Melatonin Decreases Circulating Levels of Galectin-3 and Cytokines, Motor Activity, and Anxiety Following Acute Global Cerebral Ischemia in Male Rats

Fenton-Navarro, B; Ríos, Diana Garduño; Torner, Luz; Letechipía-Vallejo, Graciela; Cervantes, Miguel

doi:10.1016/j.arcmed.2021.01.009

Cited by 9 publications

(5 citation statements)

References 60 publications

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“…Furthermore, some compounds with protective effects on stroke, such as the Chinese medicine QiShenYiQi, melatonin, and modified citrus pectin (MCP), exert their effects through decreased expression of Gal-3 [ 149 , 150 ] or its inhibition [ 151 ]. In keeping with this view, in 2020, a preliminary study has demonstrated that the administration of the Gal-3 inhibitor MCP ameliorates brain oedema and neuronal score in an experimental mouse model of subarachnoid haemorrhage [ 152 ].…”

Section: Galectin-3 In Main Neurodegenerative Diseasesmentioning

confidence: 99%

Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration

et al. 2022

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The advent of high-throughput single-cell transcriptomic analysis of microglia has revealed different phenotypes that are inherently associated with disease conditions. A common feature of some of these activated phenotypes is the upregulation of galectin-3. Representative examples of these phenotypes include disease-associated microglia (DAM) and white-associated microglia (WAM), whose role(s) in neuroprotection/neurotoxicity is a matter of high interest in the microglia community. In this review, we summarise the main findings that demonstrate the ability of galectin-3 to interact with key pattern recognition receptors, including, among others, TLR4 and TREM2 and the importance of galectin-3 in the regulation of microglia activation. Finally, we discuss increasing evidence supporting the involvement of this lectin in the main neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, multiple sclerosis, traumatic brain injury, and stroke.

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Section: Galectin-3 In Main Neurodegenerative Diseasesmentioning

confidence: 99%

Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration

et al. 2022

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“…Levels of Gal-3 in the serum of patients is associated with severity and progression of ischemic stroke [166]. Treatment with melatonin after ischemic stroke is neuroprotective, reduces levels of Gal-3 and ameliorates hyperactivity and anxiety in rats [167]. However, a recent study showed that treatment with Gal-3 is protective to stroke (MCAO in rats), preventing apoptosis and neurodegeneration [168].…”

Section: Galectin-3 Functions In Adult Strokementioning

confidence: 99%

Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases

Soares

Al‐Dalahmah

Hillis

et al. 2021

Cells

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Galectin-3 (Gal-3) is an evolutionarily conserved and multifunctional protein that drives inflammation in disease. Gal-3’s role in the central nervous system has been less studied than in the immune system. However, recent studies show it exacerbates Alzheimer’s disease and is upregulated in a large variety of brain injuries, while loss of Gal-3 function can diminish symptoms of neurodegenerative diseases such as Alzheimer’s. Several novel molecular pathways for Gal-3 were recently uncovered. It is a natural ligand for TREM2 (triggering receptor expressed on myeloid cells), TLR4 (Toll-like receptor 4), and IR (insulin receptor). Gal-3 regulates a number of pathways including stimulation of bone morphogenetic protein (BMP) signaling and modulating Wnt signalling in a context-dependent manner. Gal-3 typically acts in pathology but is now known to affect subventricular zone (SVZ) neurogenesis and gliogenesis in the healthy brain. Despite its myriad interactors, Gal-3 has surprisingly specific and important functions in regulating SVZ neurogenesis in disease. Gal-1, a similar lectin often co-expressed with Gal-3, also has profound effects on brain pathology and adult neurogenesis. Remarkably, Gal-3’s carbohydrate recognition domain bears structural similarity to the SARS-CoV-2 virus spike protein necessary for cell entry. Gal-3 can be targeted pharmacologically and is a valid target for several diseases involving brain inflammation. The wealth of molecular pathways now known further suggest its modulation could be therapeutically useful.

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“…Previous research showed reduced melatonin levels lead to anxious behavior in animals (Fenton-Navarro et al, 2021 ; Wang et al, 2021 ), and we tested whether melatonin treatment of nomo1 −/− has an ameliorative effect on their behavior. The results showed that MT treatment significantly rescued the overactive locomotor behavior of nomo1 −/ − (Fig.…”

Section: Resultsmentioning

confidence: 99%

Nomo1 deficiency causes autism-like behavior in zebrafish

Zhang,

Li,

et al. 2024

EMBO Rep

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Patients with neuropsychiatric disorders often exhibit a combination of clinical symptoms such as autism, epilepsy, or schizophrenia, complicating diagnosis and development of therapeutic strategies. Functional studies of novel genes associated with co-morbidities can provide clues to understand the pathogenic mechanisms and interventions. NOMO1 is one of the candidate genes located at 16p13.11, a hotspot of neuropsychiatric diseases. Here, we generate nomo1−/− zebrafish to get further insight into the function of NOMO1. Nomo1 mutants show abnormal brain and neuronal development and activation of apoptosis and inflammation-related pathways in the brain. Adult Nomo1-deficient zebrafish exhibit multiple neuropsychiatric behaviors such as hyperactive locomotor activity, social deficits, and repetitive stereotypic behaviors. The Habenular nucleus and the pineal gland in the telencephalon are affected, and the melatonin level of nomo1−/− is reduced. Melatonin treatment restores locomotor activity, reduces repetitive stereotypic behaviors, and rescues the noninfectious brain inflammatory responses caused by nomo1 deficiency. These results suggest melatonin supplementation as a potential therapeutic regimen for neuropsychiatric disorders caused by NOMO1 deficiency.

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Melatonin Decreases Circulating Levels of Galectin-3 and Cytokines, Motor Activity, and Anxiety Following Acute Global Cerebral Ischemia in Male Rats

Cited by 9 publications

References 60 publications

Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration

Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration

Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases

Nomo1 deficiency causes autism-like behavior in zebrafish

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