Regular ArticleIL-6 Deficiency Leads to Reduced Metallothionein-I+II Expression and Increased Oxidative Stress in the Brain Stem after 6-Aminonicotinamide Treatment
References (64)
- et al.
Expression of growth inhibitory factor (metallothionein-III) mRNA and protein following excitotoxic immature brain injury
J. Neuropathol. Exp. Neurol.
(1999) - et al.
Metallothionein-I+II induction by zinc and copper in primary cultures of rat microglia
Neurochem. Int.
(1998) - et al.
Expression of growth inhibitory factor (GIF) in normal and injured rat brains
Neurochem. Int.
(1995) The functional significance of brain metallothioneins
FASEB J.
(1996)Astrocyte metallothioneins (MTs) and their neuroprotective role
Ann. N.Y. Acad. Sci.
(1997)- et al.
Metallothioneins in brain—The role in physiology and pathology
Toxicol. Appl. Pharmacol.
(1997) Astrocytic functions and physiological reactions to injury: The potential to induce and/or exacerbate neuronal dysfunction—A forum position paper
Neurotoxicology
(1998)Metallothionein (MT) isoforms in the central nervous system (CNS): Regional and cell-specific distribution and potential functions as an antioxidant
Neurotoxicology
(1998)- et al.
Evolution of neuropathologic abnormalities associated with blood–brain barrier breakdown in transgenic mice expressing interleukin-6 in astrocytes
J. Neuropathol. Exp. Neurol.
(1995) - et al.
Transcytosis of protein through the mammalian cerebral epithelium and endothelium. III. Receptor-mediated transcytosis through the blood–brain barrier of blood-borne transferrin and antibody against the transferrin receptor
Exp. Neurol.
(1996)
Endothelial cell biology and the enigma of transcytosis through the blood–brain barrier
Adv. Exp. Med. Biol.
6-Aminonicotinamide sensitizes human tumor cell lines to cisplatin
Clin. Cancer Res.
Reactive gliosis as a consequence of interleukin-6 expression in the brain: studies in transgenic mice
Dev. Neurosci.
Temporalspatial patterns of expression of metallothionein-I and -III and other stress related genes in rat brain after kainic acid-induced seizures
Neurochem. Int.
Molecular profile of reactive astrocytes-implications for their role in neurologic disease
Neuroscience
Enhanced neurotrophic activity in Alzheimer's disease cortex is not associated with down-regulation of metallothionein-III (GIF)
Brain Res.
Development of a competitive double antibody radioimmunoassay for rat metallothionein
J. Immunoassay
Transcriptional induction of the mouse metallothionein-I gene in hydrogen peroxide-treated Hepa cells involves a composite major late transcription factor/antioxidant response element and metal response promoter elements
Nucleic Acids Res.
Effect of 6-aminonicotinamide on metabolism of astrocytes and C6-glioma cells
Metabol. Brain Dis.
The pivotal role of interleukin 6 in formation and function of hematopoietically active murine long-term bone marrow cultures
Stem Cells
Endotoxin and intracerebroventricular injection of IL-1 and IL-6 induce rat brain metallothionein-I and -II
Neurochem. Int.
Transgenic expression of interleukin 6 in the central nervous system regulates brain metallothionein-I and -III expression in mice
Mol. Brain Res.
Regulation of brain metallothioneins
Curr. Top. Neurochem.
Interleukin-6: Possible implications in human diseases
Ric. Clin. Lab.
Cytokines and the nervous system. I. Expression and recognition
Trends Neurosci.
Changes of growth inhibitory factor after stab wounds in rat brain
Brain Res.
Brain injury and growth inhibitory factor (GIF)—A minireview
Neurochem. Res.
Inhibition of NADPH supply by 6-aminonicotinamide: Effect on glutathione, nitric oxide and superoxide in J774 cells
FEBS Lett.
Patterns of growth inhibitory factor (GIF) and glial fibrillary acidic protein relative level changes differ following left middle cerebral artery occlusion in rats
Brain Res.
Impaired neuroglial activation in interleukin-6 deficient mice
Glia
Enhanced apoptosis in metallothionein null cells
Mol. Pharmacol.
Cited by (51)
Interleukin-6: Its role and mechanisms in rescuing depression-like behaviors in rat models of depression
2019, Brain, Behavior, and ImmunityCitation Excerpt :In addition, we also found that knocking-down of IL-6 could increase the expression levels of pro-inflammatory cytokines such as the IL-1β, TNF-αand IFN-γ. It has been reported that IL-6 deficiency leads to increased oxidative stress and in the number of apoptotic neurons within the brain, as well as a delay in neural regeneration as compared with that observed in normal mice (Penkowa and Hidalgo, 2000; Penkowa et al., 2000). Thus, these results suggest that tissue damage induced by oxidative stress and apoptosis may result in the production of inflammatory cytokines via feedback mechanisms.
In vivo effect of acute exposure to interleukin-6 on the developing visual system
2019, Neuroscience LettersCitation Excerpt :IL-6 levels are low in physiological conditions [5], but it increases in a number of pathological conditions [5–7]. IL-6 induces neuroprotection [8,9], regeneration of the optic nerve after crushing [10] and it is also important in the mechanism of axonal growth and recovery of function after injury [11,12]. Recently we had demonstrated that an acute intravitreal injection with IL-6 alters the laminar segregation of the uncrossed retinotectal pathway in different stages of development [13].
Exercising the worry away: How inflammation, oxidative and nitrogen stress mediates the beneficial effect of physical activity on anxiety disorder symptoms and behaviours
2013, Neuroscience and Biobehavioral ReviewsCitation Excerpt :However, oxidative damage to IL-6ra subunits leads to decreased STAT-3 and subsequent M-SOD activity. Increased levels of IL-6 can prevent this oxidative damage in a stroke reperfusion model, possibly through modulating gene expression or up-regulating anti-oxidants (Penkowa and Hidalgo, 2000). In another recent study, two weeks of voluntary wheel running in mice protected against hippocampal dentate gyrus apoptosis induced by injection of trimethytin (TMT) (Funk et al., 2011), a substance known to induced cell death via TNF-α receptor activation (Harry et al., 2008).
Cytokines and innate inflammation in the pathogenesis of human traumatic brain injury
2011, Progress in NeurobiologyCitation Excerpt :In the setting of TBI, IL6 has mostly been associated with neuroprotective actions. Using a cryolesion model and genetically manipulated mice, Penkowa and Hidalgo (2000) have described an impaired inflammatory response associated with increased neurodegeneration in IL6 deficient mice. In contrast, decreased oxidative stress and apoptotic cell death, together with increased healing and tissue repair were seen in transgenic mice overexpressing IL6 in astrocytes (Penkowa et al., 2003).
Immune and Inflammatory Responses in the Central Nervous System: Modulation by Astrocytes
2008, NeuroImmune BiologyCitation Excerpt :These mice show chronic neuroinflammation and neurodegeneration, and in the case of the IL-3 and TNF transgenic mice, demyelination and progressive motor disease are also seen [49,50]. In agreement with these in vivo models, it has been demonstrated that IL-6 protects neurons against ischemic damage and excitotoxicity [38–51]; yet, it is also largely responsible for the neuropathology associated with the multiple sclerosis (MS; Fig. 1) animal model, experimental autoimmune encephalomyelitis (EAE), since IL-6 KO mice are completely resistant to EAE [52–55]. Administration of the superantigen staphylococcal enterotoxin B, which acts through a TNF-receptor pathway, overcomes this resistance, but IL-6 is still considered crucial in perpetuating the disease [56].
Psychosocial and biochemical interactions in aging: Preliminary results from an Italian old sample of "Zincage" project
2007, Archives of Gerontology and Geriatrics
- 1
To whom correspondence should be addressed. Fax: +45-35327217. E-mail: [email protected].