Galectin-1 Enhances Astrocytic BDNF Production and Improves Functional Outcome in Rats Following Ischemia

Qu, Wensheng; Wang, Yi-hui; Wang, Jianping; Tang, Yingxin; Zhang, Qiang; Tian, Dai-Shi; Yu, Zhiyuan; Xie, Mingxing; Wang, Wei

doi:10.1007/s11064-010-0234-z

Cited by 60 publications

(47 citation statements)

References 38 publications

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“…Astrocytes are known to protect neurons from the insults of oxidative stress and excitotoxicity after brain ischemia (Rossi et al, 2007; Takano et al, 2009; Zhao and Rempe, 2010). Astrocytic brain-derived neurotrophic factor is known to reduce neuronal apoptosis in the ischemic boundary zone and improve functional recovery (Qu et al, 2010). Astrocytes are also known to play neuroprotective roles during brain ischemia by the expression of astrocyte-enriched miRNAs, including miR-181, miR-29 families, and miR-146a (Ouyang et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Astrocytes Protect Neurons in the Hippocampal CA3 Against Ischemia by Suppressing the Intracellular Ca2+ Overload

Sun

Fukushi

Wang

et al. 2018

Front. Cell. Neurosci.

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In the hippocampus, delayed neuronal death is normally seen in neurons of the CA1 region but not in those of the CA3 region. Astrocytes have been reported to play multiple supporting or pathological roles in neuronal functioning. While evidence indicates that astrocytes could exert neuroprotective effects following ischemia, the possible underlying mechanisms remain unclear. We aimed to investigate the roles of astrocytes in the process of delayed neuronal death following transient forebrain ischemia. L-α-aminoadipic acid (L-α-AAA), an astrocyte-selective gliotoxin, was injected into the hippocampal CA3 region of rats through a cranial window to selectively damage astrocytes. Immunofluorescence staining of glial fibrillary acidic protein (GFAP) was used to evaluate the effect of L-α-AAA on astrocyte numbers. Three days after the L-α-AAA injection, transient forebrain ischemia was induced by a modification of the four-vessel occlusion procedure. Seven days after transient forebrain ischemia, hematoxylin-eosin staining was performed to reveal the morphology of hippocampal pyramidal neurons. In rats with ischemia and reperfusion, regional cerebral blood flow (rCBF) and change in intracellular Ca2+ concentration ([Ca2+]i) were separately measured in CA1 and CA3 regions. L-α-AAA injection significantly decreased the number of astrocytes in CA3, but did not affect the pattern of rCBF changes upon ischemia/reperfusion. Seven days after transient forebrain ischemia, in rats receiving L-α-AAA, delayed neuronal death comparable with that in CA1 was observed in the CA3 region. In addition, the pattern of increase in [Ca2+]i due to transient forebrain ischemia was completely changed in the hippocampal CA3. The loss of astrocytes induced a persistent increase in [Ca2+]i in the CA3 region following transient ischemia, similar to what is observed in the CA1 region. Our study indicates that astrocytes in the hippocampal CA3 region exert neuroprotective effects following transient forebrain ischemia and act by suppressing the intracellular Ca2+ overload. Furthermore, our study will most likely provide a new therapeutic strategy for brain ischemic diseases, targeted to astrocytes.

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Section: Discussionmentioning

confidence: 99%

Astrocytes Protect Neurons in the Hippocampal CA3 Against Ischemia by Suppressing the Intracellular Ca2+ Overload

Sun

Fukushi

Wang

et al. 2018

Front. Cell. Neurosci.

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“…Previous studies showed that cultured astrocytes express and secrete Gal1 (Qu et al, 2010; Yin et al, 2012). Similarly, Gal1 is upregulated in GFAP+ cells in animal models of multiple sclerosis and cerebral ischemia (Qu et al, 2010; Stancic et al, 2011). Gal1-treated astrocytes show decreased proliferation and increased brain-derived neurotrophic factor (BDNF) secretion (Sasaki et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Galectin-1 in injured rat spinal cord: Implications for macrophage phagocytosis and neural repair

Gaudet

Sweet²,

Polinski³

et al. 2015

Molecular and Cellular Neuroscience

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Galectin (Gal)-1 is a small carbohydrate-binding protein and immune modulatory cytokine that is synthesized locally at the site of peripheral nerve injury. In this environment, Gal1 can promote regeneration of injured peripheral axons, in part by modifying the function of macrophages recruited to the site of injury. Unlike in injured peripheral nerves, macrophages do not promote axon regeneration in the injured central nervous system (CNS), perhaps because Gal1 levels are not regulated appropriately. Because the dynamics and cellular localization of endogenous Gal1 have not been rigorously characterized after CNS injury, we examined the spatio-temporal distribution of Gal1 in rat spinal cords subjected to a standardized contusion injury. Whereas Gal1 was not expressed in uninjured spinal cord, it was significantly upregulated after SCI, especially within the lesion core. Gal1 was expressed in ~40% of lesion-localized macrophages at 3–28 days post-injury (dpi), and in ~45% of astrocytes in the lesion border at 7–28 dpi. Most lesion-localized Gal1+ macrophages did not express the phagocytosis marker ED1, and Gal1+ cells contained less phagocytosed lipids. These data suggest time- and location-dependent regulation of Gal1 by macrophages (and astrocytes) could be important for modulating phagocytosis, inflammation/gliosis, and axon growth after SCI.

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“…In models of focal brain ischemia and stroke, galectin-1 and -3 were found to be upregulated in astrocytes and microglial cells, respectively (35)(36)(37)(38).…”

Section: Ischemic Conditions Induce the Expression Of Galectin-3 As Wmentioning

confidence: 99%

“…Although the precise functions of galectins under ischemic conditions remain unclear, galectin-1 and -3 may improve the functional recovery of the damaged brain tissues (37,38). Galectin-1, -3, and -9 are strongly expressed in mesenchymal stem cells derived from bone marrow and umbilical cord blood (44)(45)(46)(47).…”

Section: Ischemic Conditions Induce the Expression Of Galectin-3 As Wmentioning

confidence: 99%

Histological Mapping and Subtype-Specific Functions of Galectins in Health and Disease

Nio‐Kobayashi

2018

Trends in Glycoscience and Glycotechnology

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Galectins, β-galactoside-binding lectins, consist of 15 members and are broadly distributed in the mammalian body in organand cell-specific manners. This minireview summarizes current knowledge on the cellular localization of galectin subtypes in various organs including the digestive tract, lymphatic system, respiratory system, urinary system, and reproductive system. We also summarize the specific localization of galectins in the epithelium with a focus on the characteristic morphologies of epithelia. In addition, we discuss the functions of galectins in the reproductive and endocrine systems, pathogenic angiogenesis, and the regulation of stem cells. The regulatory mechanism of galectin expression is also discussed based on findings obtained from luteal cells. Various glycoconjugate ligands for galectins have been identified, and notably the ligands for galectins differ in each galectin-expressing cell. The physiological and pathological states of cells affect the expression of galectin and glycoconjugate ligands, and the extracellular environment, such as the concentration of growth factors, nutrients, and oxygen also controls the expression levels. Future studies to identify the cellular and intracellular localization of galectins using histological analyses will provide a better understanding of the potential functions of galectins in healthy and disease states.

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Galectin-1 Enhances Astrocytic BDNF Production and Improves Functional Outcome in Rats Following Ischemia

Cited by 60 publications

References 38 publications

Astrocytes Protect Neurons in the Hippocampal CA3 Against Ischemia by Suppressing the Intracellular Ca2+ Overload

Astrocytes Protect Neurons in the Hippocampal CA3 Against Ischemia by Suppressing the Intracellular Ca2+ Overload

Galectin-1 in injured rat spinal cord: Implications for macrophage phagocytosis and neural repair

Histological Mapping and Subtype-Specific Functions of Galectins in Health and Disease

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