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Endogenous stem cell-based in-situ tissue regeneration has recently gained considerable attention. In this study, we investigated the potential of a chemokine, SDF-1-mimic peptide (SMP), to promote endogenous stem cell-based in-situ wound healing. Our approach involved the development of a click crosslinked hyaluronic acid scaffold loaded with SMP (Cx-HA + SMP) to release SMP in a wound site. The Cx-HA scaffold maintained its structural integrity throughout the wound healing process and also captured endogenous stem cells. Gradual SMP release from the Cx-HA + SMP scaffold established a concentration gradient at the wound site. In animal wound experiments, Cx-HA + SMP exhibited faster wound contraction compared to Cx-HA + SDF-1. Additionally, Cx-HA + SMP resulted in approximately 1.2-1.6 times higher collagen formation compared to Cx-HA + SDF-1. SMP released from the Cx-HA + SMP scaffold promoted endogenous stem cell migration to the wound site 1.5 times more effectively than Cx-HA + SDF-1. Moreover, compared to Cx-HA + SDF-1, Cx-HA + SMP exhibited higher expression of CXCR4 and CD31, as well as the positive markers CD29 and CD44 for endogenous stem cells. The endogenous stem cells that migrated through Cx-HA + SMP regenerated into wound skin with minimal scar granule formation, similar to the normal tissue. In conclusion, SMP peptide offers greater convenience, while efficiently attracting migrating endogenous stem cells compared to the SDF protein. Our findings suggest that Cx-HA + SMP scaffolds hold promise as a strategy to enhance endogenous stem cell-based in-situ wound healing.
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http://dx.doi.org/10.1016/j.jconrel.2023.10.047 | DOI Listing |
Elife
September 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.
Innate immune cells can acquire a memory phenotype, termed trained immunity, but the mechanism underlying the regulation of trained immunity remains largely elusive. Here, we demonstrate that inhibition of Aurora kinase A (AurA) dampens trained immunity induced by β-glucan. ATAC-seq and RNA-seq analysis reveal that AurA inhibition restricts chromatin accessibility of genes associated with inflammatory pathways such as JAK-STAT, TNF, and NF-κB pathways.
View Article and Find Full Text PDFMol Ther Methods Clin Dev
September 2025
Molecular Biology Interdepartmental Program, University of California, Los Angeles, Los Angeles, CA 90095, USA.
X-linked agammaglobulinemia (XLA) is a rare inborn error of immunity caused by loss-of-function mutations in the gene encoding Bruton's tyrosine kinase (BTK). XLA patients lack mature B cells and have negligible antibody levels, leaving them susceptible to recurrent bacterial and chronic viral infections. Autologous hematopoietic stem cell gene therapy with gene-corrected HSC may serve as a promising treatment of XLA; this therapy would provide a one-time cure and would replace lifelong immunoglobulin replacement therapy.
View Article and Find Full Text PDFResearch (Wash D C)
September 2025
Department of Neurosurgery, Southwest Hospital, Third Military Medical University (Army Medical University), 400038 Chongqing, China.
Ischemic stroke (IS), a common neurological disease, lacks satisfactory treatments worldwide. Neural stem cell (NSC) therapy is a promising strategy for stroke, while microenvironmental disturbance, including but not limited to acidosis, oxidative stress, and excessive neuroinflammation, restricts the therapeutic potential of endogenous and exogenous NSC post-IS. The present study introduces the effect of common disturbance on NSC and the underlying mechanism to screen out feasible methods aiming to potentiate the reparative capacity of NSC following IS.
View Article and Find Full Text PDFExp Cell Res
September 2025
State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu City 610041, China. Electronic address:
Adipose-derived mesenchymal stem cells (ADSCs) hold great promise for bone tissue repair and regeneration. Circular RNAs (circRNAs) play a crucial role in regulating the osteogenic differentiation and bone remodeling of ADSCs; however, the underlying molecular mechanisms remain unclear. In this study, we conducted whole transcriptome sequencing (WTS) on ADSCs and constructed a competing endogenous RNA (ceRNA) regulatory network to identify the circTTC3/miR-205/mothers against decapentaplegic homolog 3 (Smad3) signaling axis.
View Article and Find Full Text PDFBiochem Biophys Res Commun
September 2025
CERVO Brain Research Centre, Quebec City, QC, Canada; Department of Medicine, Faculty of Medicine, Université Laval, Quebec City, QC, Canada. Electronic address:
Brugada syndrome is a rare inherited cardiac arrhythmia disorder primarily characterized by ventricular fibrillation, which can lead to sudden cardiac death. It follows an autosomal dominant pattern of inheritance and is most associated with dysfunction of the cardiac sodium channel Nav1.5.
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