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  • Edaravone, a ROS scavenger, ameliorates photoreceptor cell death after experimental retinal detachment. 21310909

    Purpose. To investigate whether edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger is neuroprotective against photoreceptor cell death in a rat model of retinal detachment (RD). Methods. RD was induced in adult Brown Norway rats by subretinal injection of sodium hyaluronate. Edaravone (3 mg/kg, 5 mg/kg, 10 mg/kg) or physiologic saline were administered intraperitoneally once a day until sacrifice on day 3 or 5. Oxidative stress in the retina was assessed by 4-hydroxynonenal staining or ELISA for protein carbonyl content. Photoreceptor death was assessed by TUNEL and measurement of the outer nuclear layer thickness . Western blot analysis and caspase activity assays were performed. Inflammatory cytokine secretion and inflammatory cell infiltration were evaluated by ELISA and immunostaining, respectively. Results. RD resulted in increased generation of ROS. Treatment with 5 mg/kg edaravone significantly reduced ROS level along with decrease in TUNEL positive cells in the photoreceptor layer. Caspase assay also confirmed decreased activation of caspases -3,-,8, and -9 in RD treated with edaravone. The level of the anti-apoptotic Bcl-2 was increased in detached retinas after edaravone treatment, whereas the levels of the stress-activated p-ERK1/2 were decreased. Additionally, edaravone treatment resulted in a significant decrease in the levels of TNF-α, MCP-1 and macrophage infiltration. Conclusions. Oxidative stress plays an important role in the photoreceptor cell death after RD. Edaravone treatment may aid in preventing photoreceptor cell death following RD by suppressing ROS-induced photoreceptor damage.
    Document Type:
    Reference
    Product Catalog Number:
    APT173
    Product Catalog Name:
    Caspase 9 Colorimetric Activity Assay Kit, LEHD

  • Targeting the CaMKII/ERK Interaction in the Heart Prevents Cardiac Hypertrophy. 26110816

    Activation of Ca2+/Calmodulin protein kinase II (CaMKII) is an important step in signaling of cardiac hypertrophy. The molecular mechanisms by which CaMKII integrates with other pathways in the heart are incompletely understood. We hypothesize that CaMKII association with extracellular regulated kinase (ERK), promotes cardiac hypertrophy through ERK nuclear localization.In H9C2 cardiomyoblasts, the selective CaMKII peptide inhibitor AntCaNtide, its penetratin conjugated minimal inhibitory sequence analog tat-CN17β, and the MEK/ERK inhibitor UO126 all reduce phenylephrine (PE)-mediated ERK and CaMKII activation and their interaction. Moreover, AntCaNtide or tat-CN17β pretreatment prevented PE induced CaMKII and ERK nuclear accumulation in H9C2s and reduced the hypertrophy responses. To determine the role of CaMKII in cardiac hypertrophy in vivo, spontaneously hypertensive rats were subjected to intramyocardial injections of AntCaNtide or tat-CN17β. Left ventricular hypertrophy was evaluated weekly for 3 weeks by cardiac ultrasounds. We observed that the treatment with CaMKII inhibitors induced similar but significant reduction of cardiac size, left ventricular mass, and thickness of cardiac wall. The treatment with CaMKII inhibitors caused a significant reduction of CaMKII and ERK phosphorylation levels and their nuclear localization in the heart.These results indicate that CaMKII and ERK interact to promote activation in hypertrophy; the inhibition of CaMKII-ERK interaction offers a novel therapeutic approach to limit cardiac hypertrophy.
    Document Type:
    Reference
    Product Catalog Number:
    16-283

  • Orphan nuclear receptor PNR/NR2E3 stimulates p53 functions by enhancing p53 acetylation. 22025681

    Since inactivation of tumor suppressor p53 functions is one of the most common features of human cancer cells, restoring p53 expression and activity is an important focus in cancer therapy. Here we report identification of photoreceptor-specific nuclear receptor (PNR)/NR2E3 as a positive regulator of p53 in a high-throughput genetic screen. In HeLa cells, PNR stimulated p53-responsive promoters in a p53-dependent fashion and induced apoptosis in several cell types. PNR also increased p53 protein stability and specific activity as a transcriptional activator. Our studies of the underlying mechanisms showed that PNR forms complexes with p53 and the acetyltransferase p300, stimulates p53 acetylation, and increases the expression of a subset of p53 target genes. Furthermore, PNR significantly boosted actinomycin D-stimulated p53 acetylation. The unique mechanisms by which PNR stimulates p53 acetylation and functions define this orphan nuclear receptor as a potentially valuable target and tool in p53-associated cancer therapy and offer new insights into the roles of PNR mutation in retinal diseases.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Anti-acetyl-p53 (Lys320) -2739273

    Document Type:
    Certificate of Analysis
    Lot Number:
    2739273
    Product Catalog Number:
    06-1283
    Product Catalog Name:
    Anti-acetyl-p53 (Lys320) Antibody

  • Anti-acetyl-p53 (Lys320) - 4070124

    Document Type:
    Certificate of Analysis
    Lot Number:
    4070124
    Product Catalog Number:
    06-1283
    Product Catalog Name:
    Anti-acetyl-p53 (Lys320) Antibody

  • Anti-acetyl-p53 (Lys320) - 3772443

    Document Type:
    Certificate of Analysis
    Lot Number:
    3772443
    Product Catalog Number:
    06-1283
    Product Catalog Name:
    Anti-acetyl-p53 (Lys320) Antibody