Ontology highlight
ABSTRACT:
PROVIDER: PRJNA504454 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR10117800_1.fastq.gz | Fastqsanger.gz | |||
| SRR10117800_2.fastq.gz | Fastqsanger.gz | |||
| SRR10117801_1.fastq.gz | Fastqsanger.gz | |||
| SRR10117801_2.fastq.gz | Fastqsanger.gz |
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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
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.
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Project description:Febrile seizures (FS) are the most common type of seizures in young children. Complex FS are a risk factor for mesial temporal lobe epilepsy (mTLE). Twin studies and mutations in families with complex epilepsy syndromes including FS, indicate a genetic contribution to FS susceptibility. By employing a phenotype driven genetic strategy using consomics we mapped a quantitative trait locus (QTL) for hyperthermia-induced FS susceptibility on mouse chromosome 1. Signal Recognition Particle 9 (Srp9) in the QTL was differentially expressed between parental strains, and its binding partner Srp14 was co-identified as a strong candidate gene in another FS susceptibility QTL. The SRP complex plays a key role in the synthesis of membrane proteins, such as glutamate receptors. In vivo knock-down of brain Srp9 or inhibition of protein synthesis reduced FS susceptibility. The mouse strain (CSS1) with reduced Srp9 expression and FS susceptibility, exhibited reduced hippocampal AMPA and NMDA currents. Down-regulation of Srp9 in hippocampal neurons reduced surface expression of AMPA receptor subunit GluA1. Consistent with a role of SRP9 in human FS, we detected increased hippocampal SRP9 expression in mTLE patients with antecedent FS. Comparing mTLE patients and healthy controls we found an association of a SRP9 promoter SNP (rs12403575 G/A) with FS and mTLE, which was replicated in FS patients. Our findings identify SRP9 as a novel FS susceptibility gene and implicate ER-dependent protein synthesis and glutamate receptor expression in the mechanism.
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