Bone cells regulate the formation of blood vessels during mechanical unloading

It is well known that bone development and maintenance, and bone cell activities require vascular supply, since molecules important for the bone tissue functionality reach the organ through the vasculature. In this context, bone forming cells, osteoblasts, and endothelial cells, that make up blood vessels, show a strong relationship in regulating each other functions. In case of osteoporosis caused by disuse (e.g. sedentary life style, prolonged therapeutic bed rest, immobilization or elderly), the bone is unloaded and endothelial cells produce molecules that reduce bone formation by osteoblasts, and increase bone erosion by the bone resorbing cells, osteoclasts.

However, in the same condition, how do unloaded osteoblasts affect the endothelial cells functionality? Mattia Capulli, a member of ECTS Academy, and his colleagues answered this question in a recent paper published in Calcified Tissue International. By using a Rotating Wall Vessel (RWV) Bioreactor, approved by NASA, they cultured in vitro the osteoblasts in a simulated microgravity conditions mimicking unloading. Unloaded osteoblasts produced high amount of the Vascular Endothelial Growth Factor (VEGF), necessary for blood vessel formation (angiogenesis), and increased endothelial cells viability, migration and their ability to form new vessels.

When they blocked the VEGF molecules in osteoblasts, the enhancement of angiogenesis was impaired, indicating that VEGF function is crucial in this interaction. The overproduction of VEGF by osteoblasts was also detected in vivo using an experimental model of low bone mass. This research showed how the bone forming cells, osteoblasts, producing VEGF, strongly regulate blood vessel cells stimulating their angiogenic properties. This means that, in bone, the interactions of these two type of cells might play a key role in human diseases when unloading in disuse osteoporosis is present.

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