Galectin-3 expression in delayed neuronal death of hippocampal CA1 following transient forebrain ischemia, and its inhibition by hypothermia

Satoh, Kazuro; Niwa, Masayuki; Goda, Wael; Binh, Nguyen Huy; Nakashima, Masaya; Takamatsu, Manabu; Hara, Akira

doi:10.1016/j.brainres.2011.01.049

Cited by 50 publications

(41 citation statements)

References 26 publications

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“…Hyperthermic and hypothermic conditions were found to have opposite effects, stimulation vs inhibition, on the expression of galectin-3 in the microglial cells of hippocampal brain tissues from gerbils following experimental ischemia [104,105]. Interestingly, the increased levels of galectin-3 at a high temperature (39°C) were associated with less severe apoptotic damage in brain tissues, suggesting that galectin-3 plays a protective role.…”

Section: Chimeric Type Galectin-3mentioning

confidence: 86%

Towards molecular mechanisms regulating the expression of galectins in cancer cells under microenvironmental stress conditions

Timoshenko

2015

Cell. Mol. Life Sci.

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Galectins, a family of soluble β-galactoside-binding proteins, serve as mediators of fundamental biological processes, such as cell growth, differentiation, adhesion, migration, survival, and death. The purpose of this review is to summarize the current knowledge regarding the ways in which the expression of individual galectins differs in normal and transformed human cells exposed to various stimuli mimicking physiological and pathological microenvironmental stress conditions. A conceptual point is being made and grounded that the modulation of galectin expression profiles is a key aspect of cellular stress responses. Moreover, this modulation might be precisely regulated at transcriptional and post-transcriptional levels in the context of non-overlapping transcription factors and miRNAs specific to galectins.

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Section: Chimeric Type Galectin-3mentioning

confidence: 86%

Towards molecular mechanisms regulating the expression of galectins in cancer cells under microenvironmental stress conditions

Timoshenko

2015

Cell. Mol. Life Sci.

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“…In a focal ischemia model, galectin-3 was up-regulated in OX-42+ microglia for up to 2 months after injury [68]. Galectin-3 was shown to be increased in the CA1 region of the hippocampus following transient ischemia [69]. In addition to macrophages and microglia, T cells have been reported to express galectin-3 [70].…”

Section: Galectin-3mentioning

confidence: 99%

Novel Neuroinflammatory Targets in the Chronically Injured Spinal Cord

Pajoohesh‐Ganji

Byrnes

2011

Neurotherapeutics

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Summary: Injury to the spinal cord is known to result in inflammation. To date, the preponderance of research has focused on the acute neuroinflammatory response, which begins immediately and is believed to terminate within hours to (at most) days after the injury. However, recent studies have demonstrated that postinjury inflammation is not restricted to the first few hours or days after injury, but can last for months to years after a spinal cord injury (SCI). These chronic studies have revealed that increased numbers of inflammatory cells, such as microglia and macrophages, and inflammatory factors, including cytokines, chemokines, and enzyme products are found at markedly delayed times after injury. Here we review experimental work on a selection of the novel inflammatory factors observed chronically after SCI, including the nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) oxidase enzyme and galectin-3. We will discuss the role of these proteins in inflammation with regard to both detrimental and beneficial effects of neuroinflammation after injury. Finally, the potential of these proteins to serve as therapeutic targets will be considered, and a novel therapeutic approach (i.e., the agonist for metabotropic glutamate receptor 5 [mGluR5], [RS]-2-Chloro-5-hydroxyphenylglycine [CHPG]) will be discussed. This review will demonstrate the expression and activity profiles, roles in potentiation of injury, and therapy studies of these inflammatory factors suggest that not only are these chronically expressed factors viable targets for SCI treatment, but that the therapeutic window is broader than has previously been thought.

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“…However, there is little evidence for the presence of peripheral immune cells in the central nervous system following CA/CPR. It has been demonstrated that global cerebral ischemia stimulates microglial activation and a pro-inflammatory state within the brain (Wagner et al, 2002, Langdon et al, 2008, Waid et al, 2008, Norman et al, 2011, Satoh et al, 2011). While resident microglia are clearly early mediators of neuroinflammation and likely effectors of injury, the maintenance of a sustained inflammatory state consistent with delayed neuronal injury requires the action of other immune cells, particularly T lymphocytes.…”

Section: Introductionmentioning

confidence: 99%

Pro-inflammatory T-lymphocytes rapidly infiltrate into the brain and contribute to neuronal injury following cardiac arrest and cardiopulmonary resuscitation

Deng

Carter

Traystman

et al. 2014

Journal of Neuroimmunology

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Although inflammatory mechanisms have been linked to neuronal injury following global cerebral ischemia, the presence of infiltrating peripheral immune cells remains understudied. We performed flow cytometry of single cell suspensions obtained from the brains of mice at varying time points after global cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR) to characterize the influx in lymphocytes into the injured brain. We observed that CA/CPR caused a large influx of lymphocytes within 3 hours of resuscitation that was maintained for the 3 day duration of our experiments. Using cell staining flow cytometry we observed that the large majority of infiltrating lymphocytes were CD4+ T cells. Intracellular stains revealed a large proportion of pro-inflammatory T cells expressing either TNFα or INFγ. Importantly, the lack of functional T cells in TCRα knockout mice reduced neuronal injury following CA/CPR, implicating pro-inflammatory T cells in the progression of ischemic neuronal injury. Finally, we made the remarkable observation that the novel CD4+CD40+ (Th40) population of pro-inflammatory T cells that are strongly associated with autoimmunity are present in large numbers in the injured brain. These data indicate that studies investigating the neuro-immune response after global cerebral ischemia should consider the role of infiltrating T cells in orchestrating the acute and sustained immune response.

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Galectin-3 expression in delayed neuronal death of hippocampal CA1 following transient forebrain ischemia, and its inhibition by hypothermia

Cited by 50 publications

References 26 publications

Towards molecular mechanisms regulating the expression of galectins in cancer cells under microenvironmental stress conditions

Towards molecular mechanisms regulating the expression of galectins in cancer cells under microenvironmental stress conditions

Novel Neuroinflammatory Targets in the Chronically Injured Spinal Cord

Pro-inflammatory T-lymphocytes rapidly infiltrate into the brain and contribute to neuronal injury following cardiac arrest and cardiopulmonary resuscitation

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