Search results for: Histone Demethylase Fluorescent Detection Kit
#29286083 2017/12/29 To Up
KDM3A inhibition attenuates high concentration insulin‑induced vascular smooth muscle cell injury by suppressing MAPK/NF‑κB pathways.
Previous studies have indicated that lysine (K)‑specific demethylase 3A (KDM3A) is associated with diverse diabetes‑associated cardiovascular complications in response to high glucose levels. However, the effects of KDM3A on the pathological progression of cardiovascular injuries in response to high insulin levels remain unknown. The present study aimed to explore whether KDM3A knockdown may attenuate high insulin‑induced vascular smooth muscle cell (VSMC) dysfunction, and to further investigate the underlying mechanisms. Primary VSMCs were isolated from the thoracic aorta of Sprague‑Dawley rats. Lentiviral vectors encoding control‑small interfering (si)RNA or KDM3A‑siRNA were transduced into VSMCs for 72 h, and cells were subsequently incubated in medium containing 100 nM insulin for a further 5 days. Cellular proli-feration, migration and apoptosis were measured by Cell Counting kit‑8, Transwell chamber assay and flow cytometry, respectively. Reactive oxygen species (ROS) were detected using the dihydroethidium fluorescent probe. The mRNA expression levels of interleukin‑6 and monocyte chemotactic protein‑1 were measured by reverse transcription‑quantitative polymerase chain reaction. Furthermore, the protein expression levels of KDM3A, mitogen‑activated protein kinases (MAPKs), nuclear factor (NF)‑κB/p65, B‑cell lymphoma 2 (Bcl‑2)‑associated X protein and Bcl‑2 were evaluated by west-ern blotting. Lentivirus transduction with KDM3A‑siRNA markedly reduced the elevated expression of KDM3A induced by high insulin stimulation in VSMCs. In addition, inhibition of KDM3A significantly ameliorated insulin‑induced VSMC proliferation and migration, which was accompanied by decreased ROS levels, cell apoptosis and inflammatory cytokine levels. Furthermore, KDM3A gene silencing mitigated phosphorylation of MAPKs and NF‑κB/p65 activation. In conclusion, KDM3A inhibition may exert numerous protective effects on high insulin‑stimulated VSMCs, and the underlying mechanisms may be partly associated with inactivation of MAPK/NF‑κB signaling pathways.Bo-Fang Zhang, Hong Jiang, Jing Chen, Xin Guo, Qi Hu, Shuo Yang
1617 related Products with: KDM3A inhibition attenuates high concentration insulin‑induced vascular smooth muscle cell injury by suppressing MAPK/NF‑κB pathways.
400 ug100ul96 assaysOne 96-Well Microplate Ki2 Pieces/Box 6 ml Ready-to-use 100ul96tests100ul1 ml96 assaysRelated Pathways
#27914215 2016/12/03 To Up
Lysine-Specific Demethylase 1 (LSD1) Inhibitor S2101 Induces Autophagy via the AKT/mTOR Pathway in SKOV3 Ovarian Cancer Cells.
BACKGROUND S2101 is one of the most potent LSD1 inhibitors, which can inhibit ovarian cancer cells viability. This study aimed to detect the mechanism behind the anticancer properties of S2101 in SKOV3 ovarian cells. MATERIAL AND METHODS Cell viability was tested by Cell Counting Kit-8 (CCK-8) assay. Cellular apoptosis and autophagy were evaluated by flow cytometric analysis using Annexin-V/PI staining methods and Green fluorescent protein (GFP)-fused-LC3 (GFP-LC3), respectively. Western blotting was performed for analyzing the Bax, Bcl-2, mTOR, p- mTOR, p62, LC3-I, LC3-II, AKT, and p-AKT protein expression. RESULTS Our results show that the proportion of early apoptotic and late apoptotic cells increased significantly for cells treated with S2101 at a concentration of 100 μM for 48 h. Treatment of S2101 in SKOV3 cells resulted in upregulation of Bax and downregulation of Bcl-2 in a time-dependent manner, indicating that S2101 can induce apoptosis in SKOV3. There was a downward trend in the expression of p62 when the SKOV3cells were treated with 100 µm S2101 for 12 h, 24 h and 48 h. The conversion of LC3-I to LC3-II was increased significantly at 24 h and 48 h. Autophagy was induced by S2101 in SKOV3 cells, evidenced by an increase in punctuate localization of GFP-LC3 and a change in expression of autophagy-related proteins. CONCLUSIONS S2101 treatment decreased the levels of phosphorylated AKT and mTOR. S2101 inhibits SKOV3 cells viability and induces apoptosis and autophagy. The AKT/mTOR signaling pathway was found to be affected by S2101.Shujun Feng, Ye Jin, Mengjiao Cui, Jianhua Zheng
1979 related Products with: Lysine-Specific Demethylase 1 (LSD1) Inhibitor S2101 Induces Autophagy via the AKT/mTOR Pathway in SKOV3 Ovarian Cancer Cells.
2 Pieces/Box10mg2 Pieces/Box10mg11 inhibitors10mg10mg5mg1 mg10mg 100ulRelated Pathways
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