Repression of proinflammatory cytokine and inducible nitric oxide synthase (NOS2) gene expression in activated microglia by N-acetyl-O-methyldopamine: Protein kinase a-dependent mechanism

Cho, Sunghee; Kim, Yoonseong; Cruz, Manuel; Park, Eun Mi; Chu, Chung K.; Song, Gyu Yong; Joh, Tong H.

doi:10.1002/1098-1136(20010315)33:4<324::aid-glia1031>3.0.co;2-m

Cited by 39 publications

(19 citation statements)

References 65 publications

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“…How the cAMP pathway regulates IL-1β expression is an active area of investigation. Several studies have shown that raising cAMP levels with either neurotransmitters or phosphodiesterase inhibitors reduce IL-1β levels, but the exact mechanism is still unclear (Cogswell et al, 1994, Verghese et al, 1995, Si et al, 1998, Caggiano and Kraig, 1999, Cho et al, 2001, Dello Russo et al, 2004.…”

Section: Discussionmentioning

confidence: 99%

Modulation of the cAMP signaling pathway after traumatic brain injury

Atkins

Oliva

Alonso

et al. 2007

Experimental Neurology

137

151

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Traumatic brain injury (TBI) results in both focal and diffuse brain pathologies that are exacerbated by the inflammatory response and progress from hours to days after the initial injury. Using a clinically relevant model of TBI, the parasagittal fluid-percussion brain injury (FPI) model, we found injury-induced impairments in the cyclic AMP (cAMP) signaling pathway. Levels of cAMP were depressed in the ipsilateral parietal cortex and hippocampus, as well as activation of its downstream target, protein kinase A, from 15 min to 48 hr after moderate FPI. To determine if preventing hydrolysis of cAMP by administration of a phosphodiesterase (PDE) IV inhibitor would improve outcome after TBI, we treated animals intraperitoneally with rolipram (0.3 or 3.0 mg/kg) 30 min prior to TBI, and then once per day for three days. Rolipram treatment restored cAMP to sham levels and significantly reduced cortical contusion volume and improved neuronal cell survival in the parietal cortex and CA3 region of the hippocampus. Traumatic axonal injury, characterized by β-amyloid precursor protein deposits in the external capsule, was also significantly reduced in rolipramtreated animals. Furthermore, levels of the pro-inflammatory cytokines, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), were significantly decreased with rolipram treatment. These results demonstrate that the cAMP-PKA signaling cascade is downregulated after TBI, and that treatment with a PDE IV inhibitor improves histopathological outcome and decreases inflammation after TBI. Keywordscamp; Fluid-percussion; Inflammation; Interleukin-1β; PKA; Phosphodiesterase; Rolipram; TNF-α; Traumatic brain injury; TBI Traumatic brain injury (TBI) is a prevalent, debilitating health problem, occurring in 1.4 million people each year and disabling 5 million people in the United States (Langlois et al., 2004). The subsequent progressive injury after brain trauma develops from hours to days after the initiating insult, providing an accessible time window for pharmacological therapies. Despite Address correspondence to: W. Dalton Dietrich, Scientific Director, The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, P.O. Box 016960, (R-48), Miami, FL 33101, E-mail: ddietrich@miami.edu, Phone: 305-243-2297, Fax: 305-243-3207. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Brain trauma results in contusion formation, neuronal apoptosis, and axonal tract damage. These pathologies are worsened by the inflammatory cascade set into motion by the initial injury (Morganti-Kossmann et al., 2002. Two pro-i...

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Section: Discussionmentioning

confidence: 99%

Modulation of the cAMP signaling pathway after traumatic brain injury

Atkins

Oliva

Alonso

et al. 2007

Experimental Neurology

137

151

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“…Numerous studies have shown that agents that increase intracellular cAMP levels were able to inhibit the production of LPS-induced proinflammatory cytokines [2][3][4][5][6]. The regulation of pro-inflammatory cytokines is of immediate clinical interest in the treatment of many inflammatory diseases including rheumatoid arthritis, inflammatory bowel disease, and sepsis.…”

Section: Introductionmentioning

confidence: 85%

Cilostazol protects mice against endotoxin shock and attenuates LPS-induced cytokine expression in RAW 264.7 macrophages via MAPK inhibition and NF-κB inactivation: Not involved in cAMP mechanisms

Park

Jung

Lee

et al. 2010

International Immunopharmacology

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“…Furthermore, it has been suggested that CREB is involved in suppression of cytokine gene expression in other systems (Delgado et al, 1998;Perez et al, 1999;Cho et al, 2001). Our previous studies on V 1 agonist-induced nuclear-signaling cascade demonstrated that CREB is significantly activated in cortical astrocytes in response to V 1 agonist in a time-dependent manner , which is confirmed in the current study and shown in Figure 4 A.…”

Section: Suppression Of Inflammatory Cytokines Gene Expression In Resmentioning

confidence: 99%

“…CRE-like promoter sequence is found in the promotor region of both IL-1␤ and TNF-␣ genes (Liu and Whisler, 1998;Perez et al, 1999). Suppression of LPS-induced IL-1␤ and TNF-␣ by N-acetyl-O-methyldopamine was found to be dependent on CREB activation (Cho et al, 2001). VIP-and PACAP-induced repression of TNF-␣ expression was also demonstrated to involve CREB (Delgado et al, 1998).…”

Section: Creb Involvement In Cytokine Suppressionmentioning

confidence: 99%

Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V₁Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

Zhao¹,

Brinton²

2004

J. Neurosci.

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Repression of proinflammatory cytokine and inducible nitric oxide synthase (NOS2) gene expression in activated microglia by N-acetyl-O-methyldopamine: Protein kinase a-dependent mechanism

Cited by 39 publications

References 65 publications

Modulation of the cAMP signaling pathway after traumatic brain injury

Modulation of the cAMP signaling pathway after traumatic brain injury

Cilostazol protects mice against endotoxin shock and attenuates LPS-induced cytokine expression in RAW 264.7 macrophages via MAPK inhibition and NF-κB inactivation: Not involved in cAMP mechanisms

Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V₁Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

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Repression of proinflammatory cytokine and inducible nitric oxide synthase (NOS2) gene expression in activated microglia by N-acetyl-O-methyldopamine: Protein kinase a-dependent mechanism

Cited by 39 publications

References 65 publications

Modulation of the cAMP signaling pathway after traumatic brain injury

Modulation of the cAMP signaling pathway after traumatic brain injury

Cilostazol protects mice against endotoxin shock and attenuates LPS-induced cytokine expression in RAW 264.7 macrophages via MAPK inhibition and NF-κB inactivation: Not involved in cAMP mechanisms

Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V1Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

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Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V₁Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism