NYU Dentistry Study Finds Evidence That Protein MCP-1 May Determine Bone Loss Responses to Parathyroid Hormone

Image by JOSE LUIS CALVO MARTIN & JOSE ENRIQUE GARCIA-MAURIÑO MUZQUIZ/ ISTOCK/ GETTY IMAGES PLUS

In a study published in Scientific Reports, New York University College of Dentistry (NYU Dentistry) researchers investigating the catabolic effect of parathyroid hormone (PTH) in hyperparathyroidism (HPT) showed that monocyte chemoattractant protein-1 (MCP-1) is required for catabolic responses to PTH. HTP is a condition in which an abnormally high concentration of PTH in the blood accelerates bone loss.

NYU Dentistry reports, researchers focused on the role of MCP-1 in PTH-induced osteoclast formation. The team recreated the hyperparathyroid state in mice by constantly elevating their hyperparathyroid levels. Over a two-week period, they continuously infused female wild-type and MCP-1 knockout mice with human PTH. They showed that the ability of PTH to increase osteoclast formation in vitro is markedly impaired in cells from MCP-1 knockout mice and concluded that MCP-1 is an important chemokine, or signaling protein, in PTH-induced osteoclast formation and bone resorption.

The findings support the possibility that MCP-1 could be a marker for how PTH works in humans with hyperparathyroidism, as elevated serum MCP-1 has been shown to be correlated with elevated serum PTH levels in women.

The study, “Catabolic Effects of Human PTH (1–34) on Bone: Requirement of Monocyte Chemoattractant Protein-1 in Murine Model of Hyperparathyroidism,” was published in November.

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