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  1. Article: Mechanisms of anti-inflammatory and neuroprotective actions of PPAR-gamma agonists.

    Kapadia, Ramya / Yi, Jae-Hyuk / Vemuganti, Raghu

    Frontiers in bioscience : a journal and virtual library

    2008  Volume 13, Page(s) 1813–1826

    Abstract: Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors of the nuclear hormone receptor superfamily. The 3 PPAR isoforms (alpha, delta/beta and gamma) are known to control many physiological functions including ... ...

    Abstract Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors of the nuclear hormone receptor superfamily. The 3 PPAR isoforms (alpha, delta/beta and gamma) are known to control many physiological functions including glucose absorption, lipid balance, and cell growth and differentiation. Of interest, PPAR-gamma activation was recently shown to mitigate the inflammation associated with chronic and acute neurological insults. Particular attention was paid to test the therapeutic potential of PPAR agonists in acute conditions like stroke, spinal cord injury (SCI) and traumatic brain injury (TBI), in which massive inflammation plays a detrimental role. While 15d-prostaglandin J2 (15d PGJ2) is the natural ligand of PPAR-gamma, the thiazolidinediones (TZDs) are potent exogenous agonists. Due to their insulin-sensitizing properties, 2 TZDs rosiglitazone and pioglitazone are currently FDA-approved for type-2 diabetes treatment. Recent studies from our laboratory and other groups have shown that TZDs induce significant neuroprotection in animal models of focal ischemia and SCI by multiple mechanisms. The beneficial actions of TZDs were observed to be both PPAR-gamma-dependent as well as -independent. The major mechanism of TZD-induced neuroprotection seems to be prevention of microglial activation and inflammatory cytokine and chemokine expression. TZDs were also shown to prevent the activation of pro-inflammatory transcription factors at the same time promoting the anti-oxidant mechanisms in the injured CNS. This review article discusses the multiple mechanisms of TZD-induced neuroprotection in various animal models of CNS injury with an emphasis on stroke.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/therapeutic use ; Brain Ischemia/pathology ; Humans ; Inflammation ; Ischemia ; Ligands ; Neuroprotective Agents/therapeutic use ; Oxidative Stress ; PPAR delta/metabolism ; PPAR gamma/agonists ; PPAR-beta/metabolism ; Reactive Oxygen Species ; Spinal Cord Injuries/metabolism ; Stroke
    Chemical Substances Anti-Inflammatory Agents ; Ligands ; Neuroprotective Agents ; PPAR delta ; PPAR gamma ; PPAR-beta ; Reactive Oxygen Species
    Language English
    Publishing date 2008-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2141320-4
    ISSN 1093-9946
    ISSN 1093-9946
    DOI 10.2741/2802
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5867: Show issues Location:
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  2. Article: Role of transcription factors in mediating post-ischemic cerebral inflammation and brain damage.

    Yi, Jae-Hyuk / Park, Seung-Won / Kapadia, Ramya / Vemuganti, Raghu

    Neurochemistry international

    2007  Volume 50, Issue 7-8, Page(s) 1014–1027

    Abstract: Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, ... ...

    Abstract Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, several transcription factors induced in the ischemic brain can modulate the post-ischemic inflammation. While the induction of transcription factors such as IRF1, NF-kappaB, ATF-2, STAT3, Egr1 and C/EBPbeta is thought to promote post-ischemic inflammation, activation of transcription factors such as HIF-1, CREB, c-fos, PPARalpha, PPARgamma and p53 is thought to prevent post-ischemic inflammation and neuronal damage. Of these, PPARgamma which is a ligand-activated transcription factor was recently shown to prevent inflammatory gene expression in several animal models CNS disorders. This review article discusses some of the molecular mechanisms of PPARgamma induction by its agonists following focal cerebral ischemia.
    MeSH term(s) Animals ; Brain/physiopathology ; Brain Damage, Chronic/physiopathology ; Brain Ischemia/physiopathology ; CCAAT-Enhancer-Binding Protein-beta/physiology ; Cell Adhesion Molecules/physiology ; Humans ; Inflammation/etiology ; Inflammation/physiopathology ; NF-kappa B/physiology ; Peroxisome Proliferator-Activated Receptors/physiology ; Signal Transduction ; Transcription Factors/physiology
    Chemical Substances CCAAT-Enhancer-Binding Protein-beta ; Cell Adhesion Molecules ; NF-kappa B ; Peroxisome Proliferator-Activated Receptors ; Transcription Factors
    Language English
    Publishing date 2007-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 283190-9
    ISSN 1872-9754 ; 0197-0186
    ISSN (online) 1872-9754
    ISSN 0197-0186
    DOI 10.1016/j.neuint.2007.04.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1610: Show issues Location:
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  3. Article: Decreased brain damage and curtailed inflammation in transcription factor CCAAT/enhancer binding protein beta knockout mice following transient focal cerebral ischemia.

    Kapadia, Ramya / Tureyen, Kudret / Bowen, Kellie K / Kalluri, Haviryaji / Johnson, Peter F / Vemuganti, Raghu

    Journal of neurochemistry

    2006  Volume 98, Issue 6, Page(s) 1718–1731

    Abstract: CCAAT/enhancer binding protein beta (C/EBPbeta) is a leucine-zipper transcription factor that regulates cell growth and differentiation in mammals. Expression of many pro-inflammatory genes including the cytokine interleukin-6 is known to be controlled ... ...

    Abstract CCAAT/enhancer binding protein beta (C/EBPbeta) is a leucine-zipper transcription factor that regulates cell growth and differentiation in mammals. Expression of many pro-inflammatory genes including the cytokine interleukin-6 is known to be controlled by C/EBPbeta. We report that focal cerebral ischemia induced by transient middle cerebral artery occlusion (MCAO) significantly increases C/EBPbeta gene expression in mouse brain at between 6 and 72 h of reperfusion. To understand the functional significance of C/EBPbeta in postischemic inflammation and brain damage, we induced transient MCAO in cohorts of adult C/EBPbeta null mice and their wild-type littermates. At 3 days of reperfusion following transient MCAO, C/EBPbeta null mice showed significantly smaller infarcts, reduced neurological deficits, decreased terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells, decreased intercellular adhesion molecule 1 (ICAM1) immunopositive vessels, decreased extravasated neutrophils and fewer activated microglia/macrophages, compared with their wild-type littermates. Furthermore, GeneChip analysis showed that postischemic induction of many transcripts known to promote inflammation and neuronal damage was less pronounced in the brains of C/EBPbeta-/- mice compared with C/EBPbeta+/+ mice. These results suggest a significant role for C/EBPbeta in postischemic inflammation and brain damage.
    MeSH term(s) Animals ; Apoptosis ; Brain/metabolism ; Brain/pathology ; CCAAT-Enhancer-Binding Protein-beta/deficiency ; CCAAT-Enhancer-Binding Protein-beta/genetics ; Cerebral Infarction/metabolism ; Cerebral Infarction/pathology ; Encephalitis/etiology ; Encephalitis/genetics ; Encephalitis/pathology ; Gene Expression ; In Situ Nick-End Labeling ; Intercellular Adhesion Molecule-1/metabolism ; Interleukin-6/genetics ; Ischemic Attack, Transient/complications ; Ischemic Attack, Transient/metabolism ; Ischemic Attack, Transient/pathology ; Ischemic Attack, Transient/physiopathology ; Mice ; Mice, Knockout ; Nervous System Diseases/etiology ; Nervous System Diseases/prevention & control ; Neurons/pathology ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger/metabolism ; Transcription, Genetic
    Chemical Substances CCAAT-Enhancer-Binding Protein-beta ; Interleukin-6 ; RNA, Messenger ; Intercellular Adhesion Molecule-1 (126547-89-5)
    Language English
    Publishing date 2006-09
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/j.1471-4159.2006.04056.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui II Zs.170: Show issues Location:
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  4. Article: Peroxisome proliferator-activated receptor-gamma agonists induce neuroprotection following transient focal ischemia in normotensive, normoglycemic as well as hypertensive and type-2 diabetic rodents.

    Tureyen, Kudret / Kapadia, Ramya / Bowen, Kellie K / Satriotomo, Irawan / Liang, Jin / Feinstein, Douglas L / Vemuganti, Raghu

    Journal of neurochemistry

    2007  Volume 101, Issue 1, Page(s) 41–56

    Abstract: Thiazolidinediones (TZDs) are synthetic agonists of the ligand-activated transcription factor peroxisome proliferator-activated receptor-gamma (PPARgamma). TZDs are known to curtail inflammation associated with peripheral organ ischemia. As inflammation ... ...

    Abstract Thiazolidinediones (TZDs) are synthetic agonists of the ligand-activated transcription factor peroxisome proliferator-activated receptor-gamma (PPARgamma). TZDs are known to curtail inflammation associated with peripheral organ ischemia. As inflammation precipitates the neuronal death after stroke, we tested the efficacy of TZDs in preventing brain damage following transient middle cerebral artery occlusion (MCAO) in adult rodents. As hypertension and diabetes complicate the stroke outcome, we also evaluated the efficacy of TZDs in hypertensive rats and type-2 diabetic mice subjected to transient MCAO. Pre-treatment as well as post-treatment with TZDs rosiglitazone and pioglitazone significantly decreased the infarct volume and neurological deficits in normotensive, normoglycemic, hypertensive and hyperglycemic rodents. Rosiglitazone neuroprotection was not enhanced by retinoic acid x receptor agonist 9-cis-retinoic acid, but was prevented by PPARgamma antagonist GW9662. Rosiglitazone significantly decreased the post-ischemic intercellular adhesion molecule-1 expression and extravasation of macrophages and neutrophils into brain. Rosiglitazone treatment curtailed the post-ischemic expression of the pro-inflammatory genes interleukin-1beta, interleukin-6, macrophage inflammatory protein-1alpha, monocyte chemoattractant protein-1, cyclooxygenase-2, inducible nitric oxide synthase, early growth response-1, CCAAT/enhancer binding protein-beta and nuclear factor-kappa B, and increased the expression of the anti-oxidant enzymes catalase and copper/zinc-superoxide dismutase. Rosiglitazone also increased the expression of the anti-inflammatory gene suppressor of cytokine signaling-3 and prevented the phosphorylation of the transcription factor signal transducer and activator of transcription-3 after focal ischemia. Thus, PPARgamma activation with TZDs might be a potent therapeutic option for preventing inflammation and neuronal damage after stroke with promise in diabetic and hypertensive subjects.
    MeSH term(s) Anilides/pharmacology ; Animals ; Cerebral Infarction/drug therapy ; Cerebral Infarction/physiopathology ; Cerebral Infarction/prevention & control ; Chemotaxis, Leukocyte/drug effects ; Chemotaxis, Leukocyte/physiology ; Cytokines/genetics ; Cytokines/metabolism ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/physiopathology ; Disease Models, Animal ; Encephalitis/drug therapy ; Encephalitis/metabolism ; Encephalitis/physiopathology ; Hypertension/genetics ; Hypertension/physiopathology ; Intercellular Adhesion Molecule-1/drug effects ; Intercellular Adhesion Molecule-1/metabolism ; Ischemic Attack, Transient/drug therapy ; Ischemic Attack, Transient/physiopathology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Neuroprotective Agents/chemistry ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; PPAR gamma/agonists ; PPAR gamma/antagonists & inhibitors ; PPAR gamma/metabolism ; Rats ; Rats, Inbred SHR ; Rats, Sprague-Dawley ; Superoxide Dismutase/drug effects ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Superoxide Dismutase-1 ; Suppressor of Cytokine Signaling 3 Protein ; Suppressor of Cytokine Signaling Proteins/drug effects ; Suppressor of Cytokine Signaling Proteins/metabolism ; Thiazolidinediones/chemistry ; Thiazolidinediones/pharmacology ; Thiazolidinediones/therapeutic use
    Chemical Substances 2-chloro-5-nitrobenzanilide ; Anilides ; Cytokines ; Neuroprotective Agents ; PPAR gamma ; Socs3 protein, rat ; Suppressor of Cytokine Signaling 3 Protein ; Suppressor of Cytokine Signaling Proteins ; Thiazolidinediones ; rosiglitazone (05V02F2KDG) ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Sod1 protein, mouse (EC 1.15.1.1) ; Sod1 protein, rat (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1) ; pioglitazone (X4OV71U42S)
    Language English
    Publishing date 2007-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/j.1471-4159.2006.04376.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui II Zs.170: Show issues Location:
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