Imperial College London

ProfessorSaraRankin

Faculty of MedicineNational Heart & Lung Institute

Professor of Leukocyte and Stem Cell Biology
 
 
 
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Contact

 

+44 (0)20 7594 3172s.rankin

 
 
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Assistant

 

Ms Georgina Moss +44 (0)20 7594 2151

 
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Location

 

Office no. 351Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Chan:2015:10.15252/emmm.201404487,
author = {Chan, JK and Glass, GE and Ersek, A and Freidin, A and Williams, GA and Gowers, K and Santo, AIE and Jeffery, R and Otto, WR and Poulsom, R and Feldmann, M and Rankin, SM and Horwood, NJ and Nanchahal, J},
doi = {10.15252/emmm.201404487},
journal = {EMBO Molecular Medicine},
pages = {547--561},
title = {Low-dose TNF augments fracture healing in normal and osteoporotic bone by up-regulating the innate immune response},
url = {http://dx.doi.org/10.15252/emmm.201404487},
volume = {7},
year = {2015}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - The mechanism by which trauma initiates healing remains unclear. Precise understanding of these events may define interventions for accelerating healing that could be translated to the clinical arena. We previously reported that addition of lowdose recombinant human TNF (rhTNF) at the fracture site augmented fracture repair in a murine tibial fracture model. Here, we show that local rhTNF treatment is only effective when administered within 24 h of injury, when neutrophils are the major inflammatory cell infiltrate. Systemic administration of antiTNF impaired fracture healing. Addition of rhTNF enhanced neutrophil recruitment and promoted recruitment of monocytes through CCL2 production. Conversely, depletion of neutrophils or inhibition of the chemokine receptor CCR2 resulted in significantly impaired fracture healing. Fragility, or osteoporotic, fractures represent a major medical problem as they are associated with permanent disability and premature death. Using a murine model of fragility fractures, we found that local rhTNF treatment improved fracture healing during the early phase of repair. If translated clinically, this promotion of fracture healing would reduce the morbidity and mortality associated with delayed patient mobilization.
AU - Chan,JK
AU - Glass,GE
AU - Ersek,A
AU - Freidin,A
AU - Williams,GA
AU - Gowers,K
AU - Santo,AIE
AU - Jeffery,R
AU - Otto,WR
AU - Poulsom,R
AU - Feldmann,M
AU - Rankin,SM
AU - Horwood,NJ
AU - Nanchahal,J
DO - 10.15252/emmm.201404487
EP - 561
PY - 2015///
SN - 1757-4676
SP - 547
TI - Low-dose TNF augments fracture healing in normal and osteoporotic bone by up-regulating the innate immune response
T2 - EMBO Molecular Medicine
UR - http://dx.doi.org/10.15252/emmm.201404487
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000354135500004&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - https://www.embopress.org/doi/full/10.15252/emmm.201404487
VL - 7
ER -