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CDB Seminars
All welcome

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All Seminars are held in the Gavin De Beer Lecture Theatre, Anatomy Building, Thursday 1-2pm

18 Sept: Katarzyna Anton (Tada lab) / Mae Woods (Barnes lab)

2 Oct: Helena (Wilson lab) /Maria Maiaru (Geranton lab)

16 Oct: Tom Wyatt (Charras lab) (Oates lab)

30 Oct: Harold Burgess - Title TBC (Host: Prof Steve Wilson)

31 Oct: SPECIAL SEMINAR - Sophie Jarriault (IGBMC) – Title TBC (Host: Dr Richard Poole)

6 Nov: Aude Marzo (Salinas lab)/ Maite Ogueta (Stanewsky lab)

13 Nov: (Paluch lab)/ Robert Bentham (Szabadkai lab)

27 Nov: Irene (Stern lab)/Cristina Benito(Jessen lab)

11 Dec: Marcus Ghosh (Rihel lab)/ (Chubbs lab)

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Wellcome PhD Students: Final Year Talks

Thursday 25 September

12.30-2.35pm

Room 249, 2nd Floor, Medical Sciences Building, Gower Street

12.30pm:  Scott Curran

12.55pm:  Kristina Tubby

1.20pm:  Miguel Tillo

1.45pm:  Alex Sinclair-Wilson

2.10pm:  Elena Scarpa

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Bone Biology Lab

Bone Biology Lab

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Bone Biology Lab


Research Overview

Bone growth and turnover result from the co-ordinated activities of osteoblasts (bone forming cells) and osteoclasts (bone destroying cells). Imbalance in the activities of these cells can lead to the common bone loss disorder osteoporosis.

We are interested in 'fundamental' regulators of the function of osteoclasts and osteoblasts.

Our work falls into 3 main areas:

Acidosis
We discovered that a small pH reduction (acidosis) is necessary to activate osteoclasts to excavate resorption pits on bone surfaces. We found that simultaneously, acidosis prevents mineralisation of newly formed bone by osteoblasts. The impressive responses of bone cells to extracellular pH changes probably represent a primitive ‘failsafe’ to correct systemic acidosis by releasing alkaline bone mineral (animated slide). There is increasing evidence that acidosis due to disease or diet (and perhaps excessive exercise) could play a role in bone loss disorders. Our current research is focused on understanding the mechanisms by which bone cells recognise and respond to pH changes in their environment.

Hypoxia
We have found that hypoxia (low oxygen) is a major stimulator of the formation of osteoclasts from precursor cells present in blood and bone marrow. Osteoclast formation – and thus bone resorption – is strongly increased when oxygen is reduced to as little as 1% of the atmospheric level. In contrast to its effect on osteoclasts, we observed that hypoxia strongly blocks the growth and bone-forming capacity of osteoblasts. These observations help to explain why bone is rapidly lost when the blood supply is reduced or disrupted – eg, as a result of inflammation, infection, tumours, fractures, diabetes, chronic obstructive airway diseases and ageing. Our results also explain why bone formation requires a good local blood supply. Significantly, hypoxia also causes tissue acidosis (see above). Our results emphasise the critical role of the vasculature in the maintenance of bone health (animated slide).

Nucleotides
ATP and other nucleotides are now recognised to play important and complex regulatory roles as messenger molecules for cell-to-cell communication. In collaboration with Professor Geoff Burnstock FRS, we have studied the actions of nucleotides on bone cell function. We found that numerous P2 nucleotide receptor subtypes are expressed by bone cells and that low concentrations of ATP and ADP stimulate both the formation and activity of osteoclasts, whilst selectively blocking mineralisation of newly formed bone by osteoblasts. Recent results show that skeletal changes can occur when P2 receptors are defective or deficient. This work suggests that the ATP – P2 cell signalling system offers potential for novel bone therapeutics. To help continue this research we are participating in a European consortium.

Current lab members: Isabel Orriss (Research Fellow), Jessal Patel (BBSRC/Unilever PhD Student), Mark Hajjawi (PhD Student), Tim Arnett.

Research support: Arthritis Research Campaign, BBSRC, Unilever Ltd, Amgen Ltd.

Page last modified on 07 oct 13 09:07 by Mark O R Hajjawi