Peptide Regulation of Chondrogenic Stem Cell Differentiation

Linkova, N. S.; Khavinson, Vladimir; Diatlova, A S; Myakisheva, S. N.; Ryzhak, G A

doi:10.3390/ijms24098415

Cited by 5 publications

(3 citation statements)

References 67 publications

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“…Each stage of chondrogenic differentiation of MSCs is controlled by different transcription factors (TF). TF regulates the gene expression level, and these cartilage-related indexes change dynamically during the whole process [ 44 , 45 ]. In addition, we studied by intervening gene expression, but the influence of genes on cartilage differentiation showed different trends at different time points, and there may be no obvious difference at some time points.…”

Section: Resultsmentioning

confidence: 99%

LncRNA SNHG1 enhances cartilage regeneration by modulating chondrogenic differentiation and angiogenesis potentials of JBMMSCs via mitochondrial function regulation

Liu,

Yang

et al. 2024

Stem Cell Res Ther

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Background Cartilage is a kind of avascular tissue, and it is difficult to repair itself when it is damaged. In this study, we investigated the regulation of chondrogenic differentiation and vascular formation in human jaw bone marrow mesenchymal stem cells (h-JBMMSCs) by the long-chain noncoding RNA small nucleolar RNA host gene 1 (SNHG1) during cartilage tissue regeneration. Methods JBMMSCs were isolated from the jaws via the adherent method. The effects of lncRNA SNHG1 on the chondrogenic differentiation of JBMMSCs in vitro were detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), Pellet experiment, Alcian blue staining, Masson’s trichrome staining, and modified Sirius red staining. RT-qPCR, matrix gel tube formation, and coculture experiments were used to determine the effect of lncRNA SNHG1 on the angiogenesis in JBMMSCs in vitro. A model of knee cartilage defects in New Zealand rabbits and a model of subcutaneous matrix rubber suppositories in nude mice were constructed for in vivo experiments. Changes in mitochondrial function were detected via RT-qPCR, dihydroethidium (DHE) staining, MitoSOX staining, tetramethyl rhodamine methyl ester (TMRM) staining, and adenosine triphosphate (ATP) detection. Western blotting was used to detect the phosphorylation level of signal transducer and activator of transcription 3 (STAT3). Results Alcian blue staining, Masson’s trichrome staining, and modified Sirius Red staining showed that lncRNA SNHG1 promoted chondrogenic differentiation. The lncRNA SNHG1 promoted angiogenesis in vitro and the formation of microvessels in vivo. The lncRNA SNHG1 promoted the repair and regeneration of rabbit knee cartilage tissue. Western blot and alcian blue staining showed that the JAK inhibitor reduced the increase of STAT3 phosphorylation level and staining deepening caused by SNHG1. Mitochondrial correlation analysis revealed that the lncRNA SNHG1 led to a decrease in reactive oxygen species (ROS) levels, an increase in mitochondrial membrane potential and an increase in ATP levels. Alcian blue staining showed that the ROS inhibitor significantly alleviated the decrease in blue fluorescence caused by SNHG1 knockdown. Conclusions The lncRNA SNHG1 promotes chondrogenic differentiation and angiogenesis of JBMMSCs. The lncRNA SNHG1 regulates the phosphorylation of STAT3, reduces the level of ROS, regulates mitochondrial energy metabolism, and ultimately promotes cartilage regeneration.

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Section: Resultsmentioning

confidence: 99%

LncRNA SNHG1 enhances cartilage regeneration by modulating chondrogenic differentiation and angiogenesis potentials of JBMMSCs via mitochondrial function regulation

Liu,

Yang

et al. 2024

Stem Cell Res Ther

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“…Peptides have a wide range of applications in medicine, drug delivery, and tissue engineering. − These include, among others, peptides as antimicrobial, anticancer, and cell penetrating agents, as vaccines and biosensors, as self-assembly agents to form hierarchical multiscale structures, and as interference peptides in precision medicine. − Recently, peptides based on the recognition sites of morphogenetic proteins have received attention as an alternative to protein therapy in tissue engineering to guide differentiation and maturation of transplanted cells to the desired lineage to reduce side effects like immunogenic response and tumorigenicity. − However, peptides derived from morphogenetic and other proteins have orders of magnitude lower biological activity. , This lower activity is attributed to misfolding in the absence of other protein sequences (conformational differences between the peptide as a part of the protein versus a free molecule), which further causes peptide aggregation and micelle formation . Furthermore, natural peptides are susceptible to degradation by proteolytic enzymes and their function is limited by short half-life in physiological medium .…”

Section: Introductionmentioning

confidence: 99%

A Structure Independent Molecular Fragment Interfuse Model for Mesoscale Dissipative Particle Dynamics Simulation of Peptides

Dash,

Jabbari

2024

ACS Omega

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There is a need to develop robust computational models for mesoscale simulation of the structure of peptides over large length scales toward the discovery of novel peptides for medical applications to address the issues of peptide aggregation, enzymatic degradation, and short half-life. The primary objective was to predict the structure and conformation of peptides whose native structures are not known. This work presents a new model for computation of interaction parameters between the beads in coarse-grained dissipative particle dynamics (DPD) simulation that is properly calibrated for amino acids, supports compressibility requirement of water molecules, and accounts for subtle differences in the structure of amino acids and the charge in the side chain of charged amino acids. This new model is referred to as Structure Independent Molecular Fragment Interfuse Model, abbreviated as SIMFIM, because it accounts for specific interactions between different beads, which represent molecular fragments of the amino acids, in calculating nonbonded interaction parameters in the absence of knowing the actual peptide structure. The electrostatic interactions are incorporated in this model by using a normal distribution of charges around the center of the beads to prevent the collapse of oppositely charged soft beads. The uniquely parameterized DPD force field in the SIMFIM model is optimized for a given peptide with respect to the degree of coarse-grained graining for simulating the peptide over long times and length scales. The SIMFIM model was tested in this work using four peptides, namely, TrpZip2, Rubrivinodin, Lihuanodin, and IC3-CB1/Gai peptides, whose structures were sourced from the Protein Data Bank. The SIMFIM model predicted radius of gyration (R g ) values for the peptides closer to the actual structures as compared to the conventional model, and there was less deviation between the predicted and actual structures of the peptides.

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“… 6 , 7 Stem cell-based therapies hold promise for treating TMJOA and regenerating full-thickness cartilage defects in the TMJ. 8 , 9 …”

Section: Introductionmentioning

confidence: 99%

Delivery of dental pulp stem cells by an injectable ROS-responsive hydrogel promotes temporomandibular joint cartilage repair via enhancing anti-apoptosis and regulating microenvironment

Ma,

Li,

Wei

et al. 2024

J Tissue Eng

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Temporomandibular joint (TMJ) cartilage repair poses a considerable clinical challenge, and tissue engineering has emerged as a promising solution. In this study, we developed an injectable reactive oxygen species (ROS)-responsive multifunctional hydrogel (RDGel) to encapsulate dental pulp stem cells (DPSCs/RDGel in short) for the targeted repair of condylar cartilage defect. The DPSCs/RDGel composite exhibited a synergistic effect in the elimination of TMJ OA (osteoarthritis) inflammation via the interaction between the hydrogel component and the DPSCs. We first demonstrated the applicability and biocompatibility of RDGel. RDGel encapsulation could enhance the anti-apoptotic ability of DPSCs by inhibiting P38/P53 mitochondrial apoptotic signal in vitro. We also proved that the utilization of DPSCs/RDGel composite effectively enhanced the expression of TMJOA cartilage matrix and promoted subchondral bone structure in vivo. Subsequently, we observed the synergistic improvement of DPSCs/RDGel composite on the oxidative stress microenvironment of TMJOA and its regulation and promotion of M2 polarization, thereby confirmed that M2 macrophages further promoted the condylar cartilage repair of DPSCs. This is the first time application of DPSCs/RDGel composite for the targeted repair of TMJOA condylar cartilage defects, presenting a novel and promising avenue for cell-based therapy.

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Peptide Regulation of Chondrogenic Stem Cell Differentiation

Cited by 5 publications

References 67 publications

LncRNA SNHG1 enhances cartilage regeneration by modulating chondrogenic differentiation and angiogenesis potentials of JBMMSCs via mitochondrial function regulation

LncRNA SNHG1 enhances cartilage regeneration by modulating chondrogenic differentiation and angiogenesis potentials of JBMMSCs via mitochondrial function regulation

A Structure Independent Molecular Fragment Interfuse Model for Mesoscale Dissipative Particle Dynamics Simulation of Peptides

Delivery of dental pulp stem cells by an injectable ROS-responsive hydrogel promotes temporomandibular joint cartilage repair via enhancing anti-apoptosis and regulating microenvironment

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