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Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126 [CNP53]

ABSTRACT: Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126 [CNP53]

PROVIDER: PRJNA448589 | ENA |

REPOSITORIES: ENA

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Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126 [U0126]

Project description:Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126 [U0126]

| PRJNA448590 | ENA

Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126

Project description:Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126

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Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126 [U0126]

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Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126 [CNP53]

Project description:To investigate the similarity of gene expression profile of CNP53 and U0126 treatment in growth plate.

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Gene expression profiles of rat hypertrophic zone after treatment of CNP53 or U0126

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2018-04-04 | GSE112639 | GEO

Transcription profiling of Bos taurus hypertrophic growth plate chondrocytes vs. reserve zone chondrocytes

Project description:Growth plate chondrocytes were isolated from the distal metacarpus of young dairy cattle (all under 10 mo of age), the chondrocytes were released from the extracellular matrix by digestion with Collagenase P for 4 hours, and the various zones of the growth plate were separated by density centrifugation. The least-dense Hypertrophic Zone (HZ) cells were compared to the most-dense Reserve Zone (RZ) cells. 6 pairs of HZ vs RZ were compared by microarray. Experiment Overall Design: Growth plate chondrocytes were isolated from the distal metacarpus of young dairy cattle (all under 10 mo of age), the chondrocytes were released from the extracellular matrix by digestion with Collagenase P for 4 hours, and the various zones of the growth plate were separated by density centrifugation. The least-dense Hypertrophic Zone (HZ) cells were compared to the most-dense Reserve Zone (RZ) cells. Six independent sample pairs of HZ vs RZ were compared by microarray.

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mRNA-seq analysis of hypertrophic zone of wild type (WT) and Adamts17-/- growth plates

Project description:We compared gene expression profiles of hypertrophic zone of WT and Adamts17-/- growth plates through laser microdissection (LMD) using adhesive tape, linear amplification of mRNA, and mRNA-seq analysis.

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Nonwoven-based gelatin/polycaprolactone membrane loaded with ERK inhibitor U0126 for treatment of tendon defects

Project description:Background: Tendon is a major component of musculoskeletal system connecting the muscles to the bone. Tendon injuries are very common orthopedics problems leading to impeded motion. Up to now, there still lacks effective treatments for tendon diseases. Methods: Tendon stem/progenitor cells (TSPCs) were isolated from the patellar tendons of SD rats. The expression levels of genes were evaluated by quantitative RT-PCR. Immunohistochemistry staining was performed to confirm the presence of tendon markers in tendon tissues. Bioinformatics analysis of data acquired by RNA-seq was used to find out the differentially expressed genes. Rat patellar tendon injury model was used to evaluate the effect of U0126 on tendon injury healing. Biomechanical testing was applied to evaluate the mechanical properties of newly formed tendon tissues. Results: In this study, we have shown that ERK inhibitor U0126 rather PD98059 could effectively increase the expression of tendon-related genes and promote the tenogenesis of TSPCs in vitro. To explore the underlying mechanisms, RNA sequencing was performed to identify the molecular difference between U0126-treated and control TSPCs. The result showed that GDF6 was significantly increased by U0126, which is an important factor of the TGFβ superfamily regulating tendon development and tenogenesis. In addition, NBM (nonwoven-based gelatin/polycaprolactone membrane) which mimics the native microenvironment of the tendon tissue was used as an acellular scaffold to carry U0126. The results demonstrated that when NBM was used in combination with U0126, tendon healing was significantly promoted with better histological staining outcomes and mechanical properties. Conclusion: Taken together, we have found U0126 promoted tenogenesis in TSPCs through activating GDF6, and NBM loaded with U0126 significantly promoted tendon defect healing, which provides a new treatment for tendon injury.

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