Soluble RANKL is physiologically dispensable but accelerates tumour metastasis to bone.
Asano T. et al., Nat. Metab. 2019, 1: 868–875.
Data from a study by Asano et al. suggest that membrane-bound RANKL is sufficient for most physiological RANKL functions. By contrast, soluble RANKL specifically contributes to bone metastasis by exerting a chemotactic activity in tumour cells expressing RANK thus attracting them to the bone.
Therefore, measurement of the serum RANKL level may help to identify patients who have a high risk of developing bone metastasis and inhibiting soluble RANKL alone may lead to the development of a new therapeutic strategy.
RANKL can easily be measured in serum:
√ HIGH SENSITIVITY – measurable concentrations in healthy subjects
√ Only ELISA that measures free uncomplexed soluble RANKL
√ CE-marked – widely cited in clinical studies
Also available:
OPG ELISA – most referenced
Learn more: RANKL biology: bone metabolism, the immune system, and beyond.
Ono T. et al., Inflamm. Regen. 2020; 40: 2. Full text
Spinal cord injury (SCI) induces an acute alteration in bone metabolism. Although the aetiology of the bone disturbances is not precisely known, immobilisation reduces mechanical loading and the morphology of osteocytes, which are the primary mechanosensors. Periostin and Sclerostin are secreted mostly by osteocytes and are involved in bone’s mechanical response.
In a recent study using the Biomedica Periostin ELISA and Sclerostin ELISA, individuals with spinal cord injury presented higher serum Periostin levels in the acute phase and normal values in the chronic phase.
Conversely, serum Sclerostin levels were suppressed whatever the post-injury duration in the individuals with spinal cord injury. Paraplegia vs. tetraplegia and fragility fracture status seemed to influence Sclerostin levels only.
Maïmoun et al. Periostin and Sclerostin levels in individuals with spinal cord injury and their relationship with bone mass, bone turnover, fracture and osteoporosis status. Bone. 2019 127:612-619.