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Proinsulin C-peptide modulates the expression of ERK1/2, type I collagen and RANKL in human osteoblast-like cells (Saos-2). 2017
Cristina Russo, and
Veronica Lazzaro, and
Carmine Gazzaruso, and
Samantha Maurotti, and
Yvelise Ferro, and
Piero Pingitore, and
Francesca Fumo, and
Adriana Coppola, and
Pietro Gallotti, and
Valentina Zambianchi, and
Mariangela Fodaro, and
Emanuela Galliera, and
Monica Gioia Marazzi, and
Massimiliano Marco Corsi Romanelli, and
Sandro Giannini, and
Stefano Romeo, and
Arturo Pujia, and
Tiziana Montalcini
Department of Medical and Surgical Sciences, University "Magna Graecia" of Catanzaro, Catanzaro, Italy.
A lower bone mass accompanied by a higher bone fragility with increased risk of fracture are observed in individuals with type 1 diabetes mellitus. Low C-peptide levels are associated with low lumbar mineral density in postmenopausal woman. In this work, we investigated the role of C-peptide on the osteoblast cell biology in vitro. We examined intracellular pathways and we found that C peptide activates ERK1/2 in human osteoblast-like cells (Saos-2). We also observed that proinsulin C-peptide prevents a reduction of type I collagen expression and decreases, in combination with insulin, receptor activator of nuclear factor-κB (RANKL) levels. In this work we show for the first time that Cpeptide activates a specific intracellular pathway in osteoblasts and it modulates the expression of protein involved in bone remodeling. Our results suggest that both C-peptide may have a role in bone metabolism. Further studies are needing to fully clarify its role.
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