Galectin-3 Involvement in Cognitive Processes for New Therapeutic Considerations

Mijailović, Nataša R.; Vesić, Katarina; Arsenijević, Dragana; Milojević-Rakić, Maja; Borovcanin, M.

doi:10.3389/fncel.2022.923811

Cited by 11 publications

(10 citation statements)

References 130 publications

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“…Anti-inflammatory factors secreted by M2-type microglia cells can reduce inflammation and improve ischemic brain injury. The neurotrophic factors secreted by it can promote the proliferation of neural precursor cells, accelerate the migration of neuroblasts ( 99 ), promote the maturation of new neurons, and promote the repair of the central nervous system. In addition, after ischemic stroke, M2-type microglia and macrophages, compared with M1 phenotypes, have a stronger phagocytosis capacity for necrotic neurons to remove damaged neurons, prevent secondary inflammatory reactions, and provide survival space for new neurons to maintain the homeostasis of the central nervous system under pathological conditions.…”

Section: Microglia Activation and Cns Disordersmentioning

confidence: 99%

Microglia activation in central nervous system disorders: A review of recent mechanistic investigations and development efforts

Qin

Chen

et al. 2023

Front. Neurol.

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Microglia are the principal resident immune cells in the central nervous system (CNS) and play important roles in the development of CNS disorders. In recent years, there have been significant developments in our understanding of microglia, and we now have greater insight into the temporal and spatial patterns of microglia activation in a variety of CNS disorders, as well as the interactions between microglia and neurons. A variety of signaling pathways have been implicated. However, to date, all published clinical trials have failed to demonstrate efficacy over placebo. This review summarizes the results of recent important studies and attempts to provide a mechanistic view of microglia activation, inflammation, tissue repair, and CNS disorders.

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Section: Microglia Activation and Cns Disordersmentioning

confidence: 99%

Microglia activation in central nervous system disorders: A review of recent mechanistic investigations and development efforts

Qin

Chen

et al. 2023

Front. Neurol.

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“…Future research exploiting mouse models with the neuron-specific deletion of Lifr will help delineate how LIF mediates brain responses to peripheral cancers. On the other hand, the precise identity of Gal3 receptor(s) is currently under debate, 40 – 42 rendering it a challenge to elucidate the molecular mechanism of Gal3 action on the brain. It is possible that Gal3 can function via its putative receptor(s) expressed by neurons.…”

Section: Discussionmentioning

confidence: 99%

Multiple cancer cell types release LIF and Gal3 to hijack neural signals

Xu,

Cao,

Kong

et al. 2024

Cell Res

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Neural signals can significantly influence cancer prognosis. However, how cancer cells may proactively modulate the nervous system to benefit their own survival is incompletely understood. In this study, we report an overlapping pattern of brain responses, including that in the paraventricular nucleus of the hypothalamus, in multiple mouse models of peripheral cancers. A multi-omic screening then identifies leukemia inhibitory factor (LIF) and galectin-3 (Gal3) as the key cytokines released by these cancer cell types to trigger brain activation. Importantly, increased plasma levels of these two cytokines are observed in patients with different cancers. We further demonstrate that pharmacologic or genetic blockage of cancer cell-derived LIF or Gal3 signaling abolishes the brain responses and strongly inhibits tumor growth. In addition, ablation of peripheral sympathetic actions can similarly restore antitumor immunity. These results have elucidated a novel, shared mechanism of multiple cancer cell types hijacking the nervous system to promote tumor progression.

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“…Another player of interest in the complex network of intercellular communication is GALECTIN, a β-galactosidase binding protein that is present in both the nucleus and cytoplasm. GALECTIN is involved in the control of phagocytosis and macropinocytosis ( 29 , 30 ). In summary, our study suggested that CD70 and GALECTIN may be potential biomarkers or targets for the diagnosis and treatment of HFRS.…”

Section: Discussionmentioning

confidence: 99%

Single cells and TRUST4 reveal immunological features of the HFRS transcriptome

Xiao,

Lin,

Liu

et al. 2024

Front. Med.

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The etiology of hemorrhagic fever with renal syndrome (HFRS) is significantly impacted by a variety of immune cells. Nevertheless, the existing techniques for sequencing peripheral blood T cell receptor (TCR) or B cell receptor (BCR) libraries in HFRS are constrained by both limitations and high costs. In this investigation, we utilized the computational tool TRUST4 to generate TCR and BCR libraries utilizing comprehensive RNA-seq data from peripheral blood specimens of HFRS patients. This facilitated the examination of clonality and diversity within immune libraries linked to the condition. Despite previous research on immune cell function, the underlying mechanisms remain intricate, and differential gene expression across immune cell types and cell-to-cell interactions within immune cell clusters have not been thoroughly explored. To address this gap, we performed clustering analysis on 11 cell subsets derived from raw single-cell RNA-seq data, elucidating characteristic changes in cell subset proportions under disease conditions. Additionally, we utilized CellChat, a tool for cell–cell communication analysis, to investigate the impact of MIF family, CD70 family, and GALECTIN family cytokines—known to be involved in cell communication—on immune cell subsets. Furthermore, hdWGCNA analysis identified core genes implicated in HFRS pathogenesis within T cells and B cells. Trajectory analysis revealed that most cell subsets were in a developmental stage, with high expression of transcription factors such as NFKB and JUN in Effector CD8+ T cells, as well as in Naive CD4+ T cells and Naive B cells. Our findings provide a comprehensive understanding of the dynamic changes in immune cells during HFRS pathogenesis, identifying specific V genes and J genes in TCR and BCR that contribute to advancing our knowledge of HFRS. These insights offer potential implications for the diagnosis and treatment of this autoimmune disease.

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Galectin-3 Involvement in Cognitive Processes for New Therapeutic Considerations

Cited by 11 publications

References 130 publications

Microglia activation in central nervous system disorders: A review of recent mechanistic investigations and development efforts

Microglia activation in central nervous system disorders: A review of recent mechanistic investigations and development efforts

Multiple cancer cell types release LIF and Gal3 to hijack neural signals

Single cells and TRUST4 reveal immunological features of the HFRS transcriptome

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