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Effect of vitamin D in vascular and endocrine cells


Project Description

Vitamin D3 deficiency is a common public health problem worldwide that is increasingly believed to contribute not only to decreased bone mineralisation but potentially to other serious medical conditions. Interestingly, there is even increasing evidence of links between obesity and vitamin D3 deficiency. However, the mechanisms underlying these associations remain poorly understood. This project will look at the cellular actions of 1,25(OH)2 vitamin D3 formation on vascular cells and on cells of the endocrine system, with particular regard to understanding how the vitamin D signals within the cells. Since chronic kidney disease is associated with low vitamin D levels and life-threatening vascular calcification the project will also look at the role of the vitamin D receptor in smooth muscle cells mineralisation. The techniques involved in this project include hormone assay, live cell calcium imaging, kinase assays and transfection with siRNAs for the selective knockdown of calciotropic signal regulators.

Training/techniques to be provided:

Intracellular signalling measured using a) FRET-based cell imaging and b) Epifluorescence microscopy
Cell culture, transfection, gene knockdown and cell assay. Smooth Muscle Cell mineralisation
Molecular techniques including Immunoblotting, Immunofluorescence, RT-PCR and mutagenesis

Funding Notes

Candidates are expected to hold (or be about to obtain) a minimum upper second class honours degree (or equivalent) in a related area / subject.

This project has a Band 3 fee. Details of our different fee bands can be found on our website (View Website). For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website (View Website).

Informal enquiries may be made directly to the primary supervisor.

References

Absi M, Ward DT. (2013). Increased Endothelin-1 Responsiveness in Human Coronary Artery Smooth Muscle Cells Exposed to 1,25-Dihydroxyvitamin D3. Am J Physiol Cell Physiol, 304, C666-C672.

Ward DT, Mughal MZ, Ranieri M, Dvorak MM, Valenti G, Riccardi D (2013) Molecular and Clinical Analysis of a Neonatal Severe Hyperparathyroidism Case Caused by a Stop Mutation in the Calcium-Sensing Receptor Extracellular Domain Representing in Effect a Human “Knockout”. Eur J Endocrinol. 169, K1-7

Lazarus S, Pretorius C, Khafagi F, Campion KL, Brennan SC, Conigrave AD, Brown EM, Ward DT (2011) A novel mutation of the primary protein kinase C phosphorylation site in the calcium-sensing receptor causes autosomal dominant hypocalcemia. Eur J Endocrinol. 164, 429–435.

McCormick WD, Atkinson-Dell R, Campion KL, Mun H-C, Conigrave AD, Ward DT (2010) Increased Receptor Stimulation Elicits Differential Calcium-Sensing ReceptorT888 Dephosphorylation. J Biol Chem 285, 14170-14177.

Conigrave AD, Ward DT (2013) Calcium-sensing receptor (CaSR): Pharmacological properties and signaling pathways. (Review) Best Practice & Res Clin Endocrinol & Metab 27, 315-331.

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