VCAM1 Labels a Subpopulation of Neural Stem Cells in the Adult Hippocampus and Contributes to Spatial Memory

Dan-Ying, Wang; Luo, An-Feng; Bai, Qing-Ran; Gong, Xia; Zheng, Yi; Shen, Qin; Hu, Xiaoling; Wang, Xiaomin

doi:10.1016/j.stemcr.2020.05.012

Cited by 8 publications

(9 citation statements)

References 59 publications

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“…We searched the literature for candidate genes/proteins exhibiting dynamic level changes during the transition period in NSCs. Vcam1 is expressed by both embryonic and adult NSCs 46,60 . Interestingly, the Vcam1 protein is widespread in the embryonic germinal zone and the distribution becomes more restricted in the V-SVZ during the first three postnatal weeks as radial glial transition into adult NSCs 46 .…”

Section: Resultsmentioning

confidence: 99%

“…Interestingly, the Vcam1 protein is widespread in the embryonic germinal zone and the distribution becomes more restricted in the V-SVZ during the first three postnatal weeks as radial glial transition into adult NSCs 46 . Importantly, Vcam1 maintains the subpopulation of embryonic NSCs destined to become adult neural stem cells 46 ; NSCs are prematurely depleted in Vcam1 -knockout mice 60 . Furthermore, Vcam1 is necessary for maintaining the V-SVZ structure in adults 61 .…”

Section: Resultsmentioning

confidence: 99%

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Prdm16 and Vcam1 regulate the postnatal disappearance of embryonic radial glia and the ending of cortical neurogenesis

Godoy

Zhang

et al. 2023

Preprint

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Embryonic neural stem cells (NSCs, i.e., radial glia) in the ventricular-subventricular zone (V-SVZ) generate the majority of neurons and glia in the forebrain. Postnatally, embryonic radial glia disappear and a subpopulation of radial glia transition into adult NSCs. As this transition occurs, widespread neurogenesis in brain regions such as the cerebral cortex ends. The mechanisms that regulate the postnatal disappearance of radial glia and the ending of embryonic neurogenesis remain poorly understood. Here, we show that PR domain-containing 16 (Prdm16) promotes the disappearance of radial glia and the ending of neurogenesis in the cerebral cortex. Genetic deletion of Prdm16 from NSCs leads to the persistence of radial glia in the adult V-SVZ and prolonged postnatal cortical neurogenesis. Mechanistically, Prdm16 induces the postnatal reduction in Vascular Cell Adhesion Molecule 1 (Vcam1). The postnatal disappearance of radial glia and the ending of cortical neurogenesis occur normally in Prdm16-Vcam1 double conditional knockout mice. These observations reveal novel molecular regulators of the postnatal disappearance of radial glia and the ending of embryonic neurogenesis, filling a key knowledge gap in NSC biology.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Prdm16 and Vcam1 regulate the postnatal disappearance of embryonic radial glia and the ending of cortical neurogenesis

Godoy

Zhang

et al. 2023

Preprint

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“…6E ). It was reported that VCAM1 + cells exhibited more stem cell characteristics in neural stem cell populations [ 29 ], which implies that stem cells may express high levels of VCAM1. In fact, a positive correlation between LSC level and VCAM1 expression was observed in the datasets GSE92969 and GSE115549 [ 4 , 6 ].…”

Section: Resultsmentioning

confidence: 99%

Loss of IRF7 accelerates acute myeloid leukemia progression and induces VCAM1-VLA-4 mediated intracerebral invasion

et al. 2022

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Interferon regulatory factor 7 (IRF7) is widely studied in inflammatory models. Its effects on malignant progression have been documented mainly from the perspective of the microenvironment. However, its role in leukemia has not been established. Here we used MLL-AF9-induced acute myeloid leukemia (AML) mouse models with IRF7 knockout or overexpression and xenograft mouse models to explore the intrinsic effects of IRF7 in AML. AML-IRF7−/− mice exhibited accelerated disease progression with intracerebral invasion of AML cells. AML-IRF7−/− cells showed increased proliferation and elevated leukemia stem cell (LSC) levels. Overexpression of IRF7 in AML cells decreased cell proliferation and LSC levels. Furthermore, overexpression of transforming growth-interacting factor 1 (TGIF1) rescued the enhanced proliferation and high LSC levels caused by IRF7 deficiency. Moreover, upregulation of vascular cell adhesion molecule 1 (VCAM1), which correlated with high LSC levels, was detected in AML-IRF7−/− cells. In addition, blocking VCAM1-very late antigen 4 (VLA-4) axis delayed disease progression and attenuated intracerebral invasion of AML cells. Therefore, our findings uncover the intrinsic effects of IRF7 in AML and provide a potential strategy to control central nervous system myeloid leukemia.

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“…Double-immunostaining revealed that these Mito-tracker-positive cells coexpress well with nestin ( Figure 3(b) ), suggesting the neural progenitor identity of these cells. There are two populations of progenitors in the hippocampus, active neural stem cells (aNSCs), and quiescent neural stem cells (qNSCs) [ 16 ], which could be roughly identified by morphology and play important roles in the cognitive function of the hippocampus [ 17 ], namely, aNSCs are horizontal and qNSCs are radial [ 16 ]. To explore if exogenous mitochondria regulate the behavior of neural progenitors in the hippocampus, we focused on Wnt/ β -catenin signal transduction, a pivotal signal path, which regulates the balance of qNSCs and aNSCs [ 16 ], via a Wnt signal transduction reporting mice line, TOPGAL mice [ 18 ].…”

Section: Resultsmentioning

confidence: 99%

Hippocampal Mitochondrial Transplantation Alleviates Age-Associated Cognitive Decline via Enhancing Wnt Signaling and Neurogenesis

Zhang

Wei

et al. 2022

Computational Intelligence and Neuroscience

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Gradual cognition decline and mitochondrial dysfunction are two notable changes closely associated with aging. Enhancing mitochondrial function has been assumed to be antiaging. However, most current mitochondria-promoting agents usually target 1-2 aspects of mitochondrial function. In the present study, we transplanted mitochondria isolated from young mice into the hippocampus of aged mice, which presumably boost mitochondrial function more thoroughly, examined the effects on cognition, and explored the possible underlying mechanism. Our data showed that exogenous mitochondria were efficiently internalized by nestin-positive neural progenitors in the hippocampus. Mitochondrial transplantation quickly increased ATP levels, enhanced the activity of mitochondrial complexes I, II, and IV, and decreased Tom20 expression in the hippocampus. In regard of cognitive function, mitochondria-treated mice displayed a remarkable improvement of novel object recognition and spatial memory. Utilizing the Wnt signaling reporting mouse line, TOPGAL mice, we detected activated canonical Wnt signaling in the neural progenitors of the mitochondria-treated hippocampus. Further, BrdU labeling showed that exogenous mitochondria significantly stimulated neural progenitor neurogenesis and proliferation. Taken together, our data demonstrated that exogenous mitochondria from young mice might be a novel way of rejuvenating the function of hippocampal neural progenitors to exert antiaging effects.

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VCAM1 Labels a Subpopulation of Neural Stem Cells in the Adult Hippocampus and Contributes to Spatial Memory

Cited by 8 publications

References 59 publications

Prdm16 and Vcam1 regulate the postnatal disappearance of embryonic radial glia and the ending of cortical neurogenesis

Prdm16 and Vcam1 regulate the postnatal disappearance of embryonic radial glia and the ending of cortical neurogenesis

Loss of IRF7 accelerates acute myeloid leukemia progression and induces VCAM1-VLA-4 mediated intracerebral invasion

Hippocampal Mitochondrial Transplantation Alleviates Age-Associated Cognitive Decline via Enhancing Wnt Signaling and Neurogenesis

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