1,720,967 research outputs found
Chronic tryptophan deficency impairs bone metabolism and reduces bone accrual in growing rats
No full textCaratterizzazione dei meccanismi coinvolti nell'effetto di ghrelina sulla proliferazione degli osteoblasti e sulla regolazione del cross-talk tra osteoblasti ed osteoclasti
No full textCGRP facilitates canonical WNT signaling through PKA activation in human osteoblast-like cells
No full textRuolo della serotonina nel controllo della massa ossea in condizioni di ridotta attività fisica nel ratto
No full text
Tryptophan-deficient diet is associated with impaired bone metabolism and osteopenia in growing rats
No full textWnt pathway in the aging bone of postmenopausal women and the expression og genes relevant for osteoblast commitment, differentiation and activity
No full textCaratterizzazione delle cellule mesenchimali nell'osso della popolazione senile: effetti dell'invecchiamento sulla via canonica di Wnt
No full text17β-Estradiol positively modulates growth hormone signaling through the reduction of SOCS2 negative feedback in human osteoblasts
No full textRecent evidence demonstrated an interplay between estrogens and growth hormone (GH) at cellular level. To investigate the possible mechanism/s involved, we studied the effect of 17β-estradiol (E2) on GH signaling pathways in primary culture of human osteoblasts (hOBs). Exposure of hOBs to E2 (10(-8) M) 60 min before GH (5 ng/ml) significantly increased phosphorylated STAT5 (P-STAT5) levels compared with GH alone. E2 per se had no effect on P-STAT5. E2-enhanced GH signaling was effective in increasing osteopontin, bone-sialoprotein, and IGF II mRNA expression to a greater extent than GH alone. We then studied the effect of E2 on the protein levels of the negative regulator of GH signaling, suppressor of cytokine signaling-2 (SOCS2). E2 (10(-11) M-10(-7) M) reduced dose-dependently SOCS2 protein levels without modifying its mRNA expression. The silencing of SOCS2 gene prevented E2 positive effect on GH induced P-STAT5 and on GH induced bone-sialoprotein and osteopontin mRNA expression. Treatment with the inhibitor of DNA-dependent RNA synthesis, actinomycin-D, did not prevent E2 induced decrease of SOCS2, thus suggesting a non-genomic effect. E2 promoted an increase in SOCS2 ubiquitination. To determine if increased ubiquitination of SOCS2 by E2 led to degradation by proteasome, hOBs were pretreated with the proteasome inhibitor MG132 (5 μM) which blocked E2 reduction of SOCS2. These findings demonstrate for the first time that E2 can amplify GH intracellular signaling in hOBs with an essential role played by the reduction of the SOCS2 mediated feedback loop
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