Effects of Copper on Proliferation and Autocrine Secretion of Insulin-Like Growth Factor-1 (IGF-1) and IGF-Binding Protein-3 (IGFBP-3) in Chondrocytes from Newborn Pigs In Vitro
Abstract:Chondrocytes from the lateral trochlear ridge of the distal femur taken from 1-day-old piglets were cultured in medium supplemented with 0, 7.8, 15.6, 31.2, and 62.5 μmol/L copper. Insulin-like growth factor-1 (IGF-1) and IGF-binding protein 3 (IGFBP-3) levels in culture medium were determined by radioimmunoassay. DNA synthesis in chondrocytes was measured by tritiated thymidine ((3)H-TdR) incorporation. Proliferation-promoting activity and incorporation of (3)H-TdR in chondrocytes were increased in all cultur… Show more
“…Copper deficiency in feeds and hence in animals would damage the synthesis of cartilage [19,20]. While there were few reports about the effect of copper on chondrocyte differentiation and function, our present research showed that copper can promote the proliferentiation of chondrocytes and the synthesis of cartilage matrix, affecting chondrocyte function [15,21].…”
The effects of different concentrations of copper on collagen content and alkaline phosphatase (AKP) activity from chondrocytes in newborn piglets were measured. Chondrocytes were cultured in media containing 15% fetal calf serum supplemented with 0, 15.6, 31.2, and 62.5 μmol/L copper in a 12-well culture plate. Collagen content and AKP activity from the chondrocyte extracellular matrix increased significantly in the culture media with 15.6, 31.2, and 62.5 μmol/L copper and was the highest at 31.2 μmol/L copper (P < 0.05). Thus, the results indicated that copper could promote AKP activity and collagen production by chondrocytes.
“…Copper deficiency in feeds and hence in animals would damage the synthesis of cartilage [19,20]. While there were few reports about the effect of copper on chondrocyte differentiation and function, our present research showed that copper can promote the proliferentiation of chondrocytes and the synthesis of cartilage matrix, affecting chondrocyte function [15,21].…”
The effects of different concentrations of copper on collagen content and alkaline phosphatase (AKP) activity from chondrocytes in newborn piglets were measured. Chondrocytes were cultured in media containing 15% fetal calf serum supplemented with 0, 15.6, 31.2, and 62.5 μmol/L copper in a 12-well culture plate. Collagen content and AKP activity from the chondrocyte extracellular matrix increased significantly in the culture media with 15.6, 31.2, and 62.5 μmol/L copper and was the highest at 31.2 μmol/L copper (P < 0.05). Thus, the results indicated that copper could promote AKP activity and collagen production by chondrocytes.
“…Under normal circumstances, IGFBP-3 is the main carrier of circulating IGF-1, due to its high affinity. In an in vitro study, it was observed that copper supplementation in a culture medium containing 15% fetal calf serum (FCS) could promote the autocrine secretion of IGF-1 and IGFBP-3 and stimulate chondrocyte proliferation [58]. Furthermore, an animal study, which was carried out in 60 weanling pigs, concluded that the effects of Cu in their diet to supplement their growth was related to the increased serum levels induced by Cu.…”
Copper is an essential micronutrient for humans. A cross-sectional and comparative study was done to assess serum Cu levels and serum copper/zinc (Cu/Zn) ratio and its association with nutritional indicators in a series of children and adolescents with chronic diseases. Anthropometric, biochemical, dietary, body composition, and bone densitometry assessments were carried out. Serum Cu and Zn were measured by atomic absorption spectrophotometry. Seventy-eight patients (55% women) participated. The mean serum Cu in the entire series and by nutritional status through body mass index (BMI) was normal. Serum Cu decreased significantly with age and was meaningfully higher in children than in adolescents. The risk of finding altered Cu levels in children and men was higher than in adolescents and women, respectively. Twenty-two per cent of patients had abnormal serum copper levels, 13 had hypercupremia, and four had hypocupremia. The Cu/Zn ratio was greater than 1.00 for 87% of the patients, which is an indicator of an inflammatory state. All patients with hypozincemia and hypocupremia had deficient Zn intake, but only 65% of the patients with hypercupremia had dietary Zn deficiency. Consequently, the Cu/Zn ratio could indicate an inflammatory state and a high risk of zinc deficiency in this specific child population.
“…IGF-1 can promote mammalian cell proliferation and is conducive to the growth of organisms (20,22,23). In mammals, the combination of IGF-1 and IGF-1R initiates a downstream signal transduction pathway, activating a transcription factor by transducing the extracellular signals into the nucleus.…”
Bone marrow mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) interact with each other. EPCs are able to promote the self‑renewal of MSCs as niche cells in murine bone marrow, and MSCs are able to promote EPC proliferation in vitro in a co‑culture system. It has previously been reported that MSCs can secrete insulin‑like growth factor‑1 (IGF‑1), which serves critical functions in EPC proliferation. However, the mechanism underlying the IGF‑1‑mediated proliferation of EPCs remains unclear. The aim of the present study was to reveal the molecular mechanisms regulating this process. The effects of IGF‑1, which is secreted by MSCs, on EPC proliferation via the PI3K/Akt signaling pathway were examined by MTT assay, reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The present study treated EPCs with various concentrations of IGF‑1. The results demonstrated that IGF‑1 significantly induced the proliferation of cultured EPCs. However, this effect was offset by treatment with the phosphatidylinositol 3‑kinase (PI3K) inhibitor LY294002. These results indicated that the pro‑proliferative effects of IGF‑1 are mediated in response to the PI3K/protein kinase B signaling pathway.
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