Mesenchymal stem cells for management of rheumatoid arthritis : immune modulation, repair or both?

The authors are grateful for support to their research from Arthritis Research UK (grants 19271, 19429, 19667, 20050, 20775) and the Medical Research Council (grant no. MR/L020211/1)Peer reviewedPostprin

Osteoarthritis year in review 2023 : Biology

Open Access via the Elsevier agreementPeer reviewe

Stem Cell-based Therapeutic Strategies for Cartilage Defects and Osteoarthritis

We are grateful to Medical Illustration at the University of Aberdeen for drawing the schematic in Figure 1, and to Arthritis Research UK (grants 19667, 20050, 20775, 20865, 21156) and the Medical Research Council (grants MR/L020211/1, MR/L022893/1) for supporting our work.Peer reviewedPublisher PD

Cellular therapy and tissue engineering for cartilage repair

Funding The authors are grateful to the Medical Research Council (grant numbers MR/L020211/1 and MR/L022893/1; CDB, AJR), Versus Arthritis (formerly Arthritis Research UK, grant numbers 20050, 20775, 20865, 21156, and 21800; CDB, AJR), Biosplice Therapeutics (CDB, AJR), and the Canadian Institute of Health Research (AZ, RAK) for supporting their research.Peer reviewedproo

Bone Marrow Contribution to Synovial Hyperplasia Following Joint Surface Injury

Acknowledgements We thank Dr. Andrea Augello and Dr. Donna MacCallum for advice and help with animal procedures, Susan Clark and Denise Tosh for general technical help and support, and the Arthritis and Regenerative Medicine Laboratory and Arthritis and Musculoskeletal Medicine Programme for general support and scientific discussions. We acknowledge the Iain Fraser Cytometry Centre, the animal facility staff and the Microscopy and Histology Facility, in particular Kevin Mackenzie, Gillian Milne and Lucy Wight for their support. This work was supported by Arthritis Research UK (grants 19271, 19429 and 20050). AHKR is supported by the Wellcome Trust through the Scottish Translational Medicine and Therapeutics Initiative (grant WT 085664).Peer reviewedPublisher PD

The burden of metabolic syndrome on osteoarthritic joints

Versus Arthritis (grants 19667, 20050, 20775, 20865, 21156) and the Medical Research Council (grant MR/L020211/1).Peer reviewedPublisher PD

Joint morphogenetic cells in the adult mammalian synovium

The authors thank all members of the Arthritis & Regenerative Medicine Laboratory, particularly Dr Ana Sergijenko; Drs David Kingsley, Grigori Enikolopov, Fernando Camargo and Lora Heisler for sharing transgenic mice; Drs Henning Wackerhage, Neil Vargesson, Lynda Erskine, Chris Buckley, Francesco Dell’Accio and Frank Luyten for support and helpful discussions; Staff at the University of Aberdeen’s Animal Facility, Microscopy & Histology Facility and Iain Fraser Cytometry Centre for their support. C.D.B. is grateful to Dr Frank Luyten’s support for the experiment in Fig. 8, performed in his laboratory at KU Leuven, Belgium. We are grateful for the following funding: Arthritis Research UK (Grants No. 20050, 19429 and 20775), Medical Research Council (Grant No. MR/L020211/1) and Tenovus Scotland (Grant No. G13/14). A.H.K.R. is supported by the Wellcome Trust through the Scottish Translational Medicine and Therapeutics Initiative (Grant No. WT 085664).Peer reviewedPublisher PD

Human Mesenchymal Stromal Cells Enhance Cartilage Healing in a Murine Joint Surface Injury Model

Funding: This research was funded by Versus Arthritis, grant numbers 18480, 19429 and 21156, and the Medical Research Council, grant number MR/L010453/1. Acknowledgments: We thank Pat Evans and Martin Pritchard, Histopathology Dept, RJAH Orthopaedic Hospital, for guidance on histology; Meso Scale Diagnostics, LLC for advice and the loan of equipment for analyte analyses; all members of the Arthritis and Regenerative Medicine Laboratory at the University of Aberdeen, particularly Hui Wang, Sharon Ansboro and Ausra Lionikiene for their help with mouse surgeries and tissue collection, as well as staff at the University of Aberdeen’s animal facility and microscopy and hystology facility for their supportPeer reviewedPublisher PD

BMP signalling : A significant player and therapeutic target for osteoarthritis

Acknowledgements We are immensely grateful to Prof. YiPing Chen at Tulane University, USA, for the gift of mouse strains. We thank Prof. Frank Beier of Western University, Ontario, Canada for teaching APJ the method of ACL transection. We sincerely thank Shuchi Arora and Ankita Jena for their critical comments on the manuscript. We are highly grateful to Niveda Udaykumar and Saahiba Thaleshwari for their help in blind OARSI scoring. We thank Mr. Naresh Gupta for assistance with mouse experiments. Funding This work was supported by grants from the Department of Biotechnology, India (DBT) BT/PR17362/MED/30/1648/2017 and BT/IN/DENMARK/08/JD/2016 to A.B.; Versus Arthritis Grants 19667 and 21156 to CDB and AJR, Fellowships to APJ, BK, and SFI are supported by fellowships from the Ministry of Education, Govt. of India. Fellowship to AKS was supported by Science and Engineering Research Board, Govt. of India. APJ travelled to Western University Canada with Shastri Research Student Fellowship (SRSF, 2015-‘16). A.H.K.R. was supported by the Wellcome Trust through the Scottish Translational Medicine and Therapeutics Initiative (Grant No. WT 085664).Peer reviewedPostprin

Fluorescent Risedronate Analogues Reveal Bisphosphonate Uptake by Bone Marrow Monocytes and Localization Around Osteocytes In Vivo

Bisphosphonates are effective antiresorptive agents owing to their bone-targeting property and ability to inhibit osteoclasts. It remains unclear, however, whether any non-osteoclast cells are directly affected by these drugs in vivo. Two fluorescent risedronate analogues, carboxyfluorescein-labeled risedronate (FAM-RIS) and Alexa Fluor 647–labeled risedronate (AF647-RIS), were used to address this question. Twenty-four hours after injection into 3-month-old mice, fluorescent risedronate analogues were bound to bone surfaces. More detailed analysis revealed labeling of vascular channel walls within cortical bone. Furthermore, fluorescent risedronate analogues were present in osteocytic lacunae in close proximity to vascular channels and localized to the lacunae of newly embedded osteocytes close to the bone surface. Following injection into newborn rabbits, intracellular uptake of fluorescently labeled risedronate was detected in osteoclasts, and the active analogue FAM-RIS caused accumulation of unprenylated Rap1A in these cells. In addition, CD14high bone marrow monocytes showed relatively high levels of uptake of fluorescently labeled risedronate, which correlated with selective accumulation of unprenylated Rap1A in CD14+ cells, as well as osteoclasts, following treatment with risedronate in vivo. Similar results were obtained when either rabbit or human bone marrow cells were treated with fluorescent risedronate analogues in vitro. These findings suggest that the capacity of different cell types to endocytose bisphosphonate is a major determinant for the degree of cellular drug uptake in vitro as well as in vivo. In conclusion, this study shows that in addition to bone-resorbing osteoclasts, bisphosphonates may exert direct effects on bone marrow monocytes in vivo. © 2010 American Society for Bone and Mineral Researc