Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MicroRNA let-7i is up-regulated in T cells from patients with Ankylosing Spondylitis (AS). In this study, we investigated the role of let-7i in T cells survival. Our results demonstrated down-regulation of insulin-like growth factor-1 receptor (IGF1R) in T cells from patients with AS. Luciferase reporter assay suggested IGF1R as direct target of let-7i. Overexpression of let-7i in Jurkat cells significantly suppressed IGF1R expression, which mimicked the action of IGF1R siRNA. IGF1R inhibition led to a strinking decrease in phosphorylation of mTOR and Akt, down-regulation of Bcl-2, up-regulation of Bax and cleavage of caspase 3 and PARP. Meanwhile, IGF1R inhibition induced autophagy. Autophagy induced by let-7i overexpression contributed to protect cells from apoptosis. Our data indicated that let-7i might control T cells fates in AS by targeting IGF1R.
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PMID:MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R. 2530 90

The development of ankylosing spondylitis (AS) occurs due to excessive proliferation of fibroblasts. Polydatin, a monomeric compound isolated from a traditional Chinese medicine Polygonum cuspidatum, exhibits anti-inflammatory and anti-arthritic effects. However, the mechanisms underlying the regulatory effects of polydatin on the proliferation, apoptosis and autophagy of fibroblasts obtained from patients with AS remain unclear. The aim of this study was to investigate the therapeutic effects of polydatin on symptoms associated with AS. Multiple cellular and molecular biology experiments were performed in the present study, such as cell viability assay, Western blotting, flow cytometry, monodansylcadaverine (MDC) staining and immunofluorescence assays. In the present study, the results revealed that polydatin induced the apoptosis of fibroblasts isolated from patients with AS by upregulating the expression of active caspase-3 and Bax, and downregulating the expression of Bcl-2. Meanwhile, polydatin was revealed to enhance the autophagy of fibroblasts by increasing the expression levels of LC3II, Beclin 1 and Atg5. The results of MDC and immunofluorescence assays further demonstrated that polydatin significantly induced the formation of autophagosomes in fibroblasts. Furthermore, polydatin-induced apoptosis and autophagy were markedly inhibited following treatment with the autophagy inhibitor, 3-methyladenine (3-MA). In conclusion, the results of the present study indicated that polydatin induces the apoptosis and autophagy of fibroblasts obtained from patients suffering from AS, and that polydatin may represent a therapeutic agent for the future treatment of patients with AS.
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PMID:Polydatin Regulates the Apoptosis and Autophagy of Fibroblasts Obtained from Patients with Ankylosing Spondylitis. 3033 77