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Active, phosphorylation-dependent MAP kinases, MAPK/ERK, SAPK/JNK and p38, and specific transcription factor substrates are differentially expressed following systemic administration of kainic acid to the adult rat.
Acta Neuropathol 2002; 103(4):391-407AN

Abstract

Excitotoxicity is considered a major cell death inductor in neurodegeneration. Yet the mechanisms involved in cell death and cell survival following excitotoxic insults are poorly understood. Expression of active, phosphorylation-dependent mitogen-activated extracellular signal-regulated kinases (MAPK/ERKs), stress-activated c-Jun N-terminal kinases (SAPK/JNKs) and p38 kinases, as well as their putative active, phosphorylation-dependent specific transcriptional factor substrates CREB, Elk-1, ATF-2, c-Myc and c-Jun, has been examined following systemic administration of kainic acid (KA) at convulsant doses to rats. Increased phosphorylated MAPK (MAPK(P)) immunoreactivity has been found at 3 and 6 h in the vulnerable regions entorhinal cortex and CA3, in which neurons are committed to die, as well as in sensitive regions dentate gyrus and gyrus cinguli, in which neurons will survive. JNK(P) has been observed in the entorhinal cortex and dentate gyrus, and p38(P) immunoreactivity occurs in the entorhinal cortex. Strong c-Myc(P) expression parallels MAPK(P) immunoreactivity in the entorhinal cortex, CA3, dentate gyrus and gyrus cinguli, showing that enhanced c-Myc(P) expression does not preclude cell death or cell survival. Selective decrease of CREB(P) immunoreactivity in entorhinal cortex and CA3 indicates CREB(P) reduction associated with cell death. Strong c-Jun(P) immunoreactivity has been found in the entorhinal cortex, CA3 and dentate gyrus, thus suggesting that regulation of two opposing cellular programs (cell death or cell survival) of c-Jun(P) depends on c-Jun interactions with other factors. Interestingly, ATF-2(P), and to a lesser extent Elk-1(P), is selectively increased in the dentate gyrus. These results suggest ATF-2(P) involvement in cell survival of dentate gyrus granule cells. The present results demonstrate activation of specific MAPK pathways in association with either cell death or cell survival triggered by KA. Furthermore, increased Ras activation, as seen with p21 Ras activation assay, indicates a crucial role for Ras in activating MAP kinases following excitotoxic insult.

Authors+Show Affiliations

Departament de Biologia Cel.lular i Anatomia Patològica, Hospital Princeps d'Espanya, Universitat de Barcelona, Campus de Bellvitge, Hospitalet de Llobregat, Spain. iferrer@sakma.esNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11904760

Citation

Ferrer, I, et al. "Active, Phosphorylation-dependent MAP Kinases, MAPK/ERK, SAPK/JNK and P38, and Specific Transcription Factor Substrates Are Differentially Expressed Following Systemic Administration of Kainic Acid to the Adult Rat." Acta Neuropathologica, vol. 103, no. 4, 2002, pp. 391-407.
Ferrer I, Blanco R, Carmona M, et al. Active, phosphorylation-dependent MAP kinases, MAPK/ERK, SAPK/JNK and p38, and specific transcription factor substrates are differentially expressed following systemic administration of kainic acid to the adult rat. Acta Neuropathol. 2002;103(4):391-407.
Ferrer, I., Blanco, R., Carmona, M., Puig, B., Domínguez, I., & Viñals, F. (2002). Active, phosphorylation-dependent MAP kinases, MAPK/ERK, SAPK/JNK and p38, and specific transcription factor substrates are differentially expressed following systemic administration of kainic acid to the adult rat. Acta Neuropathologica, 103(4), pp. 391-407.
Ferrer I, et al. Active, Phosphorylation-dependent MAP Kinases, MAPK/ERK, SAPK/JNK and P38, and Specific Transcription Factor Substrates Are Differentially Expressed Following Systemic Administration of Kainic Acid to the Adult Rat. Acta Neuropathol. 2002;103(4):391-407. PubMed PMID: 11904760.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Active, phosphorylation-dependent MAP kinases, MAPK/ERK, SAPK/JNK and p38, and specific transcription factor substrates are differentially expressed following systemic administration of kainic acid to the adult rat. AU - Ferrer,I, AU - Blanco,R, AU - Carmona,M, AU - Puig,B, AU - Domínguez,I, AU - Viñals,F, Y1 - 2002/01/31/ PY - 2001/07/02/received PY - 2001/09/18/accepted PY - 2002/3/21/pubmed PY - 2002/5/8/medline PY - 2002/3/21/entrez SP - 391 EP - 407 JF - Acta neuropathologica JO - Acta Neuropathol. VL - 103 IS - 4 N2 - Excitotoxicity is considered a major cell death inductor in neurodegeneration. Yet the mechanisms involved in cell death and cell survival following excitotoxic insults are poorly understood. Expression of active, phosphorylation-dependent mitogen-activated extracellular signal-regulated kinases (MAPK/ERKs), stress-activated c-Jun N-terminal kinases (SAPK/JNKs) and p38 kinases, as well as their putative active, phosphorylation-dependent specific transcriptional factor substrates CREB, Elk-1, ATF-2, c-Myc and c-Jun, has been examined following systemic administration of kainic acid (KA) at convulsant doses to rats. Increased phosphorylated MAPK (MAPK(P)) immunoreactivity has been found at 3 and 6 h in the vulnerable regions entorhinal cortex and CA3, in which neurons are committed to die, as well as in sensitive regions dentate gyrus and gyrus cinguli, in which neurons will survive. JNK(P) has been observed in the entorhinal cortex and dentate gyrus, and p38(P) immunoreactivity occurs in the entorhinal cortex. Strong c-Myc(P) expression parallels MAPK(P) immunoreactivity in the entorhinal cortex, CA3, dentate gyrus and gyrus cinguli, showing that enhanced c-Myc(P) expression does not preclude cell death or cell survival. Selective decrease of CREB(P) immunoreactivity in entorhinal cortex and CA3 indicates CREB(P) reduction associated with cell death. Strong c-Jun(P) immunoreactivity has been found in the entorhinal cortex, CA3 and dentate gyrus, thus suggesting that regulation of two opposing cellular programs (cell death or cell survival) of c-Jun(P) depends on c-Jun interactions with other factors. Interestingly, ATF-2(P), and to a lesser extent Elk-1(P), is selectively increased in the dentate gyrus. These results suggest ATF-2(P) involvement in cell survival of dentate gyrus granule cells. The present results demonstrate activation of specific MAPK pathways in association with either cell death or cell survival triggered by KA. Furthermore, increased Ras activation, as seen with p21 Ras activation assay, indicates a crucial role for Ras in activating MAP kinases following excitotoxic insult. SN - 0001-6322 UR - https://www.unboundmedicine.com/medline/citation/11904760/Active_phosphorylation_dependent_MAP_kinases_MAPK/ERK_SAPK/JNK_and_p38_and_specific_transcription_factor_substrates_are_differentially_expressed_following_systemic_administration_of_kainic_acid_to_the_adult_rat_ L2 - https://dx.doi.org/10.1007/s00401-001-0481-9 DB - PRIME DP - Unbound Medicine ER -