Our previous study showed that kainate (KA) receptor subunit GluR6 played an important role in ischemia-induced MLK3 and JNK activation and neuronal degeneration through the GluR6-PSD95-MLK3 signaling module. However, whether the KA receptors subunit GluR6 is involved in the activation of p38 MAP kinase during the transient brain ischemia/reperfusion (I/R) in the rat hippocampal CA1 subfield is still unknown. In this present study, we first evaluated the time-course of phospho-p38 MAP kinase at various time-points after 15 min of ischemia and then observed the effects of antagonist of KA receptor subunit GluR6, GluR6 antisence oligodeoxynucleotides on the phosphorylation of p38 MAP kinase induced by I/R. Results showed that inhibiting KA receptor GluR6 or suppressing the expression of KA receptor GluR6 could down-regulate the elevation of phospho-p38 MAP kinase induced by I/R. These drugs also reduced the phosphorylation of MLK3, MKK3/MKK6, MKK4, and MAPKAPK2. Additionally, our results indicated administration of three drugs, including p38 MAP kinase inhibitor before brain ischemia significantly decreased the number of TUNEL-positive cells detected at 3 days of reperfusion and increased the number of the surviving CA1 pyramidal cells at 5 days of reperfusion after 15 min of ischemia. Taken together, we suggest that GluR6-contained KA receptors can mediate p38 MAP kinase activation through a kinase cascade, including MLK3, MKK3/MKK6, and MKK4 and then induce increased phosphorylation of MAPKAPK-2 during ischemia injury and ultimately result in neuronal cell death in the rat hippocampal CA1 region.
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http://dx.doi.org/10.1002/hipo.20479 | DOI Listing |
Cell Biochem Biophys
December 2024
Biology Department, Université de Moncton, Moncton, NB, Canada.
Targeting more than one in nine men before age 70, prostate cancer is the most common type of cancer in men. The increased levels of cyclins, leading to activation of cyclin-dependent kinases (CDKs), play a critical role in the increased proliferation of prostate cancer cells. In this study, the regulation of the cyclin D1 (CCND1) promoter activity by activator protein-1 (AP-1) and SRY-related HMG-box (SOX) transcription factors has been characterized in PC3 prostate cancer cells.
View Article and Find Full Text PDFMar Drugs
November 2024
Research Institute of Basic Sciences, Incheon National University, Incheon 22012, Republic of Korea.
, a salt-tolerant plant, has demonstrated antioxidant effects, the ability to prevent prostate enlargement, antifungal properties, and skin moisturizing benefits. This study aimed to explore the anti-melanogenic potential of the 70% ethanol extract of (TME) along with its ethyl acetate (TME-EA) and water (TME-A) fractions. TME (10-200 µg/mL), TME-EA (1-15 µg/mL), and TME-A (100-1000 µg/mL) were prepared and applied to B16F10 cells with or without α-MSH for 72 h.
View Article and Find Full Text PDFCell Mol Life Sci
December 2024
National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, Nanchang, 330031, China.
Idiopathic pulmonary fibrosis (IPF) is a prevalent interstitial lung disease with high mortality. CD38 is a main enzyme for intracellular nicotinamide adenine dinucleotide (NAD) degradation in mammals. It has been reported that CD38 participated in pulmonary fibrosis through promoting alveolar epithelial cells senescence.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
December 2024
Department of Stomatology, Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, China.
Objectives: To investigate the mechanism of PHPS1 for promoting apoptosis of oral squamous cell carcinoma cells and the role of AMPK in regulating tumor angiogenesis under hypoxic conditions.
Methods: Human oral squamous cell carcinoma Ca9-22 cells cultured in hypoxic conditions (1% O) were inoculated subcutaneously in 16 nude mice, which were divided into control group and PHPS1 group (8) for treatment with 10% DMSO and 10% PHPS1 respectively. Tumor growth in the mice was monitored till 14 days after the treatment, and the xenografts were examined pathologically using HE staining.
J Cancer Res Clin Oncol
December 2024
Department of Respiratory Medicine, The Fuyang Affiliated Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Purpose: This study aims to investigate the biological roles and molecular mechanisms of Cathepsin G (CTSG) in the progression of non-small cell lung cancer (NSCLC).
Methods: Western blotting and immunohistochemistry analyses of clinical samples were performed to determine the expression levels of CTSG in patients with NSCLC. Bioinformatic analysis of clinical datasets was conducted to evaluate the correlation between CTSG and lymph node metastasis, tumor stage, and immune cell infiltration.
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