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Articular Fibrocartilage-Targeted Therapy by Microtubule Stabilization

ABSTRACT: Articular Fibrocartilage-Targeted Therapy by Microtubule Stabilization

PROVIDER: PRJNA853927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19895072_1.fastq.gz	Fastqsanger.gz
	SRR19895072_2.fastq.gz	Fastqsanger.gz
	SRR19895073_1.fastq.gz	Fastqsanger.gz
	SRR19895073_2.fastq.gz	Fastqsanger.gz
	SRR19895074_1.fastq.gz	Fastqsanger.gz

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Articular Fibrocartilage-Targeted Therapy by Microtubule Stabilization

Project description:To investigate the fibrotic effect on BMSCs by CTGF and TGFβ1 treatment, and the anti-fibrotic effect of docetaxel on fibrotic chondrocytes. We established BMSCs primary culture and treated CTGF and TGFβ1, then treated by docetaxel.

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Articular fibrocartilage-targeted therapy by microtubule stabilization.

Project description:The fibrocartilage presented on the joint surface was caused by cartilage injury or degeneration. There is still a lack of effective strategies for fibrocartilage. Here, we hypothesized that the fibrocartilage could be viewed as a raw material for the renewal of hyaline cartilage and proposed a previously unidentified strategy of cartilage regeneration, namely, "fibrocartilage hyalinization." Cytoskeleton remodeling plays a vital role in modifying the cellular phenotype. We identified that microtubule stabilization by docetaxel repressed cartilage fibrosis and increased the hyaline cartilage extracellular matrix. We further designed a fibrocartilage-targeted negatively charged thermosensitive hydrogel for the sustained delivery of docetaxel, which promoted fibrocartilage hyalinization in the cartilage defect model. Moreover, the mechanism of fibrocartilage hyalinization by microtubule stabilization was verified as the inhibition of Sparc (secreted protein acidic and rich in cysteine). Together, our study suggested that articular fibrocartilage-targeted therapy in situ was a promising strategy for hyaline cartilage repair.

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Insulin Induces Microtubule Stabilization and Regulates the Microtubule Plus-End Tracking Protein Network in Adipocytes

Project description:Insulin-stimulated glucose uptake is known to involve microtubules, although the function of microtubules and the microtubule-regulating proteins involved in insulin action are poorly understood. CLASP2, a plus-end tracking microtubule-associated protein (+TIP) that controls microtubule dynamics, was recently implicated as the first +TIP associated with insulin-regulated glucose uptake. Here, using protein-specific targeted quantitative phosphoproteomics within 3T3-L1 adipocytes, we discovered that insulin regulates phosphorylation of the CLASP2 network members G2L1, MARK2, CLIP2, AGAP3 and CKAP5 as well as EB1, revealing the existence of a previously unknown microtubule-associated protein system that responds to insulin. To further investigate, G2L1 interactome studies within 3T3-L1 adipocytes revealed that G2L1 co-immunoprecipitates CLASP2 and CLIP2 as well as the master integrators of +TIP assembly, the end binding (EB) proteins. Live-cell total internal reflection fluorescence microscopy in adipocytes revealed G2L1 and CLASP2 colocalize on microtubule plus-ends. We found that while insulin increases the number of CLASP2-containing plus-ends, insulin treatment simultaneously decreases CLASP2-containing plus-end velocity. In addition, we discovered that insulin stimulates re-distribution of CLASP2 and G2L1 from exclusive plus-end tracking to “trailing” behind the growing tip of the microtubule. Insulin treatment increases -tubulin Lysine 40 acetylation, a mechanism that was observed to be regulated by a counterbalance between GSK3 and mTOR, and also led to microtubule stabilization. Our studies introduce insulin-stimulated microtubule stabilization and plus-end trailing of +TIPs as new modes of insulin action and reveal the likelihood that a network of microtubule-associated proteins synergize to coordinate insulin-regulated microtubule dynamics.

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Stabilization of Heterochromatin by CLOCK Counteracts hMSC Senescence and Articular Degeneration

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