PMID- 23471014 OWN - NLM STAT- MEDLINE DCOM- 20130930 LR - 20171116 IS - 1872-8111 (Electronic) IS - 0168-0102 (Linking) VI - 75 IP - 4 DP - 2013 Apr TI - Differences in phosphodiesterase 3A and 3B expression after ischemic insult. PG - 340-8 LID - S0168-0102(13)00040-0 [pii] LID - 10.1016/j.neures.2013.02.006 [doi] AB - Phosphodiesterase (PDE) exists in the cardiovascular system, adipose tissue and platelets, and its inhibition increases the cellular levels of cAMP, which could activate cAMP-responsive element binding protein (pCREB). The present study was designed to map the expression of PDE3A/B in the forebrain and define the time course of PDE3 expression in the ischemic boundary zone after ischemia. The number of PDE3A-positive cells (neurons and endothelial cells) remained unchanged, while PDE3B-positive cells gradually increased after ischemia/reperfusion. In the corpus callosum, PDE3B was expressed in oligodendrocytes, oligodendrocyte progenitor cells, and astrocytes. PDE3B-expressing astrocytes showed gradual increase after ischemia/reperfusion. In the cortex, the majority of PDE3B-expressing cells before ischemia were neurons, though few were astrocytes. Ischemic insult resulted in gradual increase in PDE3B-expressing astrocytes and neurons, with larger increase in astrocytes. Expression of brain derived neurotrophic factor (BDNF) and B-cell leukemia/lymphoma 2 protein (Bcl-2) was detected in pCREB-positive cells, not in PDE3B-positive cells. Our results demonstrated that ischemic insult increased PDE3B expression, but not PDE3A, and changed the number and type of cells in a time-dependent manner. The variation of PDE3B-expression in the brain might play a crucial pathophysiological role, and regulation of PDE3B production might protect against ischemic brain damage. CI - Copyright (c) 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved. FAU - Mitome-Mishima, Yumiko AU - Mitome-Mishima Y AD - Department of Neurosurgery, Juntendo University School of Medicine, Tokyo, Japan. FAU - Miyamoto, Nobukazu AU - Miyamoto N FAU - Tanaka, Ryota AU - Tanaka R FAU - Oishi, Hidenori AU - Oishi H FAU - Arai, Hajime AU - Arai H FAU - Hattori, Nobutaka AU - Hattori N FAU - Urabe, Takao AU - Urabe T LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20130305 PL - Ireland TA - Neurosci Res JT - Neuroscience research JID - 8500749 RN - 0 (Aif1 protein, mouse) RN - 0 (CD11b Antigen) RN - 0 (Calcium-Binding Proteins) RN - 0 (Glial Fibrillary Acidic Protein) RN - 0 (Microfilament Proteins) RN - EC 2.3.1.48 (CREB-Binding Protein) RN - EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 3) RN - EC 4.2.1.11 (Phosphopyruvate Hydratase) SB - IM MH - Analysis of Variance MH - Animals MH - Brain/*enzymology/pathology MH - CD11b Antigen/metabolism MH - CREB-Binding Protein/metabolism MH - Calcium-Binding Proteins/metabolism MH - Cell Count MH - Cerebral Cortex/enzymology/pathology MH - Cerebrovascular Circulation/physiology MH - Corpus Callosum/enzymology/pathology MH - Cyclic Nucleotide Phosphodiesterases, Type 3/*metabolism MH - Disease Models, Animal MH - Gene Expression Regulation, Enzymologic/*physiology MH - Glial Fibrillary Acidic Protein/metabolism MH - In Situ Nick-End Labeling MH - Infarction, Middle Cerebral Artery/*enzymology/*pathology MH - Male MH - Mice MH - Mice, Inbred C57BL MH - Microfilament Proteins/metabolism MH - Phosphopyruvate Hydratase/metabolism MH - Phosphorylation MH - Reperfusion EDAT- 2013/03/09 06:00 MHDA- 2013/10/01 06:00 CRDT- 2013/03/09 06:00 PHST- 2012/10/22 00:00 [received] PHST- 2013/01/31 00:00 [revised] PHST- 2013/02/04 00:00 [accepted] PHST- 2013/03/09 06:00 [entrez] PHST- 2013/03/09 06:00 [pubmed] PHST- 2013/10/01 06:00 [medline] AID - S0168-0102(13)00040-0 [pii] AID - 10.1016/j.neures.2013.02.006 [doi] PST - ppublish SO - Neurosci Res. 2013 Apr;75(4):340-8. doi: 10.1016/j.neures.2013.02.006. Epub 2013 Mar 5.