Fibrillation of transferrin

Booyjzsen, Claire; Scarff, Charlotte A.; Moreton, Ben; Portman, Ian; Scrivens, James H.; Costantini, Giovanni; Sadler, Peter J.

doi:10.1016/j.bbagen.2011.11.004

Cited by 14 publications

(16 citation statements)

References 58 publications

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“…Serotransferrin (TF) glycosylation (Taniguchi et al, 2008) and aggregation (Booyjzsen et al, 2012) may play an important role in the pathophysiology of AD and also modulate the homeostasis of full-length APP (Khachaturian, 2008). Secretory carrierassociated membrane protein 1 (SCAMP1) and AP2-associated protein kinase 1 (AAK1) decreases the TF uptake by endocytosis suggesting their role in endocytosis via a mechanism, which may involve the recruitment of clathrin coats to the plasma membrane and the transGolgi network (Fernandez-Chacon et al, 2000, Conner andSchmid, 2002).…”

Section: Relationships Of Chronic Cerebral Hypoperfusion Altered Synamentioning

confidence: 99%

Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex

et al. 2017

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Chronic cerebral hypoperfusion (CCH) evokes mild cognitive impairment (MCI) and contributes to the progression of vascular dementia and Alzheimer's disease (AD). How CCH 2 induces these neurodegenerative processes that may spread along the synaptic network and whether they are detectable at the synaptic proteome level of the cerebral cortex remains to be established.In the present study, we report the synaptic protein changes in the cerebral cortex after stepwise bilateral common carotid artery occlusion (BCCAO) induced CCH in the rat. The occlusions were confirmed with Magnetic Resonance Angiography 5 weeks after the surgery.Synaptosome fractions were prepared using sucrose gradient centrifugation from cerebral cortex dissected 7 weeks after the occlusion. The synaptic protein differences between the sham operated and CCH groups were analysed with label free nanoUHPLC-MS/MS.

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Section: Relationships Of Chronic Cerebral Hypoperfusion Altered Synamentioning

confidence: 99%

Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex

et al. 2017

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“…However, TF is a high abundant protein in the plasma [20]. In present study, we applied human iPSC-derived cardiomyocytes model to evaluate the effect of TF.…”

Section: Discussionmentioning

confidence: 99%

Role of augmented transferrin during the retraining for undeveloped left ventricle

Wei

Ying

et al. 2015

J Cellular Molecular Medi

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Transposition of great arteries (TGA) is a common congenital heart disease. Left ventricle (LV) is rapidly regressing and pulmonary artery banding (PAB) is utilized to retrain the undeveloped LV. Hence, it offered a unique human disease model to investigate the process of LV hypertrophy under pressure overload. Eight late referred children with TGA were enrolled. The plasma was collected at the 30 min. before and 48 hrs after PAB, and 25 proteins were identified as having significant change in proteomic analysis. Transferrin (TF) and ceruloplasmin were then confirmed. After 48 hrs incubation with TF, the size of human induced pluripotent stem cell-derived cardiomyocytes increased by two times as large as control. Meanwhile, protein synthesis and the expression of natriuretic peptide precursor A and B were significantly enhanced. TF treatment also activated both extracellular signal-regulated kinase 1/2 and activated protein kinase singling pathways. Our data provided a link to molecular components and pathways that might be involved in LV retraining. TF severed as the carrier to delivery irons, and could directly stimulate cardiomyocytes hypertrophy. TF administration may hold therapeutic potential for the biological LV retraining.

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“…More recently, it has been observed that transferrin can form fibrils under certain conditions in vitro , and this led to an investigation to determine whether transferrin has amyloid-like properties. Synchrotron X-ray circular dichroism (XCD) was used to test whether transferrin in solution has amyloid-like properties, and this helped show that transferrin aggregation in solution does not appear to involve major structural changes to the protein, or formation of beta-pleated sheets (Booyjzsen et al, 2012). …”

Section: Iron-binding Proteins and Aggregationmentioning

confidence: 99%

The role of iron in neurodegenerative disorders: insights and opportunities with synchrotron light

Collingwood¹,

Davidson²

2014

Front. Pharmacol.

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There is evidence for iron dysregulation in many forms of disease, including a broad spectrum of neurodegenerative disorders. In order to advance our understanding of the pathophysiological role of iron, it is helpful to be able to determine in detail the distribution of iron as it relates to metabolites, proteins, cells, and tissues, the chemical state and local environment of iron, and its relationship with other metal elements. Synchrotron light sources, providing primarily X-ray beams accompanied by access to longer wavelengths such as infra-red, are an outstanding tool for multi-modal non-destructive analysis of iron in these systems. The micro- and nano-focused X-ray beams that are generated at synchrotron facilities enable measurement of iron and other transition metal elements to be performed with outstanding analytic sensitivity and specificity. Recent developments have increased the scope for methods such as X-ray fluorescence mapping to be used quantitatively rather than semi-quantitatively. Burgeoning interest, coupled with technical advances and beamline development at synchrotron facilities, has led to substantial improvements in resources and methodologies in the field over the past decade. In this paper we will consider how the field has evolved with regard to the study of iron in proteins, cells, and brain tissue, and identify challenges in sample preparation and analysis. Selected examples will be used to illustrate the contribution, and future potential, of synchrotron X-ray analysis for the characterization of iron in model systems exhibiting iron dysregulation, and for human cases of neurodegenerative disorders including Alzheimer’s disease, Parkinson’s disease, Friedreich’s ataxia, and amyotrophic lateral sclerosis.

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Fibrillation of transferrin

Cited by 14 publications

References 58 publications

Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex

Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex

Role of augmented transferrin during the retraining for undeveloped left ventricle

The role of iron in neurodegenerative disorders: insights and opportunities with synchrotron light

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