Abstract submission

In line with the tentative program, the best 15 abstract will be selected for short oral presentations. 


Instructions for abstract submission:

 See example below.

 Font: Arial 11 (title, authors, affiliations), Arial 10 (the abstract text)

Title: bold, title case

Authors: first name, followed by last name

Affiliations: indicated by numbers if there is more than 1 author affiliation, indicate University (abbreviated) and department

Body abstract should contain the following subheadings in italics: Background; Objective; Methods; Results and Conclusion.

Maximum is 300 words. If more words are used, the abstract will be truncated.

Please submit your abstract as a .doc or .docx file to bma2016@erasmusmc.nl


Example abstract:

Mice lacking the epithelial calcium channel TRPV4 have increased bone mass as a consequence of function alterations of multiple bone cell types

BCJ van der Eerden1, M Koedam1, AWCM van de Kemp2, JGJ Hoenderop2, H Weinans3, HAP Pols1, RJM Bindels2, JPTM van Leeuwen1

1Erasmus MC, Internal Medicine, 2Radboud University MC,NCMLS, Cell Physiology

Background: In bone, calcium signaling is crucial for osteoblast and osteoclast function implying that calcium channels are important for calcium transport in and out of bone during mineralisation and resorption, respectively. We recently showed that the epithelial calcium channel is expressed in osteoclasts and crucial for osteoclastic bone resorption. TRPV4 is a much more widely expressed family member and several studies have established that this channel responds to an array of stimuli, including osmolarity, heat, pH, temperature and pressure. Only very recently, it was postulated that TRPV4 deficiency leads to reduced sensing of mechanical stimuli.

Objective: Therefore, in this study we explored the role of TRPV4 in bone.

Methods and results: Real-time PCR studies demonstrated that TRPV4 mRNA is abundantly expressed in both osteoblasts and osteoclasts but even higher in cartilaginous tissues. Using μCT, mice lacking TRPV4 displayed increased cortical and trabecular bone mass (thickness and volume) compared to wildtype mice, which was partly explained by increased femoral length. Bone marrow cultures from wildtype and TRPV4 deficient mice were stimulated with M-CSF and RANKL for 6 days to generate osteoclasts. Cultures from TRPV4 knockout bone marrow demonstrated reduced numbers of osteoclasts compared to wildtype cultures as assessed by TRAP staining. This was associated with less resorption pits as shown by coomassie brilliant blue staining, indicating reduced osteoclastic activity in mice lacking TRPV4. Besides osteoclast cultures, bone marrow from both mice genotypes were used to generate osteoblasts by culturing for 21 days in the presence of β-glycerophosphate and ascorbic acid. Osteoblast differentiation and mineralisation were reduced in TRPV4 knockout cultures compared to wildtype cultures as assessed by ALP and alizarin red staining, respectively. These findings suggest that not only osteoclast function but also osteoblast function is disturbed in mice lacking TRPV4.

Conclusion: mice lacking TRPV4 have increased bone mass and size. The increased bone mass most likely results from reduced osteoclast and osteoblast differentiation and/or function, with the osteoclast dysfunction being dominant. On the other hand, cartilage cells within the growth plate appear to be stimulated following TRPV4 deficiency, although no data are available yet to confirm this. Currently, attempts are being made to further specify the role of TRPV4 in bone and to assess whether DNA polymorphisms are associated with clinical endpoints in relation to osteoporosis and/or osteoarthritis within the Rotterdam Study.




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