https://www.selleckchem.com/products/c646.html Moreover, miR-200b-3p overexpression and α-Klotho knockdown reversed the SNHG29 overexpression-induced inhibitory effects on calcified VSMCs. Our study is the first to demonstrate that SNHG29 could inhibit VSMC calcification by downregulating miR-200b-3p to activate the α-Klotho/FGFR1/FGF23 axis, suggesting SNHG29 as a novel therapeutic target for VC-associated diseases. Our study is the first to demonstrate that SNHG29 could inhibit VSMC calcification by downregulating miR-200b-3p to activate the α-Klotho/FGFR1/FGF23 axis, suggesting SNHG29 as a novel therapeutic target for VC-associated diseases.Expression of cytokines/chemokines is tightly regulated at the transcription level. This is crucial in the central nervous system to maintain neuroimmune homeostasis. IL-8 a chemoattractant, which recruits neutrophils, T cells, and basophils into the brain in response to inflammation and/or injury is secreted predominantly by neurons, microglia, and astrocytes. Here, we investigated the mechanism by which astrocytes regulate IL-8 expression. We demonstrate that while β-catenin negatively regulated IL-8 transcription, its canonical transcriptional partners, members of the TCF/LEF transcription factors (TCF1, TCF3, TCF4 and LEF1) and Activating transcription factor 2 (ATF2) positively regulated IL-8 transcription. We further identified a putative TCF/LEF binding site at -175nt close to the minimal transcription region on the IL-8 promoter, mutation of which caused a significant reduction in IL-8 promoter activity. Chromatin immunoprecipitation demonstrated binding of TCF1, TCF4, LEF1 and ATF2 on the IL-8 promoter suggesting that TCFs/LEF partner with ATF2 to induce IL-8 transcription. These findings demonstrate a novel role for β-catenin in suppression of IL-8 expression and for TCFs/LEF/ATF2 in inducing IL-8. These findings reveal a unique mechanism by which astrocytes tightly regulate IL-8 expression.Ischemic injury is a major