ACS), 2025
Keywords
migration, myokines, static loading, tenocyte, wound healing
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-238095 (URN)10.1021/acs.jproteome.5c00068 (DOI)001462713100001 ()40202163 (PubMedID)2-s2.0-105002785594 (Scopus ID)
Funder
The Kempe Foundations, JCK-2032.2The Kempe Foundations, JCSMK24-00017Magnus Bergvall Foundation, 2023-466
Available from: 2025-04-30 Created: 2025-04-30 Last updated: 2025-05-16Bibliographically approved
Zhu, J., Du, Y., Backman, L. J., Chen, J., Ouyang, H. & Zhang, W. (2024). Cellular interactions and biological effects of silk fibroin: implications for tissue engineering and regenerative medicine. Small
Open this publication in new window or tab >>Cellular interactions and biological effects of silk fibroin: implications for tissue engineering and regenerative medicine
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2024 (English)In: Small, ISSN 1613-6810, E-ISSN 1613-6829Article, review/survey (Refereed) Epub ahead of print
Abstract [en]

Silk fibroin (SF), the core structural protein derived from Bombyx mori silk, is extensively employed in tissue engineering and regenerative medicine due to its exceptional mechanical properties, favorable biocompatibility, tunable biodegradability, and versatile processing capabilities. Despite these advantages, current research predominantly focuses on SF biomaterials as structural scaffolds or drug carriers, often overlooking their potential role in modulating cellular behavior and tissue regeneration. This review aims to present a comprehensive overview of the inherent biological effects of SF biomaterials, independent of any exogenous biomolecules, and their implications for various tissue regeneration. It will cover in vitro cellular interactions of SF with various cell types, including stem cells and functional tissue cells such as osteoblasts, chondrocytes, keratinocytes, endothelial cells, fibroblasts, and epithelial cells. Moreover, it will summarize in vivo immune responses, cellular responses, and tissue regeneration following SF implantation, specifically focusing on vascular, bone, skin, cartilage, ocular, and tendon/ligament regeneration. Furthermore, it will address current limitations and future perspectives in the design of bioactive SF biomaterials. A comprehensive understanding of these cellular interactions and the biological effects of SF is crucial for predicting regenerative outcomes with precision and for designing SF-based biomaterials tailored to specific properties, enabling broader applications in regenerative medicine.

Keywords
biological effects, cellular interactions, regenerative medicine, silk fibroin, tissue engineering
National Category
Biomaterials Science
Identifiers
urn:nbn:se:umu:diva-233326 (URN)10.1002/smll.202409739 (DOI)001375783000001 ()39668424 (PubMedID)2-s2.0-85211594681 (Scopus ID)
Available from: 2025-01-02 Created: 2025-01-02 Last updated: 2025-01-02
Zhang, Q., Zhou, X., Zhang, W., Wang, X., Dou, S., Zhao, L., . . . Danielson, P. (2024). Corneal strain influences keratocyte proliferation and migration through upregulation of ALDH3A1 expression. The FASEB Journal, 38(23), Article ID e70236.
Open this publication in new window or tab >>Corneal strain influences keratocyte proliferation and migration through upregulation of ALDH3A1 expression
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2024 (English)In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 38, no 23, article id e70236Article in journal (Refereed) Published
Abstract [en]

Keratocytes are the primary resident cells in the corneal stroma. They play an essential role in maintaining corneal physiological function. Studying the factors that affect the phenotype and behavior of keratocytes offers meaningful perspectives for improving the understanding and treatment of corneal injuries. In this study, 3% strain was applied to human keratocytes using the Flexcell® Tension Systems. Real-time quantitative PCR (RT-qPCR) and western blot were used to investigate the influence of strain on the expression of intracellular aldehyde dehydrogenase 3A1 (ALDH3A1). ALDH3A1 knockdown was achieved using double-stranded RNA-mediated interference (RNAi). Immunofluorescence (IF) staining was employed to observe the impact of changes in ALDH3A1 expression on nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) nuclear translocation. Keratocyte proliferation and migration were assessed by bromodeoxyuridine (BrdU) assay and scratch wound healing assay, respectively. Mouse injury models and single-cell RNA sequencing of keratocytes from keratoconus patients were used to assess how strain influenced ALDH3A1 in vivo. Our results demonstrate that 3% strain suppresses keratocyte proliferation and increases ALDH3A1. Increased ALDH3A1 inhibits NF-κB nuclear translocation, a key step in the activation of the NF-κB signaling pathway. Conversely, ALDH3A1 knockdown promotes NF-κB nuclear translocation, ultimately enhancing keratocyte proliferation and migration. Elevated ALDH3A1 levels were also observed in mouse injury models with increased corneal strain and keratoconus patients. These findings provide valuable insights for further research into the role of corneal strain and its connection to corneal injury repair.

Place, publisher, year, edition, pages
John Wiley & Sons, 2024
Keywords
ALDH3A1, NF‐κB, biomechanics, corneal injuries, corneal strain, keratocytes, migration, proliferation
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-232831 (URN)10.1096/fj.202401392R (DOI)001372449800001 ()39652089 (PubMedID)2-s2.0-85211479281 (Scopus ID)
Funder
Swedish Research Council, 017-01138Stiftelsen Kronprinsessan Margaretas arbetsnämnd för synskadade, 2013/10Region Västerbotten, RV-979985
Available from: 2024-12-10 Created: 2024-12-10 Last updated: 2024-12-16Bibliographically approved
Dennhag, N., Kahsay, A., Nissen, I., Nord, H., Chermenina, M., Liu, J., . . . Domellöf, F. P. (2024). fhl2b mediates extraocular muscle protection in zebrafish models of muscular dystrophies and its ectopic expression ameliorates affected body muscles. Nature Communications, 15(1), Article ID 1950.
Open this publication in new window or tab >>fhl2b mediates extraocular muscle protection in zebrafish models of muscular dystrophies and its ectopic expression ameliorates affected body muscles
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2024 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 15, no 1, article id 1950Article in journal (Refereed) Published
Abstract [en]

In muscular dystrophies, muscle fibers loose integrity and die, causing significant suffering and premature death. Strikingly, the extraocular muscles (EOMs) are spared, functioning well despite the disease progression. Although EOMs have been shown to differ from body musculature, the mechanisms underlying this inherent resistance to muscle dystrophies remain unknown. Here, we demonstrate important differences in gene expression as a response to muscle dystrophies between the EOMs and trunk muscles in zebrafish via transcriptomic profiling. We show that the LIM-protein Fhl2 is increased in response to the knockout of desmin, plectin and obscurin, cytoskeletal proteins whose knockout causes different muscle dystrophies, and contributes to disease protection of the EOMs. Moreover, we show that ectopic expression of fhl2b can partially rescue the muscle phenotype in the zebrafish Duchenne muscular dystrophy model sapje, significantly improving their survival. Therefore, Fhl2 is a protective agent and a candidate target gene for therapy of muscular dystrophies.

Place, publisher, year, edition, pages
Springer Nature, 2024
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-222359 (URN)10.1038/s41467-024-46187-x (DOI)001179691200013 ()38431640 (PubMedID)2-s2.0-85186557555 (Scopus ID)
Available from: 2024-03-15 Created: 2024-03-15 Last updated: 2025-04-24Bibliographically approved
Zhou, X., Zhu, S., Li, J., Mateus, A., Williams, C., Gilthorpe, J. D. & Backman, L. J. (2024). Mechanical loading modulates AMPK and mTOR signaling in muscle cells. Journal of Proteome Research, 23(10), 4286-4295
Open this publication in new window or tab >>Mechanical loading modulates AMPK and mTOR signaling in muscle cells
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2024 (English)In: Journal of Proteome Research, ISSN 1535-3893, E-ISSN 1535-3907, Vol. 23, no 10, p. 4286-4295Article in journal (Refereed) Published
Abstract [en]

Skeletal muscle adaptation to exercise involves various phenotypic changes that enhance the metabolic and contractile functions. One key regulator of these adaptive responses is the activation of AMPK, which is influenced by exercise intensity. However, the mechanistic understanding of AMPK activation during exercise remains incomplete. In this study, we utilized an in vitro model to investigate the effects of mechanical loading on AMPK activation and its interaction with the mTOR signaling pathway. Proteomic analysis of muscle cells subjected to static loading (SL) revealed distinct quantitative protein alterations associated with RNA metabolism, with 10% SL inducing the most pronounced response compared to lower intensities of 5% and 2% as well as the control. Additionally, 10% SL suppressed RNA and protein synthesis while activating AMPK and inhibiting the mTOR pathway. We also found that SRSF2, necessary for pre-mRNA splicing, is regulated by AMPK and mTOR signaling, which, in turn, is regulated in an intensity-dependent manner by SL with the highest expression in 2% SL. Further examination showed that the ADP/ATP ratio was increased after 10% SL compared to the control and that SL induced changes in mitochondrial biogenesis. Furthermore, Seahorse assay results indicate that 10% SL enhances mitochondrial respiration. These findings provide novel insights into the cellular responses to mechanical loading and shed light on the intricate AMPK-mTOR regulatory network in muscle cells.

Place, publisher, year, edition, pages
American Chemical Society (ACS), 2024
Keywords
ADP/ATP ratio, AMPK, exercise adaptation, mechanical loading, mitochondrial biogenesis, mTOR, protein synthesis, proteomics analysis, RNA sequencing, skeletal muscle
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-229419 (URN)10.1021/acs.jproteome.4c00242 (DOI)001302852000001 ()39213513 (PubMedID)2-s2.0-85202738975 (Scopus ID)
Funder
Åke Wiberg Foundation, M20-0236Åke Wiberg Foundation, M22-0008Swedish Research Council, P2022-0010Swedish Research Council, P2023-0011Swedish Research Council, P2024-0001The Kempe Foundations, JCK-2032.2
Available from: 2024-09-09 Created: 2024-09-09 Last updated: 2024-10-28Bibliographically approved
Chen, J., Mo, Q., Long, Q., Sheng, R., Chen, Z., Luo, Y., . . . Zhang, W. (2023). Hydroxycamptothecin and substratum stiffness synergistically regulate fibrosis of human corneal fibroblasts. ACS Biomaterials Science & Engineering, 9(2), 959-967
Open this publication in new window or tab >>Hydroxycamptothecin and substratum stiffness synergistically regulate fibrosis of human corneal fibroblasts
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2023 (English)In: ACS Biomaterials Science & Engineering, E-ISSN 2373-9878, Vol. 9, no 2, p. 959-967Article in journal (Refereed) Published
Abstract [en]

Corneal fibrosis is a common outcome of inappropriate repair associated with trauma or ocular infection. Altered biomechanical properties with increased corneal stiffness is a feature of fibrosis that cause corneal opacities, resulting in severe visual impairment and even blindness. The present study aims to determine the effect of hydroxycamptothecin (HCPT) and matrix stiffness on transforming growth factor-β1 (TGF-β1)-induced fibrotic processes in human corneal fibroblasts (HTK cells). HTK cells were cultured on substrates with different stiffnesses ("soft", ∼261 kPa; "stiff", ∼2.5 × 103 kPa) and on tissue culture plastic (TCP, ∼106 kPa) and simultaneously treated with or without 1 μg/mL HCPT and 10 ng/mL TGF-β1. We found that HCPT induced decreased cell viability and antiproliferative effects on HTK cells. TGF-β1-induced expression of fibrosis-related genes (FN1, ACTA2) was reduced if the cells were simultaneously treated with HCPT. Substrate stiffness did not affect the expression of fibrosis-related genes. The TGF-β1 induced expression of FN1 on both soft and stiff substrates was reduced if cells were simultaneously treated with HCPT. However, this trend was not seen for ACTA2, i.e., the TGF-β1 induced expression of ACTA2 was not reduced by simultaneous treatment of HCPT in either soft or stiff substrate. Instead, HCPT treatment in the presence of TGF-β1 resulted in increased gene expression of keratocyte phenotype makers (LUM, KERA, AQP1, CHTS6) on both substrate stiffnesses. In addition, the protein expression of keratocyte phenotype makers LUM and ALDH3 was increased in HTK cells simultaneously treated with TGF-β1 and HCPT on stiff substrate as compared to control, i.e., without HCPT. In conclusion, we found that HCPT can reduce TGF-β1-induced fibrosis and promote the keratocyte phenotype in a substrate stiffness dependent manner. Thus, HCPT stimulation might be an approach to stimulate keratocytes in the appropriate healing stage to avoid or reverse fibrosis and achieve more optimal corneal wound healing.

Place, publisher, year, edition, pages
American Chemical Society (ACS), 2023
Keywords
corneal fibroblasts, HCPT, myofibroblast differentiation, substratum stiffness
National Category
Cell and Molecular Biology Ophthalmology
Identifiers
urn:nbn:se:umu:diva-204679 (URN)10.1021/acsbiomaterials.2c01302 (DOI)000926469500001 ()36705297 (PubMedID)2-s2.0-85147220511 (Scopus ID)
Available from: 2023-02-09 Created: 2023-02-09 Last updated: 2023-07-13Bibliographically approved
Sheng, R., Liu, J., Zhang, W., Luo, Y., Chen, Z., Chi, J., . . . Chen, J. (2023). Material stiffness in cooperation with macrophage paracrine signals determines the tenogenic differentiation of mesenchymal stem cells. Advanced Science, 10(17), Article ID 2206814.
Open this publication in new window or tab >>Material stiffness in cooperation with macrophage paracrine signals determines the tenogenic differentiation of mesenchymal stem cells
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2023 (English)In: Advanced Science, E-ISSN 2198-3844, Vol. 10, no 17, article id 2206814Article in journal (Refereed) Published
Abstract [en]

Stiffness is an important physical property of biomaterials that determines stem cell fate. Guiding stem cell differentiation via stiffness modulation has been considered in tissue engineering. However, the mechanism by which material stiffness regulates stem cell differentiation into the tendon lineage remains controversial. Increasing evidence demonstrates that immune cells interact with implanted biomaterials and regulate stem cell behaviors via paracrine signaling; however, the role of this mechanism in tendon differentiation is not clear. In this study, polydimethylsiloxane (PDMS) substrates with different stiffnesses are developed, and the tenogenic differentiation of mesenchymal stem cells (MSCs) exposed to different stiffnesses and macrophage paracrine signals is investigated. The results reveal that lower stiffnesses facilitates tenogenic differentiation of MSCs, while macrophage paracrine signals at these stiffnesses suppress the differentiation. When exposed to these two stimuli, MSCs still exhibit enhanced tendon differentiation, which is further elucidated by global proteomic analysis. Following subcutaneous implantation in rats for 2 weeks, soft biomaterial induces only low inflammation and promotes tendon-like tissue formation. In conclusion, the study demonstrates that soft, rather than stiff, material has a greater potential to guide tenogenic differentiation of stem cells, which provides comprehensive evidence for optimized bioactive scaffold design in tendon tissue engineering.

Place, publisher, year, edition, pages
John Wiley & Sons, 2023
Keywords
macrophage polarization, proteomics, stem cell, stiffness, tenogenic differentiation
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-208058 (URN)10.1002/advs.202206814 (DOI)000975347000001 ()37097733 (PubMedID)2-s2.0-85153173993 (Scopus ID)
Available from: 2023-05-30 Created: 2023-05-30 Last updated: 2023-07-13Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0002-6091-3982

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