Frizzled-1 receptor regulates adult hippocampal neurogenesis

Mardones, Muriel D.; Andaur, Gabriela A.; Varas-Godoy, Manuel; Henriquez, Jenny F.; Salech, Felipe; Behrens, María Isabel; Couve, Andrés; Inestrosa, Nibaldo C.; Varela-Nallar, Lorena

doi:10.1186/s13041-016-0209-3

Cited by 65 publications

(49 citation statements)

References 56 publications

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“…AHPs were isolated from the hippocampus of 10 female 6‐week‐old C57/BL6 mice, and cultured in monolayers as previously described . Cell suspension was plated in pretreated plates coated with poly‐ d ‐lysine and laminin (Thermo Fischer Scientific, Waltham, MA) .…”

Section: Methodsmentioning

confidence: 99%

“…Also, it was determined that soluble Wnt signaling inhibitors dickkopf‐1 (Dkk1) and secreted frizzled‐related protein 3 (sFRP3) are endogenous negative regulators of neurogenesis in the adult mouse hippocampus . More recently, a role for Wnt receptors FZD1 and FZD3 in specific stages of neurogenesis was determined . Regarding Wnt ligands, overexpression of Wnt3 that stimulates Wnt/β‐catenin signaling in adult neural progenitor cells (NPCs) induced neurogenesis in the rat hippocampus .…”

Section: Introductionmentioning

confidence: 99%

“…34,35 More recently, a role for Wnt receptors FZD1 and FZD3 in specific stages of neurogenesis was determined. 36,37 Regarding Wnt ligands, overexpression of Wnt3 that stimulates Wnt/β-catenin signaling in adult neural progenitor cells (NPCs) induced neurogenesis in the rat hippocampus. 33 However, little is known about endogenous ligands that regulate neurogenesis in the adult brain.…”

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confidence: 99%

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Wnt5a promotes differentiation and development of adult-born neurons in the hippocampus by noncanonical Wnt signaling

et al. 2019

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In the adult hippocampus, new neurons are generated in the dentate gyrus. The Wnt signaling pathway regulates this process, but little is known about the endogenous Wnt ligands involved. We investigated the role of Wnt5a on adult hippocampal neurogenesis. Wnt5a regulates neuronal morphogenesis during embryonic development, and maintains dendritic architecture of pyramidal neurons in the adult hippocampus. Here, we determined that Wnt5a knockdown in the mouse dentate gyrus by lentivirus‐mediated shRNA impaired neuronal differentiation of progenitor cells, and reduced dendritic development of adult‐born neurons. In cultured adult hippocampal progenitors (AHPs), Wnt5a knockdown reduced neuronal differentiation and morphological development of AHP‐derived neurons, whereas treatment with Wnt5a had the opposite effect. Interestingly, no changes in astrocytic differentiation were observed in vivo or in vitro, suggesting that Wnt5a does not affect fate‐commitment. By using specific inhibitors, we determined that Wnt5a signals through CaMKII to induce neurogenesis, and promotes dendritic development of newborn neurons through activating Wnt/JNK and Wnt/CaMKII signaling. Our results indicate Wnt5a as a niche factor in the adult hippocampus that promotes neuronal differentiation and development through activation of noncanonical Wnt signaling pathways.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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Wnt5a promotes differentiation and development of adult-born neurons in the hippocampus by noncanonical Wnt signaling

et al. 2019

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“…Furthermore, Wnt signaling was observed in adult mouse subventricular zone (SVZ) NSCs (16) and in adult dentate gyrus. The Wnt receptor FZD1 is mainly expressed in NSCs and serves to amplifyprogenitors and immature neurons (17). These findings provide evidence that the Wnt pathway is involved in adult stem cell maintenance and neurogenesis.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia stimulates neural stem cell proliferation by increasing HIF"‘1Î± expression and activating Wnt/Î²-catenin signaling

Zhang

Chen

et al. 2017

Cell Mol Biol (Noisy-le-grand)

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Evidence indicates that after brain injury, neurogenesis is enhanced in regions such as hippocampus, striatum, and cortex. To study the role of hypoxia-inducible factor-1 (HIF−1α) and Wnt signaling in cerebral ischemia/hypoxia-induced proliferation of neural stem cells (NSCs), we investigated the proliferation of NSCs, expression of HIF−1α, and activation of Wnt signaling under conditions of pathologic hypoxia in vitro. NSCs were isolated from 30-day-old Sprague–Dawley rats and subjected to 0.3% oxygen in a microaerophilic incubation system. Cell proliferation was evaluated by measuring the diameter of neurospheres and by bromodeoxyuridine incorporation assays. Real-time quantitative PCR and Western blotting were used to detect mRNA and protein levels of HIF-1α, β-catenin, and cyclin D1 in the NSCs. The results showed that hypoxia increased NSC proliferation and the levels of HIF-1α, β−catenin, and cyclin D1 (p < 0.05). Blockade of the Wnt signaling pathway decreased hypoxia-induced NSC proliferation, whereas activation of this pathway increased hypoxia-induced NSC proliferation (p < 0.05). Knockdown of HIF-1α with HIF-1α siRNA decreased β−catenin nuclear translocation and cyclin D1 expression, and inhibited proliferation of NSCs (p < 0.05). These findings indicate that pathologic hypoxia stimulates NSC proliferation by increasing expression of HIF-1α and activating the Wnt/β-catenin signaling pathway. The data suggest that Wnt/β-catenin signaling may play a key role in NSC proliferation under conditions of pathologic hypoxia.

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“…For example, Fzd1 regulates cell fate commitment, and Fzd1 knockdown markedly decreases newborn neurons and increases the generation of astrocytes in adult hippocampus. 14 Overexpression of Gfap-GSK3b in neural precursor cells increases NSCs, mature granule neurons and dental gyrus volume. Transgenic mice also show a higher rating in memory tasks.…”

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confidence: 99%