Gelsolin superfamily proteins: key regulators of cellular functions

Silacci, Paolo; Mazzolai, Lucia; Gauci, Charles G.; Stergiopulos, Nikolaos; Yin, Helen L.; Hayoz, Daniel

doi:10.1007/s00018-004-4225-6

Cited by 357 publications

(321 citation statements)

References 98 publications

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“…Moreover, a strong negative relationship between transgelin and saturated fatty acid accumulation in adventitial lipid was observed. Overexpression of gelsolin increases vascular endothelial cell motility (Silacci et al 2003). Gelsolin was elevated in the aorta of ApoE null mice in this study.…”

Section: Discussionsupporting

confidence: 57%

Nutritional B vitamin deficiency alters the expression of key proteins associated with vascular smooth muscle cell proliferation and migration in the aorta of atherosclerotic apolipoprotein E null mice

et al. 2014

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Low B vitamin status is linked with human vascular disease. We employed a proteomic and biochemical approach to determine whether nutritional folate deficiency and/or hyperhomocysteinemia altered metabolic processes linked with atherosclerosis in ApoE null mice. Animals were fed either a control fat (C; 4 % w/w lard) or a high-fat [HF; 21 % w/w lard and cholesterol (0/15 % w/w)] diet with different B vitamin compositions for 16 weeks. Aorta tissue was prepared and global protein expression, B vitamin, homocysteine and lipoprotein status measured. Changes in the expression of aorta proteins were detected in response to multiple B vitamin deficiency combined with a high-fat diet (P \ 0.05) and were strongly linked with lipoprotein concentrations measured directly in the aorta adventitia (P \ 0.001). Pathway analysis revealed treatment effects in the aorta-related primarily to cytoskeletal organisation, smooth muscle cell adhesion and invasiveness (e.g., fibrinogen, moesin, transgelin, vimentin). Combined B vitamin deficiency induced striking quantitative changes in the expression of aorta proteins in atherosclerotic ApoE null mice. Deregulated expression of these proteins is associated with human atherosclerosis. Cellular pathways altered by B vitamin status included cytoskeletal organisation, cell differentiation and migration, oxidative stress and chronic inflammation. These findings provide new insight into the molecular mechanisms through which B vitamin deficiency may accelerate atherosclerosis.

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Section: Discussionsupporting

confidence: 57%

Nutritional B vitamin deficiency alters the expression of key proteins associated with vascular smooth muscle cell proliferation and migration in the aorta of atherosclerotic apolipoprotein E null mice

et al. 2014

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“…Thus it is involved in the control of actin-based cell motility (Silacci et al 2004) and membrane ruffling (phagocytosis) (Witke et al 2001) of non-muscle cells. It was originally isolated from the cytoplasm of alveolar macrophages (Southwick & DiNubile 1986), the prototype of a motile and phagocytotic cell.…”

Section: Known Capg Propertiesmentioning

confidence: 99%

Dynamics of the CapG actin-binding protein in the cell nucleus studied by FRAP and FCS

Renz

Langowski

2008

Chromosome Res

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FRAP (fluorescence recovery after photobleaching) and FCS (fluorescence correlation spectroscopy) are spectroscopic methods for monitoring the dynamic distribution of proteins inside the nucleus of living cells. As an example we report our studies on the intracellular mobility of the actin-binding protein CapG in live breast cancer cells. This Gelsolin-related protein is a putative oncogene. It appears to be overexpressed especially in metastasizing breast cancer. Furthermore, the CapG protein is known to be involved in the motility control of non-muscle benign cells. Its increased expression triggers an increase in cell motility of benign cells. Thus it can be expected that in cancer cells overexpressing the CapG protein, motility, invasiveness and metastasis might be particularly promoted. Since the nuclear CapG fraction seems to be pivotal to the increase in cell motility, we focused our studies on the CapG mobility in cell nuclei of live breast cancer cells. Using FCS and FRAP we showed that the eGFP-tagged CapG is monomeric and characterized its diffusional properties on the microsecond to minute timescale. This information about the mobility and compartmentalization of CapG might help to provide insight into its function within the cell nucleus and give clues about its altered cellular function in malignant dedifferentiation. Abbreviations ACF autocorrelation function CapGGelsolin-related actin binding capping protein CapG-eGFP CapG-eGFP fusion protein eGFP enhanced green fluorescent protein FCS fluorescence correlation spectroscopy FRAP fluorescence recovery after photobleaching NLS nuclear localization signal PI 3-kinase phosphatidylinositol 3-hydroxy kinase PIP 2 -binding phospatidylinositol 4,5-bisphosphate

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“…It blocks the rapidly growing ends of actin filaments (capping), and is involved in the control of actin-based cell motility 6 and membrane ruffling (phagocytosis) 7 of nonmuscle cells. CapG was originally isolated from the cytoplasm of alveolar macrophages, 8 these being the prototype of a motile and phagocytotic cell.…”

mentioning

confidence: 99%

Invasive breast cancer cells exhibit increased mobility of the actin‐binding protein CapG

Renz

Betz

Niederacher

et al. 2008

Intl Journal of Cancer

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The CapG protein, a Gelsolin-related actin-binding protein, is expressed at higher levels in breast cancer, especially in metastasizing breast cancer, than in normal breast epithelium. Furthermore, it is known that an increased expression of the CapG protein triggers an increase in cell motility. According to in vitro experiments, it was supposed that it is the nuclear fraction of the protein, which causes the increase in cell motility. Here, we examined the dynamical distribution of the CapG protein within the living cell, i.e. the import of the CapG protein into the nucleus. The nuclear import kinetics of invasive, metastasizing breast cancer cells were compared to the import kinetics of non-neoplastic cells similar to normal breast epithelium. FRAP kinetics showed a highly significant increase in the recovery of photobleached CapG-eGFP in the cancer cells, so that a differentiation of invasive, metastasizing cells and non-invasive, non-metastasizing cells on the basis of transport processes of the CapG protein between the nucleus and the cytoplasm seems to be possible. Comprehension of the mobility and compartmentalization of the CapG protein in normal and in cancer cells in vivo could constitute a new basis to characterize the invasiveness and metastasizing potential of breast cancer. ' 2007 Wiley-Liss, Inc.

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Gelsolin superfamily proteins: key regulators of cellular functions

Cited by 357 publications

References 98 publications

Nutritional B vitamin deficiency alters the expression of key proteins associated with vascular smooth muscle cell proliferation and migration in the aorta of atherosclerotic apolipoprotein E null mice

Nutritional B vitamin deficiency alters the expression of key proteins associated with vascular smooth muscle cell proliferation and migration in the aorta of atherosclerotic apolipoprotein E null mice

Dynamics of the CapG actin-binding protein in the cell nucleus studied by FRAP and FCS

Invasive breast cancer cells exhibit increased mobility of the actin‐binding protein CapG

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