✦ LIBER ✦

Kainate-induced apoptosis correlates with c-Jun activation in cultured cerebellar granule cells

✍ Scribed by N.S. Cheung; F.Y. Carroll; J.A. Larm; P.M. Beart; S.F. Giardina

Publisher: John Wiley and Sons
Year: 1998
Tongue: English
Weight: 897 KB
Volume: 52
Category: Article
ISSN: 0360-4012
DOI: 10.1002/(sici)1097-4547(19980401)52:1<69::aid-jnr7>3.0.co;2-i

No coin nor oath required. For personal study only.

✦ Synopsis

We have investigated the involvement of c-Jun in cell death induced by exposure of primary cultures of murine cerebellar granule cells to the glutamate receptor agonist kainate (KA) and evaluated its possible use as a marker for apoptosis. Using cerebellar granule cell neurones from postnatal day 7 mice, we found that 1 hr exposure to KA (1-1000 M) induced a concentration-dependent neuronal cell death with characteristic apoptotic morphology, including cell shrinkage, neurite blebbing and DNA fragmentation. In addition KA-induced a concentration-dependent expression of c-Jun mRNA and protein as determined by in situ hybridization and immunocytochemistry respectively. DNA fragmentation was detected using terminal transferase-mediated nick-end (TUNEL) labelling and agarose gel electrophoresis. KA-induced cell death was significantly attenuated by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 50 M), which shifted the concentration-response curve significantly rightward. The number of apoptotic cell bodies, determined by TUNEL, was also reduced by CNQX (50 M), with only 15-20% of neurones staining positive after exposure to 1mM KA. In addition, the number of positively stained cells for c-Jun protein and mRNA was substantially reduced by CNQX (50 M) as determined by random and representative cell counts. These results show for the first time that KA induced apoptotic neuronal death in cultured murine cerebellar granule cells involves the induction of c-Jun mRNA and protein, suggesting the involvement of this immediate early gene in excitotoxic receptor-mediated apoptosis and its potential use as a marker for apoptotic cell death.

📜 SIMILAR VOLUMES

Inhibition of nuclear factor-κB activati

Inhibition of nuclear factor-κB activation induces apoptosis in cerebellar granule cells

✍ Patrizia Piccioli; Carola Porcile; Sabrina Stanzione; Michela Bisaglia; Adriana 📂 Article 📅 2001 🏛 John Wiley and Sons 🌐 English ⚖ 409 KB

## Abstract The nuclear factor (NF)‐κB family of transcription factors plays important roles in the regulation of many activities of neuronal cells, such as synaptic transmission, inflammation, neuroprotection, and neurotoxicity. In resting cells, NF‐κB activity is present both in the cytoplasm, as

Lactacystin, a specific inhibitor of the

Lactacystin, a specific inhibitor of the proteasome, induces apoptosis and activates caspase-3 in cultured cerebellar granule cells

✍ Laura A. Pasquini; Marcos Besio Moreno; Ana M. Adamo; Juana M. Pasquini; Eduardo 📂 Article 📅 2000 🏛 John Wiley and Sons 🌐 English ⚖ 483 KB 👁 2 views

The multicatalytic protease complex or proteasome is a fundamental nonlysosomal tool that the cell uses to process or degrade proteins at a fast rate through the ubiquitin and ATP-dependent proteolytic pathway. Examples of these important proteins include the tumor suppressor protein p53, various cy

Toki-Shakuyaku-San intervenes in apoptos

Toki-Shakuyaku-San intervenes in apoptosis induced by lowering of potassium chloride concentrations in cultured cerebellar granule cells

✍ Xiang-qian Zhang; Nobuyoshi Hagino 📂 Article 📅 1998 🏛 John Wiley and Sons 🌐 English ⚖ 972 KB

Cerebellar granular cells harvested from 8-day-old rats were cultured in a basic medium of Eagle's salt (BME) containing 10% serum and 25 mM KCl. At 7 days in vitro (DIV), the culture medium was switched to serum-free BME containing 5 mM KCl. Fluorescein diacetate/propidium iodide staining was used

Post-translational modification of spect

Post-translational modification of spectrin induced by excitatory amino acids in cultured cerebellar granule cells

✍ T. C. Petrucci; A. M. M. Di Stasi; M. Ceccarini; V. Gallo 📂 Article 📅 1991 🏛 Springer 🌐 English ⚖ 638 KB

Methylglyoxal induces apoptosis in Jurka

Methylglyoxal induces apoptosis in Jurkat leukemia T cells by activating c-Jun N-Terminal kinase

✍ Jun Du; Haruhiko Suzuki; Fumihiko Nagase; Anwarul A. Akhand; Toshihiro Yokoyama; 📂 Article 📅 2000 🏛 John Wiley and Sons 🌐 English ⚖ 227 KB 👁 2 views

Methylglyoxal (MG) is a physiological metabolite, but it is known to be toxic, inducing stress in cells and causing apoptosis. This study examines molecular mechanisms in the MG-induced signal transduction leading to apoptosis, focusing particularly on the role of JNK activation. We first confirmed

Apoptosis induced by chemotherapeutic ag

Apoptosis induced by chemotherapeutic agents involves c-Jun N-terminal kinase activation in sarcoma cell lines

✍ Takaaki Koyama; Takashi Mikami; Takashi Koyama; Atsuhiro Imakiire; Kengo Yamamot 📂 Article 📅 2006 🏛 Elsevier Science 🌐 English ⚖ 306 KB

## Abstract Molecular mechanisms underlying chemotherapeutic agent–induced apoptosis in sarcoma cells are not well known. Induction of apoptosis is regulated by several components including mitogen‐activated protein kinases (MAPKs) comprising ERK, p38MAPKs, and c‐Jun N‐terminal kinase (JNK). In the