Pharmacology of bisphosphonates

Similar documents
Musculoskeletal Clinical Correlates: Osseous Conditions in Dental Patients

Bisphosphonates. From Bench to Bedside

J. E. FISHER*, M.J.ROGERS*, J.M.HALASY, S.P.LUCKMAN, D.E.HUGHES, P.J.MASARACHIA, G. WESOLOWSKI, R.G.G.RUSSELL, G.A.RODAN, AND A. A.

Osteoclasts- What Do They Do and How Do They Do It? Prof. Steven L. Teitelbaum

Bone 49 (2011) Contents lists available at ScienceDirect. Bone. journal homepage:

Cytosolic Entry of Bisphosphonate Drugs Requires Acidification of Vesicles after Fluid-Phase Endocytosis

Activation of γδ T Cells by Bisphosphonates

The isoprenoid biosynthesis pathway and regulation of osteoblast differentiation

regulation of polarized membrane transport by rab GTPases Peter van der Sluijs;

Review Development of bisphosphonates Herbert Fleisch

Talib A. Najjar, DMD, MDS, PhD Professor Oral & Maxillofacial Surgery Rutgers University

Bisphosphonates: Mode of Action and Pharmacology

Supplementary Materials for

Osteoclast Culture Kit

Deposition of Bone by the Osteoblasts. Bone is continually being deposited by osteoblasts, and it is continually being resorbed where osteoclasts are

SUPPLEMENTARY INFORMATION

Metabolic Activities in Mevalonate Pathway could affect the Intracellular Calcium Signaling of In Situ Chondrocytes

Bisphosphonate-induced differential modulation of immune cell function in gingiva and bone marrow in vivo: Role in osteoclastmediated

Osteoclast Activity Assay Substrate

Emerging anti-cancer molecular mechanisms of aminobisphosphonates

Molecular Cell Biology - Problem Drill 17: Intracellular Vesicular Traffic

Figure S1. Western blot analysis of clathrin RNA interference in human DCs Human immature DCs were transfected with 100 nm Clathrin SMARTpool or

ABSTRACT INTRODUCTION. Hsin-Lin Cheng 1,2, Chiao-Wen Lin 3,4, Jia-Sin Yang 1,2, Ming-Ju Hsieh 1,5, Shun-Fa Yang 1,2, Ko-Hsiu Lu 6,7

Signal Transduction Cascades

Bisphosphonates in the Management of. Myeloma Bone Disease

Osteoporosis: current treatment and future prospects. Juliet Compston Professor Emeritus of Bone Medicine Cambridge Biomedical Campus

Legionella pneumophila: an intracellular pathogen of phagocytes Prof. Craig Roy

Osteoclast Culture Kit

KEY CONCEPT QUESTIONS IN SIGNAL TRANSDUCTION

Statins and osteoporosis: Can these lipid-lowering drugs also bolster bones?

Mutation in Osteoactivin Enhances RANKL-Mediated Signaling, Promoting Osteoclast Differentiation, Survival and Inhibiting Bone Resorption

Vesicle Transport. Vesicle pathway: many compartments, interconnected by trafficking routes 3/17/14

Bisphosphonates Induce Autophagy by Depleting Geranylgeranyl Diphosphate

Chapter 2. Jaw bone marrow-derived osteoclast precursors internalize more bisphosphonate than longbone marrow precursors

Siglec-15 Is A Potential Therapeutic Target For Postmenopausal Osteoporosis

Homework Hanson section MCB Course, Fall 2014

The elements of G protein-coupled receptor systems

Lysosomes and endocytic pathways 9/27/2012 Phyllis Hanson

PHSI3009 Frontiers in Cellular Physiology 2017

Review Article Bisphosphonates and Cancer: What Opportunities from Nanotechnology?

Novel bisphosphonates as inhibitors of isoprenoid biosynthesis

BONE TISSUE. Dr. Heba Kalbouneh Associate Professor of Anatomy and Histology

The molecular mechanism of nitrogen-containing bisphosphonates as antiosteoporosis drugs

Supplementary data Supplementary Figure 1 Supplementary Figure 2

How bisphosphonates work, biochemical level Jukka Mönkkönen (Kuopio, Finland) and Mike Rogers (Sydney, Australia)

(a) Significant biological processes (upper panel) and disease biomarkers (lower panel)

Involvement of PLEKHM1 in osteoclastic vesicular transport and osteopetrosis in incisors absent rats and humans

Who manipulates who in dysregulated mineralised tissue resorption? Dr Gurå Therese Bergkvist MRCVS

Module 3 Lecture 7 Endocytosis and Exocytosis

Bone mechanics bone strength and beyond

Ras and Cell Signaling Exercise

Cell Membranes. Dr. Diala Abu-Hassan School of Medicine Cell and Molecular Biology

Signal Transduction Pathways. Part 2

Pharmacological Topics of Bone Metabolism: Antiresorptive Microbial Compounds That Inhibit Osteoclast Differentiation, Function, and Survival

Principles of Genetics and Molecular Biology

Cellular Biochemistry

Synthesis of carboxyphosphonates and bisphosphonates as potential GGTase II and GGDPS inhibitors

Drugs Affecting Bone. Rosa McCarty PhD. Department of Pharmacology & Therapeutics

Biosignals, Chapter 8, rearranged, Part I

Supplementary Figure 1: Co-localization of reconstituted L-PTC and dendritic cells

RAS Genes. The ras superfamily of genes encodes small GTP binding proteins that are responsible for the regulation of many cellular processes.

Enzymes Part III: regulation II. Dr. Mamoun Ahram Summer, 2017

Propagation of the Signal

- 1 - Cell types Monocytes THP-1 cells Macrophages. LPS Treatment time (Hour) IL-6 level (pg/ml)

The Importance of Isoprenylation and Nf1 Deficiency in K-RAS induced Cancer

THE ROLE OF THE INNATE IMMUNE SYSTEM IN BISPHOSPHONATE-INDUCED OSTEONECROSIS OF THE JAW

Companion to Biosynthesis of Ketones & Cholesterols, Regulation of Lipid Metabolism Lecture Notes

Jaw bone marrow-derived osteoclast precursors internalize more bisphosphonate than long-bone marrow precursors

Glucocorticoids suppress bone formation via the osteoclast

Osteoporosis Update. Greg Summers Consultant Rheumatologist

THE ROLE OF ALTERED CALCIUM AND mtor SIGNALING IN THE PATHOGENESIS OF CYSTINOSIS

Enzyme-coupled Receptors. Cell-surface receptors 1. Ion-channel-coupled receptors 2. G-protein-coupled receptors 3. Enzyme-coupled receptors

Supplementary Materials. High affinity binding of phosphatidylinositol-4-phosphate. by Legionella pneumophila DrrA

T H E J O U R N A L O F C E L L B I O L O G Y

Bone and Cancer. Peter Croucher

Mevalonate kinase deficiency leads to decreased prenylation of Rab GTPases

An Update on Osteoporosis Treatments

Mechanism of Vesicular Transport

Chapter 20. Cell - Cell Signaling: Hormones and Receptors. Three general types of extracellular signaling. endocrine signaling. paracrine signaling

Inhibition of farnesyl pyrophosphate (FPP) and/or geranylgeranyl pyrophosphate (GGPP) biosynthesis and its implication in the treatment of cancers

Bisphosphonates for post-menopausal osteoporosis: are they all the same?

Amel Dudakovic, Andrew J. Wiemer, Kimberly M. Lamb, Laura A. Vonnahme, Sara E. Dietz, and Raymond J. Hohl

Protein Trafficking in the Secretory and Endocytic Pathways

Nature Neuroscience: doi: /nn Supplementary Figure 1. PICALM expression in brain capillary endothelium in human brain and in mouse brain.

7.06 Spring of PROBLEM SET #6

HRT and Risedronate Combined Anabolic and Antiresorptive Therapy

endomembrane system internal membranes origins transport of proteins chapter 15 endomembrane system

sfigure 1: Detection of L-fucose in normal mouse renal cortex using the plant lectin LTL

Signaling. Dr. Sujata Persad Katz Group Centre for Pharmacy & Health research

Procaspase-3. Cleaved caspase-3. actin. Cytochrome C (10 M) Z-VAD-fmk. Procaspase-3. Cleaved caspase-3. actin. Z-VAD-fmk

Cellular Physiology (PHSI3009) Contents:

Review Article Statins and prostate cancer: role of cholesterol inhibition vs. prevention of small GTP-binding proteins

Generation of post-germinal centre myeloma plasma B cell.

Review Article and Clinical Experience: PREVENTIVE AND THERAPEUTIC STRATEGIES FOR OSTEOPOROSIS (A HIGHLY EFFICACIOUS RISEDRONATE-35MG ONCE WEEKLY)

From Fragile to Firm. Monika Starosta MD. Advocate Medical Group

Lipidne mikrodomene. funkcija

Nature Immunology: doi: /ni.3866

Three-dimensional characterization of osteoclast bone-resorbing activity in the resorption lacunae

Project report October 2012 March 2013 CRF fellow: Principal Investigator: Project title:

Transcription:

Pharmacology of bisphosphonates Dr. Fraser Coxon Bone & Musculoskeletal Research Programme Institute of Medical ciences University of Aberdeen

utline Introduction to osteoclasts Culture and analysis of osteoclasts in vitro Mechanism of action of bisphosphonates Mechanism of action of phosphonocarboxylate analogues of bisphosphonates Localisation of these compounds in bone

Formation of osteoclasts steoclast precursor NFκB M-CF osteoblast 1,25() 2 D 3 PTH estrogen Pre- steoclast c-fos RANKL RANK Mature steoclast RANK = receptor activator of NFκB RANKL = RANK ligand

Identifying features of osteoclasts Multinucleated Have high levels of TRAP (tartrate( tartrate-resistant resistant acid phosphatase) Abundance of acidic vesicles α v β 3 integrin (vitronectin receptor) on the cell surface Expression of cathepsinc K Phase contrast taining for TRAP activity vitronectin receptor (green) acidic vesicles (red) Cath K activity (red) (live osteoclast)

Identifying features of resorbing osteoclasts Formation of distinct membrane domains (e.g. ruffled border) Polarisation of cytoskeleton into an F-actin F ring Resorption of bone! Actin rings visualised by staining with fluorescent phalloidin conjugates Resorption pits on bone surface visualised reflected light microscopy

steoclasts are specialised bone-resorbing cells F-actin ring sealing zone H + CK H + CK H + BNE ruffled border Bone is resorbed by the secretion of acid and cathepsin K (CK) at the ruffled border of the osteoclast

Analysis of resorbing osteoclasts steoclasts need to be cultured on a mineralised substrate Dentine Cortical bone Hydroxyapatite discs axial views: hsteoclasts on dentine 30µm hsteoclast on glass 10µm

Unusual membrane domains in osteoclasts basolateral apical basolateral apical Vesicular stomatitis virus Influenza virus - basolateral domain in epithelial cells - apical domain in epithelial cells alo et al. 1996 J Cell ci 109,, 391 LAMP-2 Ruffled border: Properties of an endosomal/lysosomal membrane Vitronectin receptor Palokangas et al 1997 J Cell ci 110,, 1767

Unique membrane domains in osteoclasts FD (apical domain) FD (apical domain) basolateral domain BL BL basolateral domain Z Z sealing zone ruffled border Bone FD- Functional secretory domain Z- sealing zone (F-actin ring)

Vesicular trafficking routes in osteoclasts FD (apical domain) FD (apical domain) basolateral domain BL BL basolateral domain Z Z sealing zone ruffled border Bone FD- Functional secretory domain Z- sealing zone (F-actin ring)

ources of osteoclast cultures

Isolation of mature osteoclasts Mince and scrape the bones to release osteoclasts washing or digestion relatively low numbers impure cultures useful for resorption assays or single cell studies Mixed culture of osteoclasts/other bone cells Pure culture of TRAP +ve osteoclasts

Generation of osteoclasts in vitro flush bone marrow from long bones high numbers fairly pure cultures useful for formation assays or biochemical analyses Isolate PBMCs from human blood eed cells in petri-dishes M-CF M-CF M-CF + RANKL M-CF + RANKL M-CF + RANKL Day 0 Day 3 Day 6 Re-seed on to resorbable substrate e.g. dentine cortical bone Day 9 Day 12 Day 15 Resorbing osteoclasts

Generation of osteoclasts in vitro- before RANKL! flush bone marrow from long bones Isolate osteoblasts from calvaria steoclast Co-culture cells in the presence of 1,25()2D3 ~ 8 Days Useful for assessing osteoblast-osteoclast interactions in osteoclast formation e.g. whether a defect is in the osteoblast or osteoclast lineage

Isolation of osteoclasts ex vivo Isolate osteoclasts using antibody to surface marker (e.g. VNR) and magnetic bead separation Pure culture of VNR +ve osteoclasts Useful for assessing the effect of a drug on osteoclasts in vivo

Bisphosphonates

Bisphosphonates bind calcium ions and target bone mineral ide chain R 1 C = P P = - - Ca 2+

Localisation of a fluorescent BP (RI) in mouse vertebra cartilage Bone marrow trabecular bone Bone Green = FAM-RI Blue = nuclei 0.1 mm

steoclasts engulf bisphosphonate into intracellular vesicles Coxon et al 2008, Bone 42:848-60 osteoclast resorption pit dentine surface zx Green- F-ALN Red- F-actin Blue-VNR green = bisphosphonate red = actin cytoskeleton

Bisphosphonates are selectively internalised from mineralised surfaces by osteoclasts Rabbit osteoclasts cultured on dentine labelled with fluorescent alendronate Bisphosphonate * * * * dextran (endocytic marker) * * * Green- F-ALN Red- F-actin Blue-VNR Green- dextran Red- F-actin Blue-VNR

Effects of BPs on osteoclast morphology cytoskeleton (F-actin ring) Ruffled border in vivo cell morphology in vitro resorbing osteoclast retraction apoptosis + RI ato et al 1991, J Clin Invest 88, 2095

Two groups of of bisphosphonates with different modes of of action imple Bisphosphonates Nitrogen-containing Bisphosphonates H 3 C Cl Cl H = P P = clodronate = P P = etidronate H 2 N N H pamidronate N = P P = H zoledronate = P P = CH 3 N H = P P = H 2 N N H ibandronate = P P = alendronate H = P P = risedronate

Bisphosphonates inhibit farnesyl diphosphate synthase in the mevalonate pathway Luckman et al,, 1998 Fisher et al,, 1999 Van Beek et al,, 1999 Keller et al,, 1999 Bergstrom et al,, 2000 Grove et al,, 2000 Dunford et al,, 2001 HMG-CoA mevalonate phosphomevalonate mevalonate diphosphate cholesterol dimethylallyl diphosphate squalene x geranyl diphosphate farnesyl diphosphate isopentenyl diphosphate FPP synthase N-BPs e.g. pamidronate alendronate Ibandronate risedronate zoledronate geranylgeranyl diphosphate

Most small GTPases are modified by prenylation -P - - P farnesyl diphosphate farnesyl transferase Ras CAA X Ras proteins Rab CXC Rab proteins -P - - P Rab geranylgeranyl transferase geranylgeranyl diphosphate geranylgeranyl Transferase I Rho CAA X Rho proteins Rap1

mall GTPases act as as molecular switches Guanine nucleotide exchange factor (GEF) GDP Ras ff GTP GEF GDP n GDI GDP Rho GDP REP Rab Translocation to membrane GTPase GDP Pi GAP GTPase activating protein (GAP) GTPase GTP Effector downstream signalling

Bisphosphonates inhibit protein prenylation Ctl HMGCoA A B A- Rab GTPases B- 21 kda GTPases [ 14 C]mevalonate dimethylallyl diphosphate isopentenyl diphosphate geranyl diphosphate FPP synthase farnesyl diphosphate FTase Ras 14 C] Ras proteins [ 14 Ras Rab [ 14 14 C] Rab proteins Geranylgeranyl Rab GGTase diphosphate GGTase I Rho Rho [ 14 family C] Rho Rap1 proteins Rap1

Bisphosphonates inhibit protein prenylation Ctl RI HMGCoA A B A- Rab GTPases B- 21 kda GTPases [ 14 C]mevalonate dimethylallyl diphosphate isopentenyl diphosphate BPs e.g. RI FPP synthase FTase Ras Rab GGTase GGTase I Rab Rho

RI disrupts the localisation of Rab6 in rabbit osteoclasts Ctrl Rab6 WGA (Golgi) merge RI

Loss of prenylated small GTPases disrupts osteoclast function cytoskeleton disruption Induction of apoptosis loss of prenylated small GTPases Rho, Rac, Cdc42 (regulate the actin cytoskeleton) Rho, Rac (regulate cell survival) Loss of the ruffled border Rabs (regulate vesicular Transport)

FPP synthase catalyses the condensation of of isoprenoid lipid chains 5-carbon 5-carbon IPP + DMAPP 10-carbon GPP + IPP 15-carbon FPP = P - P - = P - P - = P - P - = P - P - = = = = DMAPP GPP substrate DMAPP/GPP FPP synthase IPP substrate

Risedronate Risedronateco-ordinates co-ordinateswith with33magnesium magnesiumions ionsin in the the GGP GGPbinding bindingsite siteof offpp FPP Kavanagh et al 2006, Proc. Natl. Acad. ci 103, 7829-7834

Courtesy of Jean-Michel Rondeau,, Novartis

Correlation between inhibition of of FPP synthase in in vitro and anti-resorptive potency in in vivo Dunford et al, J Pharm Exp Ther 2001 10000 IC 50 (nm) for inhibition of rhfpp synthase 1000 r=0.95, p<0.0001 100 10 1 0.0001 0.001 0.01 0.1 1 Lowest effective dose (mgp( mgp/kg) in vivo

The nitrogen in in the side chain of of risedronate or or zoledronate interacts with a conserved threonine and lysine residue in in FPP synthase ideal distance is ~3Å Zoledronate Risedronate Alendronate Ibandronate 2.96 2.97 3.84 4.03 Risedronate Kavanagh et al 2006 Proc. Natl. Acad. ci Zoledronate Rondeau JM et al 2006 Chem Med Chem This interaction enables slow tight binding of the enzyme

Phosphonocarboxylate analogue of RI Bisphosphonate Phosphonocarboxylate N H P P Risedronate (RI) N H P C NE10790 (3-PEHPC) 50x lower affinity for bone 5,000x lower anti-resorptive potency

NE10790 is a novel inhibitor of Rab GGTase Ctl RI [ 14 C]mevalonate Coxon et al 2001 J Biol Chem 276,, 48213 A B DMAPP/IPP A- Rab GTPases B- 21 kda GTPases FPP synthase farnesyl diphosphate (FPP) FTase [ 14 Ras C] Ras 14 C] Ras [ 14 14 C] Rab proteins Geranylgeranyl diphosphate (GGPP) Rab GGTase GGTase I [ 14 C] Rho proteins Rap1 Rab Rho Rho Rab

NE10790 is a novel inhibitor of Rab GGTase Ctl RI NE10790 [ 14 C]mevalonate Coxon et al 2001 J Biol Chem 276,, 48213 A B DMAPP/IPP A- Rab GTPases B- 21 kda GTPases FPP synthase NE10790 farnesyl diphosphate (FPP) FTase [ 14 Ras C] Ras 14 C] Rab Rab Rab Geranylgeranyl diphosphate (GGPP) Rab GGTase GGTase I Ras [ 14 C] Rho proteins Rap1 Rho Rho

NE10790 disrupts localisation of Rab6 in rabbit osteoclasts Ctrl Rab6 WGA (Golgi) merge NE10790

Family of small GTPases (21-28kDa) 28kDa) with more than 70 human isoforms The Rab family of small GTPases Rab GTPases are crucial regulators of vesicle trafficking: Vesicle formation Vesicle motility Vesicle docking Membrane fusion Try chwartz? chwartz et al (2007) J Cell ci 120: 3905-3910 3910

% of ctrl NE10790 inhibits bone resorption in vitro without affecting the cytoskeleton 140 120 100 80 60 40 20 0 RI RI 0.1 1 10 100 Concentration (µm)( % of ctrl 140 120 100 80 60 40 20 0 NE10790 NE10790 0.1 0.5 1 Concentration (mm( mm) Resorption area actin rings

Inhibition of Rab prenylation alters vesicular trafficking in osteoclasts in vitro Control Coxon et al 2001, J Biol Chem 276, 48213-48222 48222 1mM NE10790

EM Inhibition of Rab prenylation alters vesicular trafficking in osteoclasts in vitro Coxon et al 2001, J Biol Chem 276, 48213-48222 48222 Control 1mM NE10790 confocal (axial views) *

Do these drugs inhibit protein prenylation in osteoclasts in vivo?

Do Do these compounds inhibit protein prenylation in in vivo? 2mgP/kg NE10790 or RI 24 hrs 23c6 & anti- mouse IgG- coated Dynal beads VNR +ve osteoclasts Purified osteoclast pellet In vitro prenylation assay using rh Rab GGTase Assay for unprenylated Rap1A

BPs and PCs inhibit protein prenylation in osteoclasts in vivo Unprenylated Rabs detected by prenylating with [ 3 H]GGPP in vitro: +ve: : osteoclast fraction -ve:: non-osteoclast osteoclast bone marrow cells J774 cells in vitro Ctl NE10790 CTL +ve -ve 0.5mg/kg RI +ve -ve 45mg/kg PC +ve -ve Rab Rab Rab proteins prenylated in vitro Rab Rab Rab in vitro prenylation assay western blotting for unprenylated Rap1A: CTL RI PC Rab Rab Rab Rab Rab 3 H 3 H unprenylated Rap1A actin +ve -ve +ve -ve +ve -ve

Are the effects of BPs really due to inhibition of FPP?

Loss of geranylgeranylated proteins accounts for inhibition of resorption by BPs Fisher et al 1999, Proc Natl Acad ci, 96:133-138; Coxon et al 2000, J Bone Miner Res 15:1467-1476 1476 120 mevalonate 100 ALN Bone resorption (% of control) 80 60 40 Farnesol (F) farnesyl diphosphate farnesylated proteins 20 0 Ctrl 60µM ALN ALN+ GG ALN+ F geranylgeranyl diphosphate Geranylgeranylated Rho proteins Risedronate (µm) + GG 0 12.5 25 50 12.5 25 50 β-actin geranylgeraniol (GG) Geranylgeranylated Rab proteins unprenylated Rab 6

Loss of geranylgeranylated proteins accounts for inhibition of resorption by BPs Coxon et al 2000, J Bone Miner Res 15:1467-1476 1476 Coxon et al 2003, Calcif Tissue Int 72:80-84 84 mevalonate steoclast polarisation: BPs farnesyl diphosphate FTI-277 farnesylated proteins Ctrl steoclast resorption: Resorption GGTI-298 area (mm 2 ) 0.1 geranylgeranyl 0.08 Geranylgeranylated diphosphate Rho proteins 0.06 0.04 0.02 Geranylgeranylated 0 Rab proteins Ctrl 10µM FTI 5µM10µM FTI FTI 10µM GGTI 5µM 10µM GGTI GGTI

ummary Assays using osteoclasts in vitro and ex vivo have enabled us to determine the mechanism of action of bisphosphonates and the related phosphonocarboxylates Inhibition of prenylation of small GTPases Morphological analysis of osteoclasts treated with these compounds has also shed light on the importance of prenylated small GTPases for osteoclast function

Localisation of BPs and PCs in bone

Bisphosphonates have different affinities for hydroxyapatite Nancollas et al 2006, Bone 38: 617-627 627 The R 2 side-chain of BPs also contributes to bone affinity HAP Adsorption Affinity Constants at ph 7.4 4 KL/10 6 L mol -1 3 2 1 ZL ALN RI 0 CL ETD RI IBN ALN ZL Lawson, Triffitt, Ebetino & Russell ABMR & Davos 2005 & 2006

Are osteocytes exposed to bisphosphonates in vivo? Photo by Lilian Plotkin and Lynda Bonewald Lower affinity BPs should be able to gain access to more sites in bone than higher affinity BPs which will get stuck at sites of first contact

Anti-apoptotic effect of BPs on osteocytes (ML-Y4 cells) BPs can open Connexin 43 hemichannels and activate anti-apoptotic apoptotic signalling pathways via ERK % etoposide- induced apoptosis 150 100 50 0 risedronate * * * * 150 100 50 0 etidronate * * * * * * -50 0 10-11 10-10 10-9 10-8 10-7 10-6 10-5 -50 0 10-11 10-10 10-9 10-8 10-7 10-6 10-5 concentration (M) concentration (M) IC 50 values in the nm range! Plotkin, Manolagas, Bellido, Bone 39 (2006) 443-452

Methods Mice or rats injected subcutaneously with fluorescently labelled conjugates (fluorescein, rhodamine or AlexaFluor 647) of RI and 3-PEHPC Animals sacrificed 24h later and tibiae fixed and embedded in MMA resin Resin blocks cut transversely and bone examined directly by confocal microscopy

F-RI localises to osteocyte lacunae in mouse cortical bone osteocyte Vascular channel Green- F-RI Blue-nuclei Red- wheat germ agglutinin

Acknowledgements Bone Research Group, Aberdeen Mike Rogers Miep Helfrich Adam Taylor Anke Roelofs Debbie cott Aysha Khalid University of xford Graham Russell Jim Dunford Procter & Gamble Pharmaceuticals Hal Ebetino Mark Lundy University of outhern California Charles McKenna Imperial College, London Miguel eabra Mimi Mules Queen Mary, University of London Alan Boyde