PMID- 25319623 OWN - NLM STAT- MEDLINE DCOM- 20150618 LR - 20141016 IS - 1099-1352 (Electronic) IS - 0952-3499 (Linking) VI - 27 IP - 12 DP - 2014 Dec TI - ConBr, a lectin from Canavalia brasiliensis seeds, modulates signaling pathways and increases BDNF expression probably via a glycosylated target. PG - 746-54 LID - 10.1002/jmr.2401 [doi] AB - In the central nervous system, many receptors, ion channels and neurotransmitter transporters are glycoproteins, where the glycan chains are modulator elements. Lectins are proteins, which recognize and bind carbohydrate complexes. We have previously shown that ConBr, a lectin purified from Canavalia brasiliensis seeds, produced antidepressant-like effect and blocked hippocampal neurotoxicity induced by quinolinic acid and glutamate. Noteworthy, all these effects occurred in a dependence of its carbohydrate recognition domain. Therefore, the present study was undertaken in order to elucidate intracellular signaling pathways regulated by ConBr that may be potentially associated with the antidepressant and neuroprotective effects previously reported to be dependent on carbohydrate interaction. ConBr (10 microg/site) was injected into the ventricle (i.c.v.) of mice, and the hippocampi were removed 0.5, 1, 3, 6, 8, 12, 18, and 24 h after treatment. Our results showed that in the period of 0.5-3 h, ConBr induced activation of the protein kinases Akt, ERK1, and PKA. Furthermore, the phosphorylation of CREB-Ser133 was stimulated by ConBr (1-6 h), while brain-derived neurotrophic factor (BDNF) mRNA was increased at 12 h and BDNF protein at 18-24 h. Our data suggest that an early activation of protein kinases may trigger CREB-dependent BDNF transcription, resulting in a subsequent increase of BDNF protein in response to ConBr. Later, increment of Akt phosphorylation was observed 24 h after ConBr administration, possibly due to BDNF/TrkB-dependent activation of Akt. Our findings indicate that ConBr is a multifunctional molecule capable to activate signaling pathways involved in neuroplasticity and neuroprotection. CI - Copyright (c) 2014 John Wiley & Sons, Ltd. FAU - Rieger, Debora K AU - Rieger DK AD - Departamento de Bioquimica, Centro de Ciencias Biologicas, Universidade Federal de Santa Catarina, Florianopolis, SC, 88040-900, Brazil. FAU - Cunha, Rodrigo M S AU - Cunha RM FAU - Lopes, Mark William AU - Lopes MW FAU - Costa, Ana Paula AU - Costa AP FAU - Budni, Josiani AU - Budni J FAU - Rodrigues, Ana Lucia S AU - Rodrigues AL FAU - Walz, Roger AU - Walz R FAU - Teixeira, Edson H AU - Teixeira EH FAU - Nascimento, Kyria S AU - Nascimento KS FAU - Cavada, Benildo S AU - Cavada BS FAU - Leal, Rodrigo B AU - Leal RB LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - J Mol Recognit JT - Journal of molecular recognition : JMR JID - 9004580 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Cyclic AMP Response Element-Binding Protein) RN - 0 (Plant Lectins) RN - 0 (Protein Kinase Inhibitors) RN - 0 (RNA, Messenger) RN - 0 (lectin, Canavalia) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) RN - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases) RN - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/*genetics/metabolism MH - Canavalia/*chemistry MH - Cyclic AMP Response Element-Binding Protein/metabolism MH - Cyclic AMP-Dependent Protein Kinases/metabolism MH - Extracellular Signal-Regulated MAP Kinases/metabolism MH - Gene Expression Regulation/drug effects MH - Glycosylation/drug effects MH - Hippocampus/drug effects/metabolism MH - Injections, Intraventricular MH - Male MH - Mice MH - Models, Biological MH - Phosphorylation/drug effects MH - Plant Lectins/*pharmacology MH - Protein Kinase Inhibitors/pharmacology MH - Proto-Oncogene Proteins c-akt/metabolism MH - RNA, Messenger/genetics/metabolism MH - Seeds/*chemistry MH - Signal Transduction/*drug effects MH - Time Factors OTO - NOTNLM OT - BDNF OT - CREB OT - ConBr OT - lectin OT - neuroprotection OT - protein kinases EDAT- 2014/10/17 06:00 MHDA- 2015/06/19 06:00 CRDT- 2014/10/17 06:00 PHST- 2013/10/18 00:00 [received] PHST- 2014/05/29 00:00 [revised] PHST- 2014/06/01 00:00 [accepted] PHST- 2014/10/17 06:00 [entrez] PHST- 2014/10/17 06:00 [pubmed] PHST- 2015/06/19 06:00 [medline] AID - 10.1002/jmr.2401 [doi] PST - ppublish SO - J Mol Recognit. 2014 Dec;27(12):746-54. doi: 10.1002/jmr.2401.