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PhD
Studentship
- Royal
Vetinary
College
Department
of Veterinary
Basic Sciences
Applications
are invited
for a 3
years PhD
studentship
within
the department
of Veterinary
Basic Sciences
at the
Royal Veterinary
College,
Camden
Town, London.
The project
will investigate
the skeletal
effects
and signaling
mechanisms
of glucagon-like
peptide
1 (GLP-1)
in bone.
One major
complication
of type
2 diabetes
is a greater
risk of
fractures
than is
present
in the
general
population,
as a result
of deteriorating
bone quality.
GLP-1 receptor
agonists
(GLP-1RA)
are increasingly
used as
anti-diabetic
therapy
and this
study will
investigate
if they
could have
additional
beneficial
effects
by reducing
these skeletal
diabetic
complications.
The main
objectives
of this
PhD studentship
will be:
1) to analyse
the long-term
in vivo
effects
of GLP-1
RA on bone
mass and
architecture
in control
and diabetic
rats; 2)
to determine
the cellular
distribution
of GLP-1
receptor
expression
and the
direct
effects
of GLP-1
RA on bone
cell differentiation
and function
in vitro;
3) to establish
the signaling
pathways
involved
in the
skeletal
effects
of GLP-1RA
in bone
cells.
The position
will involve
cell cultures,
in vivo
experiments
in rat,
molecular
and cellular
biology
techniques,
as well
as bone
histology
and micro-CT
analysis
of bone.
We are
seeking
a highly
motivated
researcher
who has,
or expects
to obtain,
a good
degree
in the
biological
sciences.
Prospective
applicants
are encouraged
to contact
Dr Chantal
Chenu (email:
cchenu@rvc.ac.uk;
tel: (+44)
20 7468
5045).
A generic
advertisement
for this
PhD studentship
will appear
shortly
in the
New Scientist,
and the
RVC and
FindaPhD.com
websites
Interviews
are likely
to take
place in
January
2013.
The studentship
will commence
in summer
2013
Deciphering
the regulatory
mechanisms
responsible
for mineralisation
of the
skeleton
Contact & Principal Supervisor: Prof Colin Farquharson - colin.farquharson@roslin.ed.ac.uk
Tel: 0131 651 9176.
Co-supervisor: Dr Vicky MacRae - vicky.macrae@roslin.ed.ac.uk
Bone formation is a carefully orchestrated process mediated by promoters and inhibitors of the mineralisation process. If the process is not properly regulated, the result can be too little of the mineral or too much - either of which can compromise bone health. Tissue-nonspecific alkaline phosphatase (TNAP) plays a crucial role promoting mineralisation of the collagenous extracellular matrix by restricting the concentration of the calcification inhibitor inorganic pyrophosphate (PPi). PHOSPHO1 – an enzyme discovered at the Roslin Institute – is a phosphatase with specificity for phosphoethanolamine and phosphocholine and has a role in scavenging Pi from matrix vesicle (MV) membrane phospholipids to favour intravesicular mineral deposition. Phospho1 knockout mice display spontaneous bone fractures, bowed long bones, osteomalacia and scoliosis in early life. Importantly, ablation of both TNAP and PHOSPHO1 function leads to complete absence of skeletal mineralisation (Huesa et al. 2011; Yadav et al. 2011). It is the aim of this studentship to determine how TNAP and PHOSPHO1 cooperatively work together to promote bone mineralisation This hypothesis-driven studentship will determine if the first step of MV mineralisation involves the convergence of two independent biochemical pathways a) intra-vesicular Pi generation by the enzymatic action of PHOSPHO1 and b) influx of Pi generated in the perivascular space by the activities of TNAP and NPP1, via phosphate transporters.
This project has relevance to ageing and animal health.
This project will involve training in various cellular and molecular biology techniques and will include in vivo studies with mice and in vitro approaches such as cell culture, immunohistochemistry, in situ hybridisation, western blotting, quantitative PCR and DNA transfection studies.
Identifying novel genes controlling vascular calcification
The Roslin Institute, University of Edinburgh
This studentship is for 4 years and is available from Sept 2012.
Further enquires should be made to Dr Vicky MacRae – vicky.macrae@roslin.ed.ac.uk
Vascular calcification (VC) is a significant risk factor in the development of cardiovascular disease, and involves the deposition of calcium phosphate mineral in arteries and cardiac muscle. VC has severe clinical consequences, however, the mediators and mechanisms of VC have yet to be fully elucidated. Many of the underlying principles on calcification are based on our understanding of bone mineralisation, which occurs through hydroxyapatite deposition in the extracellular matrix. This depends on a regulated balance of factors such as calcium and inorganic phosphate concentrations, in the presence of matrix proteins and mineralisation inhibitors including inorganic pyrophosphate and osteopontin.
Microarray analysis recently undertaken in our laboratory has identified a number of potential novel genes that are associated with vascular calcification. The characterisation of these genes will be the focus of this project. Functional data will be obtained from in-vitro models. We will study the calcification potential of cultured primary VSMCs and/or VSMC lines and undertake gain and loss of function studies. Where appropriate transgenic mouse models will also be used.
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