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Lactate plays a critical role as an energy substrate, metabolite, and signaling molecule in hepatocellular carcinoma (HCC). Intracellular lactate-derived protein lysine lactylation (Kla) is identified as a contributor to the progression of HCC. Liver cancer stem cells (LCSCs) are believed to be the root cause of phenotypic and functional heterogeneity in HCC. However, the impact of Kla on the biological processes of LCSCs remains poorly understood. Here enhanced glycolytic metabolism, lactate accumulation, and elevated levels of lactylation are observed in LCSCs compared to HCC cells. H3K56la was found to be closely associated with tumourigenesis and stemness of LCSCs. Notably, a comprehensive examination of the lactylome and proteome of LCSCs and HCC cells identified the ALDOA K230/322 lactylation, which plays a critical role in promoting the stemness of LCSCs. Furthermore, this study demonstrated the tight binding between aldolase A (ALDOA) and dead box deconjugate enzyme 17 (DDX17), which is attenuated by ALDOA lactylation, ultimately enhancing the regulatory function of DDX17 in maintaining the stemness of LCSCs. This investigation highlights the significance of Kla in modulating the stemness of LCSCs and its impact on the progression of HCC. Targeting lactylation in LCSCs may offer a promising therapeutic approach for treating HCC.

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A malignant tumor is a frequent and common disease that severely threatens human health. Many mechanisms, such as cell signaling pathway, anti-apoptosis mechanism, cell stemness, metabolism, and cell phenotype, have been studied to explain the reasons for chemotherapy, radioresistance, and tumor recurrences in antitumor treatment. Cancer stem cells (CSCs) are important tumor cell subclasses that can potentially organize and regulate stem cell properties. Growing evidence suggests that CSCs can initiate tumors and constitute a significant factor in metastasis, recurrence, and treatment resistance. The inability to completely target and remove CSCs is a considerable obstacle in tumor treatment. Therefore, drugs and therapeutic strategies that can effectively intervene with CSCs are essential for the treatment of different tumor types. However, the current strategies and efficacy of targeted elimination of CSCs are very limited. Oxidative stress has been recognized to play a crucial role in cancer pathophysiology. Moreover, reactive oxygen species (ROS) production and imbalance of the built-in cellular antioxidant defense system are hallmarks of tumor and cancer etiology. The current paper will focus on the regulation and mechanism behind oxidative stress in tumors and cancer stem cells and its tumor therapy applications. Additionally, the article discusses the role of CSCs in causing tumor treatment resistance and recurrence based on a redox perspective. The study also emphasizes that targeted modulation of oxidative stress in CSCs has great potential in tumor therapy, providing novel prospects for tumor therapy.

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Cancer is the second leading cause of elevated mortality worldwide. Thus, the development of drugs and treatments is needed to enhance the survival rate of the cancer-affected population. Recently, gut microbiota research in the healthy development of the human body has garnered widespread attention. Many reports indicate that changes in the gut microbiota are strongly associated with chronic inflammation-related diseases, including colitis, liver disease, and cancer within the intestine and the extraintestinal tract. Different gut bacteria are vital in the occurrence and development of tumors within the gut and extraintestinal tract. The human gut microbiome has significant implications for human physiology, including metabolism, nutrient absorption, and immune function. Moreover, diet and lifestyle habits are involved in the evolution of the human microbiome throughout the lifetime of the host and are involved in drug metabolism. Probiotics are a functional food with a protective role in cancer development in animal models. Probiotics alter the gut microbiota in the host; thus, beneficial bacterial activity is stimulated, and detrimental activity is inhibited. Clinical applications have revealed that some probiotic strains could reduce the occurrence of postoperative inflammation among cancer patients. An association network was constructed by analyzing the previous literature to explore the role of probiotics from the anti-tumor perspective. Therefore, it provides direction and insights for research on tumor treatment.

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Schisantherin A (STA) is a traditional Chinese medicine extracted from the plant Schisandra chinensis, which has a wide range of anti-inflammatory, antioxidant, and other pharmacological effects. This study investigates the anti-hepatocellular carcinoma effects of STA and the underlying mechanisms. STA significantly inhibits the proliferation and migration of Hep3B and HCCLM3 cells in vitro in a concentration-dependent manner. RNA-sequencing showed that 77 genes are upregulated and 136 genes are downregulated in STA-treated cells compared with untreated cells. KEGG pathway analysis showed significant enrichment in galactose metabolism as well as in fructose and mannose metabolism. Further gas chromatography-mass spectrometric analysis (GC-MS) confirmed this, indicating that STA significantly inhibits the glucose metabolism pathway of Hep3B cells. Tumor xenograft in nude mice showed that STA has a significant inhibitory effect on tumor growth in vivo. In conclusion, our results indicate that STA can inhibit cell proliferation by regulating glucose metabolism, with subsequent anti-tumor effects, and has the potential to be a candidate drug for the treatment of liver cancer.

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Keloids are fibroproliferative skin disorder caused by abnormal healing of injured or irritated skin and are characterized by excessive extracellular matrix (ECM) synthesis and deposition, which results in excessive collagen disorders and calcinosis, increasing the remodeling and stiffness of keloid matrix. The pathogenesis of keloid is very complex, and may include changes in cell function, genetics, inflammation, and other factors. In this review, we aim to discuss the role of biomechanical factors in keloid formation. Mechanical stimulation can lead to excessive proliferation of wound fibroblasts, deposition of ECM, secretion of more pro-fibrosis factors, and continuous increase of keloid matrix stiffness. Matrix mechanics resulting from increased matrix stiffness further activates the fibrotic phenotype of keloid fibroblasts, thus forming a loop that continuously invades the surrounding normal tissue. In this process, mechanical force is one of the initial factors of keloid formation, and matrix mechanics leads to further keloid development. Next, we summarized the mechanotransduction pathways involved in the formation of keloids, such as TGF-ß/Smad signaling pathway, integrin signaling pathway, YAP/TAZ signaling pathway, and calcium ion pathway. Finally, some potential biomechanics-based therapeutic concepts and strategies are described in detail. Taken together, these findings underscore the importance of biomechanical factors in the formation and progression of keloids and highlight their regulatory value. These findings may help facilitate the development of pharmacological interventions that can ultimately prevent and reduce keloid formation and progression.

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Cancer stem cells drive tumor initiation, progression, and recurrence, which compromise the effectiveness of anti-tumor drugs. Here, we report that demethylzeylasteral (DML), a triterpene anti-tumor compound, suppressed tumorigenesis of liver cancer stem cells (LCSCs) by interfering with lactylation of a metabolic stress-related histone. Using RNA sequencing (RNA-seq) and gas chromatography-mass spectrometric (GC-MS) analysis, we showed that the glycolysis metabolic pathway contributed to the anti-tumor effects of DML, and then focused on lactate downstream regulation as the molecular target. Mechanistically, DML opposed the progress of hepatocellular carcinoma (HCC), which was efficiently facilitated by the increase in H3 histone lactylation. Two histone modification sites: H3K9la and H3K56la, which were found to promote tumorigenesis, were inhibited by DML. In addition, we used a nude mouse tumor xenograft model to confirm that the anti-liver cancer effects of DML are mediated by regulating H3 lactylation in vivo. Our findings demonstrate that DML suppresses the tumorigenicity induced by LCSCs by inhibiting H3 histone lactylation, thus implicating DML as a potential candidate for the supplementary treatment of hepatocellular carcinoma.

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Diosmetin (DSM), a newly discovered natural flavonoid, found in citrus plants and olive leaves, has been reported to inhibit the progression of cancer when used as a food supplement. This study aimed to investigate DSM's anti-hepatocellular carcinoma (HCC) properties and possible molecular mechanisms. Hep3B and HCCLM3 cells were selected to evaluate the anti-HCC properties of DSM in vitro. RNA sequencing (RNA-seq) was used to identify the possible molecular targets and pathways. Gas chromatography-mass spectrometry (GC-MS) was used to evaluate the effect of DSM treatment on the primary metabolites of HCCLM3 cells. Tumor xenograft was performed in nude mice to examine the anti-HCC properties of DSM in vivo. The results showed that DSM inhibited the proliferation and migration of HCC cells in vitro in a dose-dependent manner. RNA-seq identified 4459 differentially expressed genes (DEGs) that were highly enriched in the cell cycle pathway. In addition, DSM regulated cell growth by arresting the cell cycle in the G1 phase by decreasing the expression of BCL2, CDK1, and CCND1. Furthermore, metabolomics analysis revealed that DSM interfered with the lipid metabolism pathway of HCC cells by significantly inhibiting the synthesis of metabolites, such as acetic acid, decanoic acid, glycerol, and L-proline. Subcutaneous tumor formation experiments revealed that DSM significantly reduced the tumor volume and weight when compared to the control. Immunohistochemical analysis further revealed that DSM treatment significantly decreased the expression of the proliferative marker KI67. Our findings demonstrated that DSM exhibited antitumor effects on HCC cells by inhibiting cell proliferation via cell cycle arrest and interfering with lipid metabolism.

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Cepharanthine (CEP), a natural compound extracted from Stephania cepharantha Hayata, has been found to have the potential to treat a variety of tumors in recent years. This study aims to evaluate the anti-hepatocellular carcinoma (HCC) effect of CEP and determine its in-depth mechanism. In this study, Hep3B and HCCLM3 cells were selected to evaluate the antitumor effects of CEP in vitro, whereas tumor xenograft in nude mice was performed to make in vivo anti-tumor assessment. RNA-sequence (RNA-seq) was used to identify possible molecular targets and pathways. Further, gas chromatography mass spectrometry (GC-MS) was performed to assess the differential metabolites involved in mediating the effect of CEP on the HCC cell line. Our results showed that CEP treatment resulted in the dose-dependent inhibition of cell viability, migration, and proliferation and could also induce apoptosis in HCC cells. RNA-seq following CEP treatment identified 168 differentially expressed genes (DEGs), which were highly enriched in metabolism-associated pathways. In addition, CEP down-regulated many metabolites through the amino acid metabolism pathway. In vivo experiment showed that CEP significantly suppressed tumor growth. Our results indicate that CEP has significant antitumor effects and has the potential to be a candidate drug for HCC treatment.

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This study aimed to determine whether hesperetin (HPT) has chondroprotective effects against the TNF-α-induced inflammatory response of chondrocytes and related mechanisms and clarify the impact of HPT on osteoarthritis (OA) induced by anterior cruciate ligament transection (ACLT). Under tumor necrosis factor-α (TNF-α) stimulation, rat chondrocytes were treated with or without HPT. The CCK-8 assay was used to detect viability and cytotoxicity. RT-qPCR and Western blot were used to examine the expression of aggrecan, collagen type II, and inflammatory and proliferative genes/proteins in chondrocytes. Flow cytometry was used to check the cell cycle to determine whether HPT protects chondrocytes against the inhibitory effect of TNF-α on chondrocyte proliferation. In addition, RNA sequencing was used to discover possible molecular targets and pathways and then validate these pathways with specific protein phosphorylation levels. Finally, immunofluorescence staining was used to examine the phosphorylation of the AMP-activated protein kinase (AMPK) pathway. The results showed that HPT restored the upregulation of interleukin 1ß (IL-1ß), PTGS2, and MMP-13 induced by TNF-α. In addition, HPT reversed the degradation of the extracellular matrix of chondrocytes induced by TNF-α. HPT also reversed the inhibitory effect of TNF-α on chondrocyte proliferation. RNA sequencing revealed 549 differentially expressed genes (DEGs), of which 105 were upregulated and 444 were downregulated, suggesting the potential importance of the AMPK pathway. Progressive analysis showed that HPT mediated the repair of TNF-α-induced chondrocyte damage through the AMPK signaling pathway. Thus, local treatment of HPT can improve OA induced by ACLT. These findings indicated that HPT has significant protective and anti-inflammatory effects on chondrocytes through the AMPK signaling pathway, effectively preventing cartilage degradation. Given the various beneficial effects of HPT, it can be used as a potential natural drug to treat OA.

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Visnagin is a furanochromone and one of the main compounds of Ammi visnaga L. that had been used to treat nephrolithiasis in Ancient Egypt. Nowadays, visnagin was widely used to treat angina pectoris, urolithiasis and hypertriglyceridemia. The potential mechanisms of visnagin involved in inflammation and cardiovascular disease were also identified. But the protective effect of visnagin on myocardial ischemia/reperfusion injury has not been confirmed. Our aim was, for the first time, to investigate the potential protective effect of visnagin on cardiac function after myocardial ischemia-reperfusion injury in a rat model, and to identify its underlying mechanism involving the inhibition of apoptosis and induction of autophagy. Thirty SD rats were randomly divided into sham group, ischemia/reperfusion group (IR), ischemia/reperfusion with visnagin (IR + visnagin) group. Myocardial ischemia/Reperfusion injury model was established. Hemodynamic measurements and echocardiography were used to analyze cardiac function, TUNEL staining and caspase activity, LC3 dots were detected with immunofluorescence staining, LC3 expression was evaluated by western blot analysis, transmission electron microscopy (TEM) was used to detect autophagosomes. Compared with the sham group and visnagin group, the cardiac dysfunction, LC3II, autophagy flow in the IR+ visnagin group increased significantly (P<0.01), but the activity of caspase-3 and caspase-9 and the apoptotic in the IR + visnagin group decreased significantly (P<0.01). In conclusion, visnagin may play a protective role in ischemia/reperfusion injury by inducing autophagy and reducing apoptosis.

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AIMS: Intervertebral disc degeneration (IVDD) has been regarded as the main cause of low back pain, which affects 80% of adults and still lack effective treatment. In IVDD, nucleus pulposus (NP) cell apoptosis has widely existed. Lysyl oxidase (LOX) has been demonstrated to protect chondrocyte against apoptosis in the TNF-α-treated human chondrocytes. Therefore, in this study, we investigated the anti-apoptosis effect of LOX on TNF-α-treated rat NP cells. MAIN METHODS: Real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and western blot analyses were used to detect the expression of LOX in TNF-α-treated rat NP cells. Then, the toxicity of exogenous LOX and its protective effect was evaluated by Cell Counting kit-8 (CCK-8). NP cell apoptosis was evaluated by flow cytometry analysis and TUNEL assay. The regulatory effects of LOX on the expression of extracellular matrix (ECM) molecules in TNF-α-treated rat NP cells were measured by RT-qPCR, western blot, and ELISA analyses. The molecular mechanism of LOX in regulating NP cell apoptosis was investigated by RT-qPCR and western blot analyses. KEY FINDINGS: The expression of LOX in TNF-α-treated rat NP cells was significantly decreased. Exogenous LOX preserved the cell viability, reduced the rate of apoptosis and improved the ECM secretion in TNF-α-treated rat NP cells. Further molecular mechanism investigation showed that LOX inhibited the Fas/FasL and p53 pathways. SIGNIFICANCES: LOX played an anti-apoptotic role in TNF-α-treated rat NP cells which could be a promising reagent in IVDD treatment.

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Tumor protein p53-binding protein 2 (TP53BP2), a member of the apoptosis-stimulating protein of p53 (ASPP) family, has previously been reported to be associated with tumor development. However, to the best of our knowledge, the role of TP53BP2 in neuroblastoma has not been elucidated. The aim of the present study was to investigate the function of TP53BP2 in the proliferation and autophagy of neuroblastoma. An expression vector that expresses TP53BP2-specific short hairpin RNA (shTP53BP2) was used for the experimental group and green fluorescent protein short hairpin RNA was used as a control. Cell proliferation was measured using MTT assays, self-renewal was evaluated using soft agar assays, light chain 3 (LC3) II expression level was examined by western blot and immunofluorescence analysis, and the autophagy-related 3 homolog (ATG3), autophagy-related 5 homolog (ATG5) and autophagy-related 9 homolog (ATG7) expression levels were examined using the reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A genomics analysis revealed that TP53BP2 expression was associated with the survival of patients with neuroblastoma. Western blot and RT-qPCR assays indicated that TP53BP2 could be implicated in neuroblastoma, as the proliferative ability of the experimental group decreased compared with that of the control group (P<0.001) and the expression levels of genes associated with autophagy, including LC3 II. ATG3, ATG5 and ATG7, increased in the experimental group. In conclusion, an increased expression of TP53BP2 in patients with neuroblastoma may be associated with poor survival and shTP53BP2 may decrease the proliferative abilities of neuroblastoma cells, including BE(2)C and SK-N-DZ cell lines. In addition, the LC3 II, ATG3, ATG5 and ATG7 expression levels increased and were associated with increased rates of autophagy following upregulation of TP53BP2.

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Growth differentiation factor 11 (GDF11), also known as bone morphogenetic protein 11, a member of the transforming growth factor-ß superfamily, has been reported to be involved in colorectal cancer. However, the roles of GDF11 in Chinese patients with liver cancer and the underlying mechanisms have remained elusive. The present study assessed the expression of GDF11 in 10 paired samples of cancerous and normal tissues from Chinese liver cancer patients. The results indicated that the expression of GDF11 was significantly lower in cancerous tissues than in normal tissues. In vitro, the expression of GDF11 was reduced in a panel of liver cancer cell lines compared with that in a normal liver cell line at the mRNA and protein level. Treatment with GDF11 reduced the viability of HepG2 for up to 72 h and GDF11 treatment reduced the viability of SMMC-7721 after 48 and 72 h. Furthermore, GDF11 activated Smad2/3 signaling in HepG2 cells. In conclusion, GDF11 has a tumor suppressor role in liver cancer, exerts its effects through Smad2/3 signaling and may serve as a novel tumor marker in liver cancer diagnosis.

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Growth differentiation factor (GDF11) is a member of TGF-ß/BMP superfamily that activates Smad and non-Smad signaling pathways and regulates expression of its target nuclear genes. Since its discovery in 1999, studies have shown the involvement of GDF11 in normal physiological processes, such as embryonic development and erythropoiesis, as well as in the pathophysiology of aging, cardiovascular disease, diabetes mellitus, and cancer. In addition, there are contradictory reports regarding the role of GDF11 in aging, cardiovascular disease, diabetes mellitus, osteogenesis, skeletal muscle development, and neurogenesis. In this review, we describe the GDF11 signaling pathway and its potential role in development, physiology and disease.

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This study investigates whether platelet-rich plasma (PRP) is an activator of tendon-derived stem cells (TDSCs) to promote regeneration of Achilles tendon post-rupture in rats. In the in vitro study, PRGF (activated PRP) significantly enhanced cell DNA synthesis, improved viability and promoted proliferation, while facilitating cell migration and the recruitment of TDSCs. In addition, TDSCs were mixed with collagen and PRP to form collagen-TDSC constructs (CTC) and PRP-collagen-TDSC constructs (PCTCs). After 3 weeks of culture in vitro, we found that most of the encapsulated TDSCs in the CTCs and PCTCs were still alive, while cells in the PCTCs showed a more aligned arrangement compared to the CTCs. In addition, the micro-structure of PCTC showed more obvious fibre-like tissues and formed a cyclic microvascular structure. The tenocyte-related genes types I and III collagen, Tenascin-C and Scleraxis of TDSCs in the PCTCs and CTCs were upregulated with time, and PCTCs showed more significance than CTCs (p < 0.05). After in vivo transplantation, the CTCs and PCTCs showed stimulatory effects on Achilles tendon healing. Moreover, the PCTCs improved the macroscopic appearance, histological morphology and biomechanical strength of ruptured Achilles tendon better than CTC. These results indicate that PRP can activate TDSCs to improve the quality of Achilles tendon rupture healing in the early stages. Copyright © 2015 John Wiley & Sons, Ltd.

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Synovial inflammation plays an important role in the pathogenesis and progress of osteoarthritis (OA). There is an urgent need to find safe and effective drugs that can reduce the inflammation and regulate the pathogenesis of cytokines of the OA disease. Here, we investigated the effect of icariin, the major pharmacological active component of herb Epimedium on human osteoarthritis fibroblast-like synoviocytes (OA-FLSs). The OA-FLSs were isolated from patients with osteoarthritis and cultured in vitro with different concentrations of icariin. Then, cell viability, proliferation, and migration were investigated; MMP14, GRP78, and IL-1ß gene expression levels were detected via qRT-PCR. Icariin showed low cytotoxicity to OA-FLSs at a concentration of under 10 µM and decreased the proliferation of the cells at concentrations of 1 and 10 µM. Icariin inhibited cell migration with concentrations ranging from 0.1 to 1 µM. Also, the expression of three cytokines for the pathogenesis of OA which include IL-1ß, MMP14 and GRP78 was decreased by the various concentrations of icariin. These preliminary results imply that icariin might be an effective compound for the treatment of OA disease.

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Wound healing scaffolds provide cells with structural integrity and can also deliver biological agents to establish a skin tissue-specific microenvironment to regulate cell functions and to accelerate the healing process. In this study, we fabricated biodegradable nanofibrous scaffolds with an emulsion electrospinning technique. The scaffolds were composed of polycaprolactone, hyaluronan and encapsulating epidermal growth factor. The morphology and core-sheath structure of the nanofibers were characterized by scanning electron microscopy and transmission electron microscopy. The scaffolds were also characterized for chemical composition and hydrophilicity with a Fourier-transform infrared analysis, energy dispersive spectroscopy and the water contact angle. An in vitro model protein bovine serum albumin and epidermal growth factor release study was conducted to evaluate the sustained release potential of the core-sheath structured nanofibers with and without the hyaluronan component. Additionally, an in vitro cultivation of human skin keratinocytes (HaCaT) and fibroblasts on polycaprolactone/hyaluronan and polycaprolactone/hyaluronan-epidermal growth factor scaffolds showed a significant synergistic effect of hyaluronan and epidermal growth factor on cell proliferation and infiltration. Furthermore, there was an up-regulation of the wound-healing-related genes collagen I, collagen III and TGF-ß in polycaprolactone/hyaluronan/epidermal growth factor scaffolds compared with control groups. In the full-thickness wound model, the enhanced regeneration of fully functional skin was facilitated by epidermal regeneration in the polycaprolactone/hyaluronan/epidermal growth factor treatment group. Our findings suggest that bioactivity and hemostasis of the hyaluronan-based nanofibrous scaffolds have the capability to encapsulate and control the release of growth factors that can serve as skin tissue engineering scaffolds for wound healing.

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Comparative therapeutic significance of tendon-derived stem cells (TDSCs) and bone marrow mesenchymal stem cells (BMSCs) transplantation to treat ruptured Achilles tendon was studied. Three groups of SD rats comprising 24 rats each, designated as TDSCs and BMSCs, and nontreated were studied for regenerative effects through morpho-histological evaluations and ultimate failure load. For possible mechanism in tendon repair/regeneration through TDSCs and BMSCs, we measured Collagen-I (Col-I), Col-III gene expression level by RT-PCR, and Tenascin-C expression via immunofluorescent assay. TDSCs showed higher agility in tendon healing with better appearance density and well-organized longitudinal fibrous structure, though BMSCs also showed positive effects. Initially the ultimate failure load was considerably higher in TDSCs than other two study groups during the weeks 1 and 2, but at week 4 it attained an average or healthy tendon strength of 30.2 N. Similar higher tendency in Col-I/III gene expression level during weeks 1, 2, and 4 was observed in TDSCs treated group with an upregulation of 1.5-fold and 1.1-fold than the other two study groups. Immunofluorescent assay revealed higher expression of Tenascin-C in TDSCs at week 1, while both TDSCs and BMSCs treated groups showed detectable CM-Dil-labelled cells at week 4. Compared with BMSCs, TDSCs showed higher regenerative potential while treating ruptured Achilles tendons in rats.

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Tendons and ligaments exhibit limited regenerative capacity following injury, with damaged tissue being replaced by a fibrotic scar. The physiological role of scar tissue is complex and has been studied extensively. In this study, we demonstrate that rat tendons contain a unique subpopulation of cells exhibiting stem cell characteristics, including clonogenicity, multipotency, and self-renewal capacity. Additionally, these putative stem cells expressed markers consistent with neural crest stem cells (NCSCs). Using immunofluorescent labeling, we identified P75(+) (p75 neurotrophin receptor) cells in the perivascular regions of the native rat tendon. Importantly, P75(+) cells were frequently localized near vascular cells and increased in number within the peritenon after injury. Ultrastructural analysis showed that perivascular cells detached from vessels in response to injury, migrated into the interstitial space, and deposited extracellular matrix. Characterization of P75(+) cells isolated from the scar tissue indicated that this population also expressed the NCSC markers, Vimentin, Sox10, and Snail. In conclusion, our results suggest that neural crest-like stem cells of perivascular origin reside within the rat peritenon and give rise to scar-forming stromal cells following tendon injury.

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