001     136528
005     20240424120353.0
024 7 _ |a 10.1186/1742-2094-9-44
|2 doi
024 7 _ |a pmid:22373413
|2 pmid
024 7 _ |a pmc:PMC3359160
|2 pmc
037 _ _ |a DZNE-2020-02850
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Röhnert, Peter
|b 0
245 _ _ |a Dipeptidyl peptidase IV, aminopeptidase N and DPIV/APN-like proteases in cerebral ischemia.
260 _ _ |a London
|c 2012
|b BioMed Central
264 _ 1 |3 online
|2 Crossref
|b Springer Science and Business Media LLC
|c 2012-02-28
264 _ 1 |3 print
|2 Crossref
|b Springer Science and Business Media LLC
|c 2012-12-01
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1713881149_10934
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
|0 0
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520 _ _ |a Cerebral inflammation is a hallmark of neuronal degeneration. Dipeptidyl peptidase IV, aminopeptidase N as well as the dipeptidyl peptidases II, 8 and 9 and cytosolic alanyl-aminopeptidase are involved in the regulation of autoimmunity and inflammation. We studied the expression, localisation and activity patterns of these proteases after endothelin-induced occlusion of the middle cerebral artery in rats, a model of transient and unilateral cerebral ischemia.Male Sprague-Dawley rats were used. RT-PCR, immunohistochemistry and protease activity assays were performed at different time points, lasting from 2 h to 7 days after cerebral ischemia. The effect of protease inhibitors on ischemia-dependent infarct volumes was quantified 7 days post middle cerebral artery occlusion. Statistical analysis was conducted using the t-test.Qualitative RT-PCR revealed these proteases in ipsilateral and contralateral cortices. Dipeptidyl peptidase II and aminopeptidase N were up-regulated ipsilaterally from 6 h to 7 days post ischemia, whereas dipeptidyl peptidase 9 and cytosolic alanyl-aminopeptidase were transiently down-regulated at day 3. Dipeptidyl peptidase 8 and aminopeptidase N immunoreactivities were detected in cortical neurons of the contralateral hemisphere. At the same time point, dipeptidyl peptidase IV, 8 and aminopeptidase N were identified in activated microglia and macrophages in the ipsilateral cortex. Seven days post artery occlusion, dipeptidyl peptidase IV immunoreactivity was found in the perikarya of surviving cortical neurons of the ipsilateral hemisphere, whereas their nuclei were dipeptidyl peptidase 8- and amino peptidase N-positive. At the same time point, dipeptidyl peptidase IV, 8 and aminopeptidase N were targeted in astroglial cells. Total dipeptidyl peptidase IV, 8 and 9 activities remained constant in both hemispheres until day 3 post experimental ischemia, but were increased (+165%) in the ipsilateral cortex at day 7. In parallel, aminopeptidase N and cytosolic alanyl-aminopeptidase activities remained unchanged.Distinct expression, localization and activity patterns of proline- and alanine-specific proteases indicate their involvement in ischemia-triggered inflammation and neurodegeneration. Consistently, IPC1755, a non-selective protease inhibitor, revealed a significant reduction of cortical lesions after transient cerebral ischemia and may suggest dipeptidyl peptidase IV, aminopeptidase N and proteases with similar substrate specificity as potentially therapy-relevant targets.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
|0 G:(DE-HGF)POF3-342
|c POF3-342
|f POF III
|x 0
542 _ _ |i 2012-02-28
|2 Crossref
|u http://www.creativecommons.org/licenses/by/2.0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Enzyme Inhibitors
|2 NLM Chemicals
650 _ 7 |a Glial Fibrillary Acidic Protein
|2 NLM Chemicals
650 _ 7 |a Glycosphingolipids
|2 NLM Chemicals
650 _ 7 |a RNA, Messenger
|2 NLM Chemicals
650 _ 7 |a inositolphosphorylceramide
|2 NLM Chemicals
650 _ 7 |a CD13 Antigens
|0 EC 3.4.11.2
|2 NLM Chemicals
650 _ 7 |a Dipeptidyl-Peptidases and Tripeptidyl-Peptidases
|0 EC 3.4.14.-
|2 NLM Chemicals
650 _ 7 |a Dpp8 protein, rat
|0 EC 3.4.14.-
|2 NLM Chemicals
650 _ 7 |a Dipeptidyl Peptidase 4
|0 EC 3.4.14.5
|2 NLM Chemicals
650 _ 7 |a Phosphopyruvate Hydratase
|0 EC 4.2.1.11
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Brain Ischemia: complications
|2 MeSH
650 _ 2 |a Brain Ischemia: drug therapy
|2 MeSH
650 _ 2 |a Brain Ischemia: enzymology
|2 MeSH
650 _ 2 |a CD13 Antigens: genetics
|2 MeSH
650 _ 2 |a CD13 Antigens: metabolism
|2 MeSH
650 _ 2 |a Cerebral Infarction: enzymology
|2 MeSH
650 _ 2 |a Cerebral Infarction: etiology
|2 MeSH
650 _ 2 |a Dipeptidyl Peptidase 4: genetics
|2 MeSH
650 _ 2 |a Dipeptidyl Peptidase 4: metabolism
|2 MeSH
650 _ 2 |a Dipeptidyl-Peptidases and Tripeptidyl-Peptidases: genetics
|2 MeSH
650 _ 2 |a Dipeptidyl-Peptidases and Tripeptidyl-Peptidases: metabolism
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Enzyme Inhibitors: therapeutic use
|2 MeSH
650 _ 2 |a Functional Laterality
|2 MeSH
650 _ 2 |a Gene Expression Regulation, Enzymologic: physiology
|2 MeSH
650 _ 2 |a Glial Fibrillary Acidic Protein: metabolism
|2 MeSH
650 _ 2 |a Glycosphingolipids: therapeutic use
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Phosphopyruvate Hydratase: metabolism
|2 MeSH
650 _ 2 |a RNA, Messenger: metabolism
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a Rats, Sprague-Dawley
|2 MeSH
650 _ 2 |a Time Factors
|2 MeSH
700 1 _ |a Schmidt, Werner
|0 P:(DE-2719)9000421
|b 1
|u dzne
700 1 _ |a Emmerlich, Patrick
|b 2
700 1 _ |a Goihl, Alexander
|b 3
700 1 _ |a Wrenger, Sabine
|b 4
700 1 _ |a Bank, Ute
|b 5
700 1 _ |a Nordhoff, Karsten
|b 6
700 1 _ |a Täger, Michael
|b 7
700 1 _ |a Ansorge, Siegfried
|b 8
700 1 _ |a Reinhold, Dirk
|b 9
700 1 _ |a Striggow, Frank
|0 P:(DE-2719)9000420
|b 10
|e Last author
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773 1 8 |a 10.1186/1742-2094-9-44
|b : Springer Science and Business Media LLC, 2012-02-28
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|p 557
|3 journal-article
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|t Journal of Neuroinflammation
|v 9
|y 2012
|x 1742-2094
773 _ _ |a 10.1186/1742-2094-9-44
|g Vol. 9, no. 1, p. 557
|0 PERI:(DE-600)2156455-3
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|t Journal of neuroinflammation
|v 9
|y 2012
|x 1742-2094
856 4 _ |y OpenAccess
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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913 1 _ |a DE-HGF
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21