AQP4 knockout impairs proliferation, migration and neuronal differentiation of adult neural stem cells

Kong, Hui; Fan, Yi; Xie, Juan; Ding, Jingzhong; Sha, Luolin; Shi, Xueru; Sun, Xiu‐Lan; Hu, Gang

doi:10.1242/jcs.035758

Cited by 130 publications

(130 citation statements)

References 81 publications

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“…For instance, we reported that cells with endogenous or exogenous, stable or transient, expression of AQP3 treated with Auphen, a potent inhibitor of the glycerol permeability of AQP3, 59 were arrested in the S-G2/M phases of the cell cycle, suggesting the possibility that the inhibition of AQP3 permeability somehow detains the progression of the cell cycle, thereby slowing cell proliferation. 18 In agreement with our results others have found that cell cycle of neurospheres derived from adult neuron stem cells of the subventricular zone (SVZ) in AQP4 knockout mice get arrested at the G2-M stage, 87 functionally implicating AQP4 in the activation and differentiation of the mice SVZ neurogenic niche.…”

Section: Cell Cycle and Aqpssupporting

confidence: 92%

“…In contrast, overexpression of AQP1, AQP8 and AQP9 was observed after lactacystin treatment. [126][127][128] However, favoring a role for AQP4 in apoptosis, Kong et al 87 observed increased basal apoptosis in adult neural stem cells obtained from KO AQP4 ¡/¡ mice.…”

Section: Apoptosis and Aqpsmentioning

confidence: 99%

“…More recent studies have demonstrated involvement of AQP1 in the differentiation of stem-like cells in rat bile duct formation, 144 development of human corneal keratocytes 145 and renewal of limbal basal epithelium from a corneal epithelial stem cell niche, 146 all important roles associated with cell proliferation and differentiation. Moreover, impaired proliferation, migration and neuronal differentiation has been demonstrated in adult neural stem cells derived from AQP4 knockout mice 87 indicating a role for AQP4 in the activation and differentiation of the mice SVZ neurogenic niche.…”

Section: Apoptosis and Aqpsmentioning

confidence: 99%

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Role of aquaporins in cell proliferation: What else beyond water permeability?

2016

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In addition to the extensive data demonstrating the importance of mammalian AQPs for the movement of water and some small solutes across the cell membrane, there is now a growing body of evidence indicating the involvement of these proteins in numerous cellular processes seemingly unrelated, at least some of them in a direct way, to their canonical function of water permeation. Here, we have presented a broad range of evidence demonstrating that these proteins have a role in cell proliferation by various different mechanisms, namely, by allowing fast cell volume regulation during cell division; by affecting progression of cell cycle and helping maintain the balance between proliferation and apoptosis, and by crosstalk with other cell membrane proteins or transcription factors that, in turn, modulate progression of the cell cycle or regulate biosynthesis pathways of cell structural components. In the end, however, after discussing all these data that strongly support a role for AQPs in the cell proliferation process, it remains impossible to conclude that all these other functions attributed to AQPs occur completely independently of their water permeability, and there is a need for new experiments designed specifically to address this interesting issue.

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Section: Cell Cycle and Aqpssupporting

confidence: 92%

Section: Apoptosis and Aqpsmentioning

confidence: 99%

Section: Apoptosis and Aqpsmentioning

confidence: 99%

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Role of aquaporins in cell proliferation: What else beyond water permeability?

2016

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“…Moreover, spontaneous repetitive Ca 2þ spikes may arise in human mesenchymal stem cells (HMSCs) [30,58], adult mice neural stem cells [59], and human cardiac progenitor cells (HCPCs) [60]. Similar to VEGF-induced Ca 2þ waves in ECFCs, the oscillatory response to serum as well as the spontaneous Ca 2þ transients in HMSCs [30] were shaped by the interplay between InsP 3 -dependent Ca 2þ release and SOCE [43,44,57].…”

Section: Discussionmentioning

confidence: 99%

Vascular Endothelial Growth Factor Stimulates Endothelial Colony Forming Cells Proliferation and Tubulogenesis by Inducing Oscillations in Intracellular Ca2+ Concentration

et al. 2011

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Endothelial progenitor cells (EPCs) home from the bone marrow to the site of tissue regeneration and sustain neovascularization after acute vascular injury and upon the angiogenic switch in solid tumors. Therefore, they represent a suitable tool for cell-based therapy (CBT) in regenerative medicine and provide a novel promising target in the fight against cancer. Intracellular Ca2+ signals regulate numerous endothelial functions, such as proliferation and tubulogenesis. The growth of endothelial colony forming cells (ECFCs), which are EPCs capable of acquiring a mature endothelial phenotype, is governed by store-dependent Ca2+ entry (SOCE). This study aimed at investigating the nature and the role of VEGF-elicited Ca2+ signals in ECFCs. VEGF induced asynchronous Ca2+ oscillations, whose latency, amplitude, and frequency were correlated to the growth factor dose. Removal of external Ca2+ (0Ca2+) and SOCE inhibition with N-(4-[3,5-bis(trifluoromethyl)-1H-pyrazol-1-yl]phenyl)-4-methyl-1,2,3-thiadiazole-5-carboxamide (BTP-2) reduced the duration of the oscillatory signal. Blockade of phospholipase C-γ with U73122, emptying the inositol-1,4,5-trisphosphate (InsP3)-sensitive Ca2+ pools with cyclopiazonic acid (CPA), and inhibition of InsP3 receptors with 2-APB prevented the Ca2+ response to VEGF. VEGF-induced ECFC proliferation and tubulogenesis were inhibited by the Ca2+-chelant, BAPTA, and BTP-2. NF-κB activation by VEGF was impaired by BAPTA, BTP-2, and its selective blocker, thymoquinone. Thymoquinone, in turn, suppressed VEGF-dependent ECFC proliferation and tubulogenesis. These data indicate that VEGF-induced Ca2+ oscillations require the interplay between InsP3-dependent Ca2+ release and SOCE, and promote ECFC growth and tubulogenesis by engaging NF-κB. This novel signaling pathway might be exploited to enhance the outcome of CBT and chemotherapy.

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“…70 Aquaporin-4, responsible for water and ion homeostasis in the central nervous system, is also expressed in NSCs and plays important roles in the proliferation, survival, migration and neuronal differentiation of adult VZ NSCs via modulation of intracellular Ca 2+ dynamics. 71 Highly selective pharmacological tools are still lacking for these particular large pore-type channels. Their usefulness as therapeutic targets must therefore be put on hold until such tools are discovered.…”

Section: Involvement Of Other Types Of Channelsmentioning

confidence: 99%