Research group - Sara Windahl
Our research aims to understand the molecular mechanisms that control the bone-strengthening effects of load / exercise. We also study how tartrate-resistant-acid phosphatase (TRAP / Acp 5) affects bone strength and length, cancer and metastasis.
Research group leader - Sara Windahl
Sara WindahlAssistant senior lecturer
Our lab is interested in bone biology, with the long-term research aim to facilitate development of new treatment strategies that strengthen the skeleton, improve bone length, and reduce the spread of cancer metastases to bone.
The short term aims are to investigate the mechanisms whereby the protein TRAP/ACP5 affects endemic diseases and syndromes such as osteoporosis, metastases, and severe short stature. The studies are divided into a number of sub-projects with the aim to investigate the mechanisms whereby (1) load/exercise increase bone strength, (2) TRAP/ACP5 affects bone length, and (3) TRAP/ACP5 and load can prevent the spread of cancer to the skeleton.
Some of our most common diseases are osteoporosis, breast- and prostate cancer. The risk of osteoporosis and cancer increases with age. With an aging population, the number of patients will increase and thus also the suffering and societal costs. Mutations in ACP5 leads to Spondyloenchondrodysplasia, a rare but severe form of skeletal dysplasia affecting not only the skeleton but often also the nervous and immune systems. it is itself not a disease, but the underlying causes and effects on other organs may be. The possibilities to cure osteoporosis and severe short stature, and prevent metastases to the skeleton are currently limited. The information derived from these studies should suggest whether ACP5 is amenable to therapeutic interference, and in turn inform therapeutic strategies to augment bone strength, treat severe stature and reduce cancer metastases.
Previous group members
Sophia Åhman, Master student
STAT3 Hyperactivation Due to SOCS3 Deletion in Murine Osteocytes Accentuates Responses to Exercise- and Load-Induced Bone Formation.
McGregor NE, Walker EC, Chan AS, Poulton IJ, Cho EH, Windahl SH, Sims NA
J Bone Miner Res 2022 Mar;37(3):547-558
Mapping Regional Cortical Bone Responses to Local Changes in Loading and Systemic Stimuli.
Windahl SH, Delisser PJ, Galea GL
Methods Mol Biol 2021 ;2221():275-289
Bone gain following loading is site-specifically enhanced by prior and concurrent disuse in aged male mice.
Galea GL, Delisser PJ, Meakin L, Price JS, Windahl SH
Bone 2020 04;133():115255
αSMA Osteoprogenitor Cells Contribute to the Increase in Osteoblast Numbers in Response to Mechanical Loading.
Matthews BG, Wee NKY, Widjaja VN, Price JS, Kalajzic I, Windahl SH
Calcif Tissue Int 2020 02;106(2):208-217
Changes in mechanical loading affect arthritis-induced bone loss in mice.
Liphardt AM, Windahl SH, Sehic E, Hannemann N, Gustafsson KL, Bozec A, Schett G, Engdahl C
Bone 2020 02;131():115149
Vitamin A decreases the anabolic bone response to mechanical loading by suppressing bone formation.
Lionikaite V, Henning P, Drevinge C, Shah FA, Palmquist A, Wikström P, Windahl SH, Lerner UH
FASEB J 2019 04;33(4):5237-5247
Body weight homeostat that regulates fat mass independently of leptin in rats and mice.
Jansson JO, Palsdottir V, Hägg DA, Schéle E, Dickson SL, Anesten F, Bake T, Montelius M, Bellman J, Johansson ME, Cone RD, Drucker DJ, Wu J, Aleksic B, Törnqvist AE, Sjögren K, Gustafsson JÅ, Windahl SH, Ohlsson C
Proc Natl Acad Sci U S A 2018 01;115(2):427-432
Correction to: Compressive loading of the murine tibia reveals site-specific micro-scale differences in adaptation and maturation rates of bone.
Bergström I, Kerns JG, Törnqvist AE, Perdikouri C, Mathavan N, Koskela A, Henriksson HB, Tuukkanen J, Andersson G, Isaksson H, Goodship AE, Windahl SH
Osteoporos Int 2018 09;29(9):2161
Prednisolone treatment reduces the osteogenic effects of loading in mice.
Bergström I, Isaksson H, Koskela A, Tuukkanen J, Ohlsson C, Andersson G, Windahl SH
Bone 2018 07;112():10-18
We are located at ANA Futura, Campus Syd, Flemingsberg.