Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases
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...
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oai:doaj.org-article:e15b078cf39b435ea88580a4252dd4512021-11-25T17:10:48ZNovel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases10.3390/cells101130472073-4409https://doaj.org/article/e15b078cf39b435ea88580a4252dd4512021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3047https://doaj.org/toc/2073-4409Galectin-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.Luana C. SoaresOsama Al-DalahmahJames HillisChristopher C. YoungIsaiah AsbedMasanori SakaguchiEric O’NeillFrancis G. SzeleMDPI AGarticlegalectinGalectin-3neurogenesissubventricular zonestem cellsinflammationBiology (General)QH301-705.5ENCells, Vol 10, Iss 3047, p 3047 (2021) |
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galectin Galectin-3 neurogenesis subventricular zone stem cells inflammation Biology (General) QH301-705.5 |
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galectin Galectin-3 neurogenesis subventricular zone stem cells inflammation Biology (General) QH301-705.5 Luana C. Soares Osama Al-Dalahmah James Hillis Christopher C. Young Isaiah Asbed Masanori Sakaguchi Eric O’Neill Francis G. Szele Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases |
description |
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. |
format |
article |
author |
Luana C. Soares Osama Al-Dalahmah James Hillis Christopher C. Young Isaiah Asbed Masanori Sakaguchi Eric O’Neill Francis G. Szele |
author_facet |
Luana C. Soares Osama Al-Dalahmah James Hillis Christopher C. Young Isaiah Asbed Masanori Sakaguchi Eric O’Neill Francis G. Szele |
author_sort |
Luana C. Soares |
title |
Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases |
title_short |
Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases |
title_full |
Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases |
title_fullStr |
Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases |
title_full_unstemmed |
Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases |
title_sort |
novel galectin-3 roles in neurogenesis, inflammation and neurological diseases |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/e15b078cf39b435ea88580a4252dd451 |
work_keys_str_mv |
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