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Signaling Pathway Defective in Osteoporotic Osteoblasts

May explain impaired osteoblast proliferation

FRIDAY, Dec. 21 (HealthDay News) -- Signaling through the insulin-like growth factor-1 (IGF-I) receptor is impaired in osteoblasts from osteoporotic patients, possibly explaining the impaired osteoblast proliferation in osteoporosis, according to the results of a study published online Dec. 13 in Endocrinology.

Sebastio Perrini, and colleagues from the University of Bari School of Medicine in Bari, Italy, compared IGF-I signaling in primary cultures of human osteoblasts from patients with osteoporosis and normal controls.

The researchers found that the IGF-I receptor in osteoporotic osteoblasts had higher basal tyrosine phosphorylation and reduced stimulated phosphorylation by IGF-I. This increase in basal phosphorylation was associated with increased basal tyrosine phosphorylation of IRS-2 and activation of Erk. Basal IRS-1, Akt, and GSK-3 phosphorylation was similar in osteoporotic and control osteoblasts and increased on IGF-I stimulation. Both basal and induced DNA synthesis after IGF-I treatment was reduced in osteoporotic osteoblasts.

"Collectively, our data show that altered osteoblast proliferation in human osteoporosis may result from dysregulation of IGF-I receptor signaling, including constitutive activation of the IRS-2/Erk signaling pathway, which becomes unresponsive to IGF-I, and defective induction of the IRS-1/Akt signaling pathway," Perrini and colleagues conclude.

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