The Response of Human Colonocytes to Folate Deficiency in Vitro: Functional and Proteomic Analyses

Duthie, Susan J.; Mavrommatis, Yiannis; Rucklidge, Garry J.; Reid, Mark D.; Duncan, Gary; Moyer, Mary Pat; Pirie, Lynn P.; Bestwick, Charles

doi:10.1021/pr700751y

Cited by 39 publications

(47 citation statements)

References 47 publications

(87 reference statements)

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“…Moreover, a proteomics analysis of cells cultured without folate (Duthie et al, 2008) identified 13 proteins that correspond with our results. Nine of these 13 proteins are contained in the group of 14 proteins that are common to HTT1800 and HTT2800 exposure.…”

Section: Discussionsupporting

confidence: 87%

Proteomics-based safety evaluation of multi-walled carbon nanotubes

Haniu

Matsuda

Takeuchi

et al. 2010

Toxicology and Applied Pharmacology

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Section: Discussionsupporting

confidence: 87%

Proteomics-based safety evaluation of multi-walled carbon nanotubes

Haniu

Matsuda

Takeuchi

et al. 2010

Toxicology and Applied Pharmacology

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“…These included collagen VI, α 1 and 2C2 isoforms, vimentin (VIM), tubulin-α (TUBA1B), β -actin (ACTB), vinculin isoform, plastin 3 (PLS3), lamin A/C isoform 2, chaperonin TCP1, caldesmon 1 (CALD1), cofilin 1 and transgelin 2. Changes in cytoskeletal proteins have been also reported for a patient cell line belonging to the cblD complementation group [ 74 ] and also, for human fibroblasts [ 75 ] and colonocytes [ 76 ] under conditions of folate deficiency. Collagen VI, isoform 2C2 was upregulated in cblC fibroblasts.…”

Section: Cytoskeleton: Assembly and Remodelingmentioning

confidence: 65%

Proteomics of vitamin B12 processing

Hannibal

DiBello

Jacobsen³

2013

Clinical Chemistry and Laboratory Medicine

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The causes of cobalamin (B 12 , Cbl) deficiency are multifactorial. Whether nutritional due to poor dietary intake, or functional due to impairments in absorption or intracellular processing and trafficking events, the major symptoms of Cbl deficiency include megaloblastic anemia, neurological deterioration and in extreme cases, failure to thrive and death. The common biomarkers of Cbl deficiency (hyperhomocysteinemia and methylmalonic acidemia) are extremely valuable diagnostic indicators of the condition, but little is known about the changes that occur at the protein level. A mechanistic explanation bridging the physiological changes associated with functional B 12 deficiency with its intracellular processers and carriers is lacking. In this article, we will cover the effects of B 12 deficiency in a cblC -disrupted background (also referred to as MMACHC) as a model of functional Cbl deficiency. As will be shown, major protein changes involve the cytoskeleton, the neurological system as well as signaling and detoxification pathways. Supplementation of cultured MMACHC-mutant cells with hydroxocobalamin (HOCbl) failed to restore these variants to the normal phenotype, suggesting that a defective Cbl processing pathway produces irreversible changes at the protein level.

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“…Proteins were separated by isoelectric focusing in the first dimension [BioRad immobilised pH gradient (IPG) strips (pi range 3-10)] and SDS-PAGE in the second dimension on 8-16 acrylamide gels (18 9 18 cm) as described previously (Duthie et al 2008). Gels were stained with Coomassie blue and imaged on a BioRad GS710 flat bed imager followed by image analysis using PD Quest version 8.0.1.…”

Section: D Gel Electrophoresis Of Aorta Tissuesmentioning

confidence: 99%

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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The Response of Human Colonocytes to Folate Deficiency in Vitro: Functional and Proteomic Analyses

Cited by 39 publications

References 47 publications

Proteomics-based safety evaluation of multi-walled carbon nanotubes

Proteomics-based safety evaluation of multi-walled carbon nanotubes

Proteomics of vitamin B12 processing

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

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