scholarly journals Hypoxia-Induced Mesenchymal Stem Cells Exhibit Stronger Tenogenic Differentiation Capacities and Promote Patellar Tendon Repair in Rabbits

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Guanyin Chen ◽  
Wangqian Zhang ◽  
Kuo Zhang ◽  
Shuning Wang ◽  
Yuan Gao ◽  
...  
Keyword(s):  
Patellar Tendon ◽  
Tendon Repair ◽  
Biomechanical Properties ◽  
Clinical Results ◽  
Medical Problem ◽  
Tendon Injury ◽  
Tenogenic Differentiation ◽  
Tgf Β1

Tendon injury is a common but tough medical problem. Unsatisfactory clinical results have been reported in tendon repair using mesenchymal stem cell (MSC) therapy, creating a need for a better strategy to induce MSCs to tenogenic differentiation. This study was designed to examine the effect of hypoxia on the tenogenic differentiation of different MSCs and their tenogenic differentiation capacities under hypoxia condition in vitro and to investigate the in vivo inductility of hypoxia in tenogenesis. Adipose tissue-derived MSCs (AMSCs) and bone marrow-derived MSCs (BMSCs) were isolated and characterized. The expression of hypoxia-induced factor-1 alpha (Hif-1α) was examined to confirm the establishment of hypoxia condition. qRT-PCR, western blot, and immunofluorescence staining were used to evaluate the expression of tendon-associated marker Col-1a1, Col-3a1, Dcn, and Tnmd in AMSCs and BMSCs under hypoxia condition, compared with Tgf-β1 induction. In vivo, a patellar tendon injury model was established. Normoxic and hypoxic BMSCs were cultured and implanted. Histological, biomechanical, and transmission electron microscopy analyses were performed to assess the improved healing effect of hypoxic BMSCs on tendon injury. Our in vitro results showed that hypoxia remarkably increased the expression of Hif-1α and that hypoxia not only promoted a significant increase in tenogenic markers in both AMSCs and BMSCs compared with the normoxia group but also showed higher inductility compared with Tgf-β1. In addition, hypoxic BMSCs exhibited higher potential of tenogenic differentiation than hypoxic AMSCs. Our in vivo results demonstrated that hypoxic BMSCs possessed better histological and biomechanical properties than normoxic BMSCs, as evidenced by histological scores, patellar tendon biomechanical parameters, and the range and average of collagen fibril diameters. These findings suggested that hypoxia may be a practical and reliable strategy to induce tenogenic differentiation of BMSCs for tendon repair and could enhance the effectiveness of MSCs therapy in treating tendon injury.

Hypoxia promotes tenocyte differentiation of mesenchymal stem cells

2020 ◽  
Author(s):  
Guanyin Chen ◽  
wangqian zhang ◽  
Jintao Gu ◽  
Yuan Gao ◽  
Lei He ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Patellar Tendon ◽  
Tendon Repair ◽  
Clinical Results ◽  
Tendon Injury ◽  
Tenogenic Differentiation ◽  
Tgf Β1

Abstract Background: Tendon injury is a common but tough medical problem. Unsatisfactory clinical results have been reported in tendon repair using mesenchymal stem cells (MSCs) therapy, creating a need for a better strategy to induce MSCs to tenogenic differentiation. This study was designed to investigate the role of hypoxia in the tenogenic differentiation of MSCs in vitro and in vivo and to compare the tenogenic differentiation capacities of different MSCs under hypoxia condition in vitro. Methods: Adipose tissue-derived MSCs (AMSCs) and bone marrow-derived MSCs (BMSCs) were isolated and characterized by the expression of MSC-specific markers and tri-lineage differentiation. The expression of hypoxia induced factor-1 alpha (Hif-1α) and the proliferation of AMSCs and BMSCs were examined in order to confirm the establishment of hypoxia condition. qRT-PCR, western blot, and immunofluorescence staining were used to evaluate the expression of tendon-associated marker Col-1a1, Col-3a1, Dcn, and Tnmd in AMSCs and BMSCs under hypoxia and/or Tgf-β1 condition. In vivo, a patellar tendon injury model was established. Normoxic and hypoxic BMSCs were cultured and implanted. Histological, biomechanical and transmission electron microscopy analyses were performed to assess the improved healing effect of hypoxic BMSCs on tendon injury. Results: Hypoxia remarkably increased the expression of Hif-1α and the proliferation of AMSCs and BMSCs. Our in vitro results detected that hypoxia not only promoted a significant increase in tenogenic markers in both AMSCs and BMSCs compared with the normoxia group, but also showed higher inductility compared with Tgf-β1. In addition, hypoxic BMSCs exhibited higher potential of tenogenic differentiation than hypoxic AMSCs. Our in vivo results demonstrated that hypoxic BMSCs possessed better histological and biomechanical properties than those of normoxic BMSCs, as evidenced by histological scores, quantitative analysis of immunohistochemical staining for Col-1a1 and Tnmd, the range and average of collagen fibril diameters and patellar tendon biomechanical tests. Conclusions: These findings suggested that hypoxia may be a practical and reliable strategy to induce tenogenic differentiation of BMSCs for tendon repair and could enhance the effectiveness of MSCs therapy in treating tendon injury.

scholarly journals Mkx Mediates Tenogenic Differentiation But Incompletely Inhibits The Proliferation of Hypoxic MSCs

2021 ◽  
Author(s):  
Guanyin Chen ◽  
Dong Fan ◽  
Wangqian Zhang ◽  
Shuning Wang ◽  
Jintao Gu ◽  
...  
Keyword(s):  
Tendon Repair ◽  
Biomechanical Properties ◽  
Tendon Injury ◽  
Cell Counting ◽  
Differentiation Markers ◽  
Proliferation Capacity ◽  
Tenogenic Differentiation ◽  
Differentiation And Proliferation

Abstract Background: Hypoxia has been shown to be able to induce tenogenic differentiation of mesenchymal stem cells (MSCs) which lead hypoxia-induced MSCs to be a potential treatment for tendon injury. However, little is known about the mechanism underlying the tenogenic differentiation process of hypoxic MSCs, which limited the application of differentiation-inducing therapies in tendon repair. This study was designed to investigate the role of Mohawk homeobox (Mkx) in tenogenic differentiation and proliferation of hypoxic MSCs.Methods: Adipose-derived MSCs (AMSCs) and bone marrow-derived MSCs (BMSCs) were isolated, identified and cultured as our previous study. qRT-PCR, western blot, and immunofluorescence staining were performed to evaluate the expression of Mkx and other tendon-associated markers in AMSCs and BMSCs under hypoxia condition. Small interfering RNA technique was applied to observe the effect of Mkx levels on the expression of tendon-associated markers in normoxic and hypoxic BMSCs. Hypoxic BMSCs infected with Mkx-specific short hair RNA (shRNA) or scramble were implanted into the wound gaps of injured patellar tendons to assess the effect of Mkx levels on tendon repair. In addition, cell counting kit‑8 and colony formation unit assays were adopted to determine the proliferation capacity of normoxic or hypoxic BMSCs infected with or without Mkx-specific shRNA.Results: Our data showed that the expression of Mkx significantly increased in hypoxic AMSCs, and increased much more in hypoxic BMSCs. Our results also detected that the expression of tenogenic differentiation markers after down-regulation of Mkx were significantly decreased not only in normoxic BMSCs, but also in hypoxic BMSCs which paralleled the inferior histological evidences, worse biomechanical properties and smaller diameters of collagen fibrils in vivo. In addition, our in vitro data demonstrated that the optical density values and the clone numbers of both normoxic and hypoxic BMSCs were significantly increased after knockdown of Mkx, and were also significantly enhanced in both AMSCs and BMSCs in hypoxia condition under which the expression of Mkx was up-regulated.Conclusions: These findings strongly suggested that Mkx mediated hypoxia-induced tenogenic differentiation of MSCs, but could not completely repress the proliferation of hypoxic MSCs.

scholarly journals Mkx mediates tenogenic differentiation but incompletely inhibits the proliferation of hypoxic MSCs

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Guanyin Chen ◽  
Dong Fan ◽  
Wangqian Zhang ◽  
Shuning Wang ◽  
Jintao Gu ◽  
...  
Keyword(s):  
Tendon Repair ◽  
Biomechanical Properties ◽  
Tendon Injury ◽  
Cell Counting ◽  
Differentiation Markers ◽  
Proliferation Capacity ◽  
Tenogenic Differentiation ◽  
Differentiation And Proliferation

Abstract Background Hypoxia has been shown to be able to induce tenogenic differentiation and proliferation of mesenchymal stem cells (MSCs) which lead hypoxia-induced MSCs to be a potential treatment for tendon injury. However, little is known about the mechanism underlying the tenogenic differentiation and proliferation process of hypoxic MSCs, which limited the application of differentiation-inducing therapies in tendon repair. This study was designed to investigate the role of Mohawk homeobox (Mkx) in tenogenic differentiation and proliferation of hypoxic MSCs. Methods qRT-PCR, western blot, and immunofluorescence staining were performed to evaluate the expression of Mkx and other tendon-associated markers in adipose-derived MSCs (AMSCs) and bone marrow-derived MSCs (BMSCs) under hypoxia condition. Small interfering RNA technique was applied to observe the effect of Mkx levels on the expression of tendon-associated markers in normoxic and hypoxic BMSCs. Hypoxic BMSCs infected with Mkx-specific short hair RNA (shRNA) or scramble were implanted into the wound gaps of injured patellar tendons to assess the effect of Mkx levels on tendon repair. In addition, cell counting kit-8 assay, colony formation unit assay, cell cycle analysis, and EdU assay were adopted to determine the proliferation capacity of normoxic or hypoxic BMSCs infected with or without Mkx-specific shRNA. Results Our data showed that the expression of Mkx significantly increased in hypoxic AMSCs and increased much higher in hypoxic BMSCs. Our results also detected that the expression of tenogenic differentiation markers after downregulation of Mkx were significantly decreased not only in normoxic BMSCs, but also in hypoxic BMSCs which paralleled the inferior histological evidences, worse biomechanical properties, and smaller diameters of collagen fibrils in vivo. In addition, our in vitro data demonstrated that the optical density values, the clone numbers, the percentage of cells in S phage, and cell proliferation potential of both normoxic and hypoxic BMSCs were all significantly increased after knockdown of Mkx and were also significantly enhanced in both AMSCs and BMSCs in hypoxia condition under which the expression of Mkx was upregulated. Conclusions These findings strongly suggested that Mkx mediated hypoxia-induced tenogenic differentiation of MSCs but could not completely repress the proliferation of hypoxic MSCs.

scholarly journals Electrospun Water-Borne Polyurethane Nanofibrous Membrane as a Barrier for Preventing Postoperative Peritendinous Adhesion

2019 ◽  
Vol 20 (7) ◽  
pp. 1625 ◽  
Author(s):  
Shih-Heng Chen ◽  
Pang-Yun Chou ◽  
Zhi-Yu Chen ◽  
Feng-Huei Lin
Keyword(s):  
Tendon Repair ◽  
Major Complication ◽  
Biomechanical Properties ◽  
Tendon Injury ◽  
Electrospinning Process ◽  
In Vivo Studies ◽  
Surrounding Tissue ◽  
Water Borne

Peritendinous adhesion is a major complication after tendon injury and the subsequent repairs or reconstructions. The degree of adhesion can be reduced by the interposition of a membranous barrier between the traumatized tendon and the surrounding tissue. In the present study, electrospun water-borne polyurethane (WPU) nanofibrous membranes (NFMs) were created for use after the reparation or reconstruction of tendons to reduce adhesion. In the electrospinning process, water was employed as the solvent for WPU, and this solvent was ecofriendly and nontoxic. The nanofibrous architecture and pore size of the WPU NFMs were analyzed. Their microporosity (0.78–1.05 µm) blocked the penetration of fibroblasts, which could result in adhesion and scarring around the tendon during healing. The release of WPU mimicked the lubrication effect of the synovial fluid produced by the synovium around the tendon. In vitro cell studies revealed that the WPU NFMs effectively reduced the number of fibroblasts that became attached and that there was no significant cytotoxicity. In vivo studies with the rabbit flexor tendon repair model revealed that WPU NFMs reduced the degree of peritendinous adhesion, as determined using a gross examination; a histological cross section evaluation; and measurements of the range of motion of interphalangeal joints (97.1 ± 14.7 and 79.0 ± 12.4 degrees in proximal and distal interphalangeal joints respectively), of the length of tendon excursion (11.6 ± 1.9 cm), and of the biomechanical properties.

scholarly journals Tenogenic differentiation of mesenchymal stem cells

2018 ◽  
Vol 3 (3) ◽  
pp. 2473011418S0030
Author(s):  
Seung Yeol Lee ◽  
Hyang Kim ◽  
Kyoung Min Lee
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Tendon Repair ◽  
Human Tonsil ◽  
Differentiation Potential ◽  
Lineage Differentiation ◽  
Tenogenic Differentiation ◽  
Surface Marker Analysis

Category: Basic Sciences/Biologics Introduction/Purpose: Tendon repair has been a challenging issue for surgeons in treating. Although tissue engineering with mesenchymal stem cells (MSC) have been used for tendon repair in both in vivo and in vitro, the stem cells are obtained through invasive procedures, and there is usually a lack of adequate numbers for clinical use. The purpose of this study was to compare the potential of tri-lineage differentiation and to investigate the potential of tenogenic differentiation of human tonsil derived MSCs (T-MSCs), bone marrow derived MSCs (BM-MSCs), and adipose tissue derived MSCs (AD-MSCs). Methods: Each tissue was obtained from 8 patients. After isolation of MSCs, flow cytometry analysis was used to characterize the phenotypes of the MSCs. Differentiation capacity to adipo-, osteo-, and chondrocytes were induced by culturing each MSCs for 3 weeks in commercially available media. Each MSCs was treated with 5ng/ml and 10ng/ml of TGF-ß3 with vehicle control. Results: Immunophenotypic surface marker analysis of BM-MSC, AD-MSC, and TMSCs revealed that these MSCs expressed a typical MSCs. mRNA expression levels of the markers for tri-lineage differentiation were significantly lower in TMSC than other MSCs. The tenogenic transcription factor, scleraxis, showed a statistically significant increase in all MSCs differentiation groups except for the 7th day TMSC differentiation group (Figure). Gene expression of tenascin-C, an ECM glycoprotein, was specifically expressed in the T-MSC differentiation group at 14 days (Figure). Comparing the ratio of collagen 1 to collagen 3 genes, the BM-MSC showed a decrease in the ratio on days 3 and 7 unlike AD-MSCs and TMSCs. Only TMSC showed a significant increase in the ratio compared with other MSCs on the 14th day. Conclusion: The tonsil-MSC has low fat, bone and cartilage differentiation potential and has excellent tendon-specific differentiation potential, thus being highly useful as a tendon-tailored cell therapy agent.

scholarly journals Regorafenib-Attenuated, Bleomycin-Induced Pulmonary Fibrosis by Inhibiting the TGF-β1 Signaling Pathway

2021 ◽  
Vol 22 (4) ◽  
pp. 1985
Author(s):  
Xiaohe Li ◽  
Ling Ma ◽  
Kai Huang ◽  
Yuli Wei ◽  
Shida Long ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Kinase Inhibitor ◽  
In Vivo Experiments ◽  
Age Related ◽  
And Migration ◽  
Tgf Β1

Idiopathic pulmonary fibrosis (IPF) is a fatal and age-related pulmonary disease. Nintedanib is a receptor tyrosine kinase inhibitor, and one of the only two listed drugs against IPF. Regorafenib is a novel, orally active, multi-kinase inhibitor that has similar targets to nintedanib and is applied to treat colorectal cancer and gastrointestinal stromal tumors in patients. In this study, we first identified that regorafenib could alleviate bleomycin-induced pulmonary fibrosis in mice. The in vivo experiments indicated that regorafenib suppresses collagen accumulation and myofibroblast activation. Further in vitro mechanism studies showed that regorafenib inhibits the activation and migration of myofibroblasts and extracellular matrix production, mainly through suppressing the transforming growth factor (TGF)-β1/Smad and non-Smad signaling pathways. In vitro studies have also indicated that regorafenib could augment autophagy in myofibroblasts by suppressing TGF-β1/mTOR (mechanistic target of rapamycin) signaling, and could promote apoptosis in myofibroblasts. In conclusion, regorafenib attenuates bleomycin-induced pulmonary fibrosis by suppressing the TGF-β1 signaling pathway.

scholarly journals Concurrent YAP/TAZ and SMAD signaling mediate vocal fold fibrosis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ryosuke Nakamura ◽  
Nao Hiwatashi ◽  
Renjie Bing ◽  
Carina P. Doyle ◽  
Ryan C. Branski
Keyword(s):  
Vocal Fold ◽  
Vocal Folds ◽  
Nuclear Accumulation ◽  
Smad Pathway ◽  
Surgical Interventions ◽  
Smad Signaling ◽  
Iatrogenic Damage ◽  
Tgf Β1

AbstractVocal fold (VF) fibrosis is a major cause of intractable voice-related disability and reduced quality of life. Excision of fibrotic regions is suboptimal and associated with scar recurrence and/or further iatrogenic damage. Non-surgical interventions are limited, putatively related to limited insight regarding biochemical events underlying fibrosis, and downstream, the lack of therapeutic targets. YAP/TAZ integrates diverse cell signaling events and interacts with signaling pathways related to fibrosis, including the TGF-β/SMAD pathway. We investigated the expression of YAP/TAZ following vocal fold injury in vivo as well as the effects of TGF-β1 on YAP/TAZ activity in human vocal fold fibroblasts, fibroblast-myofibroblast transition, and TGF-β/SMAD signaling. Iatrogenic injury increased nuclear localization of YAP and TAZ in fibrotic rat vocal folds. In vitro, TGF-β1 activated YAP and TAZ in human VF fibroblasts, and inhibition of YAP/TAZ reversed TGF-β1-stimulated fibroplastic gene upregulation. Additionally, TGF-β1 induced localization of YAP and TAZ in close proximity to SMAD2/3, and nuclear accumulation of SMAD2/3 was inhibited by a YAP/TAZ inhibitor. Collectively, YAP and TAZ were synergistically activated with the TGF-β/SMAD pathway, and likely essential for the fibroplastic phenotypic shift in VF fibroblasts. Based on these data, YAP/TAZ may evolve as an attractive therapeutic target for VF fibrosis.

scholarly journals Prrx1 promotes stemness and angiogenesis via activating TGF-β/smad pathway and upregulating proangiogenic factors in glioma

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Zetao Chen ◽  
Yihong Chen ◽  
Yan Li ◽  
Weidong Lian ◽  
Kehong Zheng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Therapeutic Strategy ◽  
Critical Role ◽  
Glioma Stem Cells ◽  
Promoter Regions ◽  
Aberrant Expression ◽  
Smad Pathway ◽  
Tgf Β1

AbstractGlioma is one of the most lethal cancers with highly vascularized networks and growing evidences have identified glioma stem cells (GSCs) to account for excessive angiogenesis in glioma. Aberrant expression of paired-related homeobox1 (Prrx1) has been functionally associated with cancer stem cells including GSCs. In this study, Prrx1 was found to be markedly upregulated in glioma specimens and elevated Prrx1 expression was inversely correlated with prognosis of glioma patients. Prrx1 potentiated stemness acquisition in non-stem tumor cells (NSTCs) and stemness maintenance in GSCs, accompanied with increased expression of stemness markers such as SOX2. Prrx1 also promoted glioma angiogenesis by upregulating proangiogenic factors such as VEGF. Consistently, silencing Prrx1 markedly inhibited glioma proliferation, stemness, and angiogenesis in vivo. Using a combination of subcellular proteomics and in vitro analyses, we revealed that Prrx1 directly bound to the promoter regions of TGF-β1 gene, upregulated TGF-β1 expression, and ultimately activated the TGF-β/smad pathway. Silencing TGF-β1 mitigated the malignant behaviors induced by Prrx1. Activation of this pathway cooperates with Prrx1 to upregulate the expression of stemness-related genes and proangiogenic factors. In summary, our findings revealed that Prrx1/TGF-β/smad signal axis exerted a critical role in glioma stemness and angiogeneis. Disrupting the function of this signal axis might represent a new therapeutic strategy in glioma patients.

scholarly journals Resveratrol Enhances Inhibition Effects of Cisplatin on Cell Migration and Invasion and Tumor Growth in Breast Cancer MDA-MB-231 Cell Models In Vivo and In Vitro

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2204
Author(s):  
Meng-Die Yang ◽  
Yang Sun ◽  
Wen-Jun Zhou ◽  
Xiao-Zheng Xie ◽  
Qian-Mei Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Tumor Growth ◽  
Cell Viability ◽  
Synergistic Effects ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tgf Β1

Triple-negative breast cancer (TNBC) is a refractory type of breast cancer that does not yet have clinically effective drugs. The aim of this study is to investigate the synergistic effects and mechanisms of resveratrol combined with cisplatin on human breast cancer MDA-MB-231 (MDA231) cell viability, migration, and invasion in vivo and in vitro. In vitro, MTS assays showed that resveratrol combined with cisplatin inhibits cell viability as a concentration-dependent manner, and produced synergistic effects (CI < 1). Transwell assay showed that the combined treatment inhibits TGF-β1-induced cell migration and invasion. Immunofluorescence assays confirmed that resveratrol upregulated E-cadherin expression and downregulated vimentin expression. Western blot assay demonstrated that resveratrol combined with cisplatin significantly reduced the expression of fibronectin, vimentin, P-AKT, P-PI3K, P-JNK, P-ERK, Sma2, and Smad3 induced by TGF-β1 (p < 0.05), and increased the expression of E-cadherin (p < 0.05), respectively. In vivo, resveratrol enhanced tumor growth inhibition and reduced body weight loss and kidney function impairment by cisplatin in MDA231 xenografts, and significantly reduced the expressions of P-AKT, P-PI3K, Smad2, Smad3, P-JNK, P-ERK, and NF-κB in tumor tissues (p < 0.05). These results indicated that resveratrol combined with cisplatin inhibits the viability of breast cancer MDA231 cells synergistically, and inhibits MDA231 cells invasion and migration through Epithelial-mesenchymal transition (EMT) approach, and resveratrol enhanced anti-tumor effect and reduced side of cisplatin in MDA231 xenografts. The mechanism may be involved in the regulations of PI3K/AKT, JNK, ERK and NF-κB expressions.

scholarly journals A composite scaffold of Wharton’s jelly and chondroitin sulphate loaded with human umbilical cord mesenchymal stem cells repairs articular cartilage defects in rat knee

2021 ◽  
Vol 32 (4) ◽  
Author(s):  
Zhong Li ◽  
Yikang Bi ◽  
Qi Wu ◽  
Chao Chen ◽  
Lu Zhou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Articular Cartilage ◽  
Composite Scaffold ◽  
Biomechanical Properties ◽  
Cartilage Defects ◽  
Human Umbilical Cord ◽  
Composite Scaffolds ◽  
Articular Cartilage Defects

AbstractTo evaluate the performance of a composite scaffold of Wharton’s jelly (WJ) and chondroitin sulfate (CS) and the effect of the composite scaffold loaded with human umbilical cord mesenchymal stem cells (hUCMSCs) in repairing articular cartilage defects, two experiments were carried out. The in vitro experiments involved identification of the hUCMSCs, construction of the biomimetic composite scaffolds by the physical and chemical crosslinking of WJ and CS, and testing of the biomechanical properties of both the composite scaffold and the WJ scaffold. In the in vivo experiments, composite scaffolds loaded with hUCMSCs and WJ scaffolds loaded with hUCMSCs were applied to repair articular cartilage defects in the rat knee. Moreover, their repair effects were evaluated by the unaided eye, histological observations, and the immunogenicity of scaffolds and hUCMSCs. We found that in vitro, the Young’s modulus of the composite scaffold (WJ-CS) was higher than that of the WJ scaffold. In vivo, the composite scaffold loaded with hUCMSCs repaired rat cartilage defects better than did the WJ scaffold loaded with hUCMSCs. Both the scaffold and hUCMSCs showed low immunogenicity. These results demonstrate that the in vitro construction of a human-derived WJ-CS composite scaffold enhances the biomechanical properties of WJ and that the repair of knee cartilage defects in rats is better with the composite scaffold than with the single WJ scaffold if the scaffold is loaded with hUCMSCs.

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