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Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder [dataset 1]

ABSTRACT: Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder [dataset 1]

PROVIDER: PRJNA997890 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25396164_1.fastq.gz	Fastqsanger.gz
	SRR25396164_2.fastq.gz	Fastqsanger.gz
	SRR25396165_1.fastq.gz	Fastqsanger.gz
	SRR25396165_2.fastq.gz	Fastqsanger.gz
	SRR25396166_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder [dataset 2]

Project description:Frozen shoulder (FS) is characterized by pain and limited range of motion (ROM). Inflammation and fibrosis are accepted as main pathologic processes associated with the development of FS. However, the intrinsic mechanisms underlying pathologic fibrosis remain unclear. We aimed to elucidate the key molecules involved in pathologic fibrosis and explore new therapeutic targets for FS. Synovial fibroblasts isolated from patient biopsies were identified using immunofluorescence. Western blotting, RT-qPCR, cell adhesion tests, and would-healing assays were used to evaluate the fibrosis-related functions of synovial fibroblasts. Elevated cluster of differentiation 36 (CD36) expression was detected in FS using western blotting and immunohistochemistry. Salvianolic acid b (SaB) inhibited CD36, blocking synovial fibroblast-induced inflammation and fibrosis. Our RNA-seq data showed that knocking down CD36 dramatically impaired the capacity of synovial fibroblasts for cell adhesion and that the PI3K-Akt signaling pathway may be crucial to the fibrotic process of FS. By up-regulating CD36 and inhibiting the phosphorylation of Akt, we demonstrated that CD36 promotes pathologic fibrosis by activating the PI3k-Akt pathway. Finally, rats treated with SaB had improved ROM and less collagen fiber deposition than the FS model group. Conclusions: SaB attenuates inflammation and inhibited the CD36-mediated activation of the PI3K-Akt signaling pathway to block pathologic fibrosis of FS in in vitro and in vivo models.

2023-07-24 | GSE238053 | GEO

Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder [dataset 1]

2023-07-24 | GSE238052 | GEO

Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder.

Project description:Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder.

| PRJNA997826 | ENA

Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder [dataset 2]

Project description:Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder [dataset 2]

| PRJNA997891 | ENA

MicrRNA-26a deficiency attenuates the severity of frozen shoulder in a mouse immobilization model

Project description:The main pathogenesis of the frozen shoulder is thought to be the inflammation of the intra-articular synovium and subsequent fibrosis of the shoulder joint capsule. However, the molecular pathogenesis of the frozen shoulder is still unknown. A class of non-coding RNAs, microRNAs (miRNAs) contribute to various diseases including musculoskeletal diseases. MicroRNA-26a (miR-26a) has been reported to be associated with fibrosis in several organs. This study aims to reveal the role of miR-26a on fibrosis in the shoulder capsule using a frozen shoulder model in miR-26a deficient (miR-26a KO) mice. MiR-26 KO and wild type (WT) mice were investigated using a frozen shoulder model. The range of motion of the shoulder, histopathological analysis such as synovitis, and fibrosis related-genes expression in the model mice were evaluated to determine the role of miR-26a. In WT mice, both inflammatory cell infiltration and thickening of the inferior shoulder joint capsule were observed after 1 week of immobilization, and this thickening further progressed over the subsequent 6 weeks. However, the immobilized shoulder in miR-26a KO mice consistently exhibited significantly better range of motion compared with WT mice at each point, and histological changes were notably less severe. The expression of inflammation- and fibrosis-related genes was decreased in the miR-26a KO mice compared with WT mice at 1 and 6 weeks. Together, miR-26a deficiency attenuated the severity of frozen shoulder in the immobilization model mouse. The present study suggests that miR-26a has the potential to be a target miRNA for therapeutic approach to frozen shoulder.

2024-09-01 | GSE256308 | GEO

A single cell atlas of frozen shoulder capsule identifies features associated with inflammatory fibrosis resolution

Project description:Single cell transcriptomic data of shoulder capsule from foetal, adult comparator (normal) and frozen shoulder (disease).

2023-10-02 | E-MTAB-12304 | biostudies-arrayexpress

A single cell atlas of frozen shoulder capsule identifies features associated with inflammatory fibrosis resolution (Bulk RNA-seq of capsular fibroblasts co-cultured with MDMs)

Project description:Bulk transcriptomic data of shoulder capsule fibroblasts isolated from frozen shoulder co-cultured with Dexamethasone (DEX) or LPS treated monocyte-derived macrophages (MDM), which were isolated from blood cones and stimulated with M-CSF, for 72 hours. The stimulated MDMs have been characterised as MerTKhigh(DEX) and MerTKlow(LPS). Unstimulated, DEX and LPS stimulated MDM were co-cultured with ex vivo shoulder capsule-derived fibroblasts from patients with frozen shoulder. Fibroblasts were then FACS isolated and RNA-sequencing analysis performed. As an additional control ex vivo fibroblasts were also profiled without co-culture (stimulation=”none”).

2023-10-02 | E-MTAB-12312 | biostudies-arrayexpress

Tuina reverses capsule fibrosis in Frozen Shoulder as indicated via phosphoproteomics

Project description:Frozen shoulder (FS) is a common disorder often treated with Tuina, but the mechanisms involved remain unclear. We employed proteomics to investigate the mechanisms associated with the treatment of capsule fibrosis in FS rats. We used a method composed of three weeks of cast immobilization to establish a model of FS. We then administered Tuina once daily for 14 days, identified differentially expressed proteins (DEPs) using phosphoproteomics. Then we used bioinformatics methods to study the mechanism of tuina therapy

2024-01-09 | PXD047468 | Pride

Tuina reverses capsule fibrosis in Frozen Shoulder as indicated via protemocis

Project description:Frozen shoulder (FS) is a common disorder often treated with Tuina, but the mechanisms involved remain unclear. We employed proteomics to investigate the mechanisms associated with the treatment of capsule fibrosis in FS rats. We used a method composed of three weeks of cast immobilization to establish a model of FS. We then administered Tuina once daily for 14 days, identified differentially expressed proteins (DEPs) using proteomics. Then we used bioinformatics methods to study the mechanism of tuina therapy

2024-01-09 | PXD047467 | Pride

Salvianolic acid B attenuates inflammation and prevent pathologic fibrosis by inhibiting CD36-mediated activation of the PI3K-Akt signaling pathway in frozen shoulder

Project description:Frozen shoulder (FS) is characterized by pain and limited range of motion (ROM). Inflammation and fibrosis are accepted as main pathologic processes associated with the development of FS. However, the intrinsic mechanisms underlying pathologic fibrosis remain unclear. We aimed to elucidate the key molecules involved in pathologic fibrosis and explore new therapeutic targets for FS. Synovial fibroblasts isolated from patient biopsies were identified using immunofluorescence. Western blotting, RT-qPCR, cell adhesion tests, and would-healing assays were used to evaluate the fibrosis-related functions of synovial fibroblasts. Elevated cluster of differentiation 36 (CD36) expression was detected in FS using Western blotting and immunohistochemistry. Salvianolic acid b (SaB) inhibited CD36, blocking synovial fibroblast-induced inflammation and fibrosis. Our RNA-seq data showed that knocking down CD36 dramatically impaired the capacity of synovial fibroblasts for cell adhesion and that the PI3K-Akt signaling pathway may be crucial to the fibrotic process of FS. By up-regulating CD36 and inhibiting the phosphorylation of Akt, we demonstrated that CD36 promotes pathologic fibrosis by activating the PI3k-Akt pathway. Finally, rats treated with SaB had improved ROM and less collagen fiber deposition than the FS model group. Conclusion: SaB attenuates inflammation and inhibited the CD36-mediated activation of the PI3K-Akt signaling pathway to block pathologic fibrosis of FS in vitro and in vivo models.

| S-EPMC10427508 | biostudies-literature

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