Water flux in cell motility: Expanding the mechanisms of membrane protrusion

Loitto, Vesa; Karlsson, Thommie; Magnusson, Karl‐Eric

doi:10.1002/cm.20357

Cited by 56 publications

(53 citation statements)

References 92 publications

(114 reference statements)

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“…Previous data from our group and others have shown how this AHL communication affect human host cells such as migration and phagocytosis [4,147,152,155,156,188,225,237,238]. In cell motility the aquaporins play an important role for the formation membrane protrusions [17,40,58,77,80]. Here we therefore studied the impact of lasI/rhlI genes in P. aeruginosa on macrophage phagocytosis and AQP9 expression.…”

Section: Resultsmentioning

confidence: 94%

“…In inflammation and infection the volume and shape regulation of cells is highly important in the recognition of cell damage, cell motility, as well as in phagocytosis [17,48,[57][58][59]. Cell migration is a prerequisite for human life and development and it is an essential part of the human immune response.…”

Section: Cell Migrationmentioning

confidence: 99%

“…As mentioned earlier several groups have shown the importance of AQPs in cell migration [13,18,30,48,58,75]. Karlsson et al [31,40,76], have, for instance, shown how AQP9 is involved in the formation of cellular protrusion and blebs, as well as in the process of cell migration.…”

Section: Aquaporins In Cell Migrationmentioning

confidence: 99%

“…Thus allowing the actin polymerization with all its protein machinery to take place, rendering formation of cellular protrusions such as filopodia [48,49,58]. AQP9 has also been proposed to be involved in both single cell and multicellular migration.…”

Section: Aquaporins In Cell Migrationmentioning

confidence: 99%

“…This is largely driven by transmembrane water fluxes through AQPs, primarily AQP9 in leukocytes [31,40,58]. Since phagocytosis of wild type P. aeruginosa was increased compared to its lasI-/rhlI-mutant, we addressed whether AQP9 was involved in this process by looking at the expression levels of AQP9 in macrophages after P. aeruginosa infection.…”

Section: Increased Aqp9 Protein Levels P Aeruginosa Infected Macrophmentioning

confidence: 99%

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Aquaporins in Infection and Inflammation

Holm¹

2016

Linköping University Medical Dissertations

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About the cover:The front cover displays a human, blood-derived macrophage stained for aquaporin 9.During the course of the research underlying this thesis, Angelika Holm was enrolled in Forum Scientium, a multidisciplinary doctoral programme at Linköping University Printed by LiU-Tryck, Linköping, Sweden, 2016 "Be brave, even if you're not, pretend to be. No one can tell the difference."To that young, awkward, tall girl who dared to dream of something else, something more:You did it. SUPERVISOR Elena VikströmDepartment of Clinical and Experimental Medicine Linköping University Linköping Sweden When cells of the innate immune system encounter pathogens they need to respond and prepare for migration and phagocytosis and do so through volume regulatory processes. The Gramnegative bacterium Pseudomonas aeruginosa utilizes a small molecule-based communication system, called quorum sensing (QS) to control the production of its virulence factors and biofilms. We found that P. aeruginosa with a complete QS system elicits a stronger phagocytic response in human blood-derived macrophages compared to its lasI-/rhlI-mutant lacking the production of the QS molecules N-butyryl-L-homoserine lactone (C4-HSL) and N-3-oxododecanoyl-L-homoserine lactone (3O-C12-HSL). Infection with P. aeruginosa further increases the expression of AQP9 and induces re-localisation of AQP9 to the front and trailing ends of macrophages. Moreover, the 3O-C12-HSL alone elevates the expression of AQP9, redistribute the water channel to the front and rear ends and increases the cell area and volume of macrophages. Both infection with the wild type P. aeruginosa and the treatment with 3O-C12-HSL change the nano-structural architecture of the AQP9 distribution in macrophages. ASSISTANT SUPERVISORS Karl-Eric MagnussonViruses use the intracellular machinery of the invaded cells to produce and assemble new viral bodies. Intracellular AQPs are localised in a membranes of cellular organelles to regulate their function and morphology. C3H10T1/2 fibroblasts transiently expressing green fluorescent protein (GFP)-AQP6 show a reduced expression of AQP6 after Hazara virus infection and an increased cell area. Overexpressing AQP6 in C3H10T1/2 cells reduces the infectivity of Hazara virus indicating that AQP6 expression has a protective role in virus infections.Ion and water channels in the epithelial cell lining tightly regulate the water homeostasis. In microscopic colitis (MC), patients suffer from severe watery diarrhoeas. For the first time, we have shown that the expression of AQP1, 8 and 11 and the sodium/hydrogen exchanger NHE1 are reduced in colonic biopsies from MC patients compared to healthy control individuals. Following treatment with the glucocorticoid budesonide the patients experienced a rapid recovery and we observed a restored or increased expression of the AQPs and NHE1 during treatment, suggesting a role for AQPs in the diarrhoeal mechanisms in MC.Taken together, this thesis provides new evidence on the importance of water homeostasis regulatio...

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Section: Resultsmentioning

confidence: 94%

Section: Cell Migrationmentioning

confidence: 99%

Section: Aquaporins In Cell Migrationmentioning

confidence: 99%

Section: Aquaporins In Cell Migrationmentioning

confidence: 99%

Section: Increased Aqp9 Protein Levels P Aeruginosa Infected Macrophmentioning

confidence: 99%

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Aquaporins in Infection and Inflammation

Holm¹

2016

Linköping University Medical Dissertations

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A novel role for MLC1 in regulating astrocyte–synapse interactions

Kater

Baumgart

Badia‐Soteras

et al. 2023

Glia

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Loss of function of the astrocyte membrane protein MLC1 is the primary genetic cause of the rare white matter disease Megalencephalic Leukoencephalopathy with subcortical Cysts (MLC), which is characterized by disrupted brain ion and water homeostasis. MLC1 is prominently present around fluid barriers in the brain, such as in astrocyte endfeet contacting blood vessels and in processes contacting the meninges. Whether the protein plays a role in other astrocyte domains is unknown. Here, we show that MLC1 is present in distal astrocyte processes, also known as perisynaptic astrocyte processes (PAPs) or astrocyte leaflets, which closely interact with excitatory synapses in the CA1 region of the hippocampus. We find that the PAP tip extending toward excitatory synapses is shortened in Mlc1-null mice. This affects glutamatergic synaptic transmission, resulting in a reduced rate of spontaneous release events and slower glutamate re-uptake under challenging conditions. Moreover, while PAPs in wildtype mice retract from the synapse upon fear conditioning, we reveal that this structural plasticity is disturbed in Mlc1-null mice, where PAPs are already shorter. Finally, Mlc1-null mice show reduced contextual fear memory. In conclusion, our study uncovers an unexpected role for the astrocyte protein MLC1 in regulating the structure of PAPs. Loss of MLC1 alters excitatory synaptic transmission, prevents normal PAP remodeling induced by fear conditioning and disrupts Mandy S. J. Kater and Katharina F. Baumgart shared first authorship.

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Aquaporin-1 facilitates angiogenic invasion in the pathological neovasculature that accompanies cirrhosis

et al. 2010

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Increasing evidence suggests that hepatic fibrosis and pathological angiogenesis are interdependent processes that occur in parallel. Endothelial cell invasion is requisite for angiogenesis, and thus studies of the mechanisms governing liver endothelial cell (LEC) invasion during cirrhosis are of great importance. Emerging research implicates amoeboid-type motility and membrane blebbing as features that may facilitate invasion through matrix-rich microenvironments. Aquaporins (AQPs) are integral membrane water channels, recognized for their importance in epithelial secretion and absorption. However, recent studies also suggest links between water transport and cell motility or invasion. Therefore, the purpose of this study was to test the hypothesis that AQP-1 is involved in amoeboid motility and angiogenic invasion during cirrhosis. AQP-1 expression and localization was examined in normal and cirrhotic liver tissues derived from human and mouse. AQP-1 levels were modulated in LEC using retroviral overexpression or small interfering RNA (siRNA) knockdown and functional effects on invasion, membrane blebbing dynamics, and osmotic water permeability were assayed. Results demonstrate that AQP-1 is upregulated in the small, angiogenic, neovasculature within the fibrotic septa of cirrhotic liver. AQP-1 overexpression promotes fibroblast growth factor (FGF)-induced dynamic membrane blebbing in LEC, which is sufficient to augment invasion through extracellular matrix. Additionally, AQP-1 localizes to plasma membrane blebs, where it increases osmotic water permeability and locally facilitates the rapid, trans-membrane flux of water. Conclusion: AQP-1 enhances osmotic water permeability and FGF-induced dynamic membrane blebbing in LEC and thereby drives invasion and pathological angiogenesis during cirrhosis. (HEPATOLOGY 2010;52:238-248)

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Water flux in cell motility: Expanding the mechanisms of membrane protrusion

Cited by 56 publications

References 92 publications

Aquaporins in Infection and Inflammation

Aquaporins in Infection and Inflammation

A novel role for MLC1 in regulating astrocyte–synapse interactions

Aquaporin-1 facilitates angiogenic invasion in the pathological neovasculature that accompanies cirrhosis

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