2012Unpublished venueRequires access

Expression of RANKL and OPG in primary osteoblasts

Jesús Delgado‐Calle, Carolina Sañudo, Manuel Sumillera, Garcés Cm, Riancho Ja, José A. Riancho

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Abstract

Summary Objective: Osteoblasts are specialized cells responsible for bone formation. Furthermore, these cells modulate osteoclast formation and maturation, mainly by the production of RANKL and OPG. We previously reported that the bone tissue of osteoporotic patients showed increased RANKL expression and RANKL/OPG ratio when compared to osteoarthritic patients. Thus we decided to explore whether this aberrant expression may be related to an abnormal expression of these genes by osteoblasts. The aim of this study was to explore the transcriptional levels of these factors in primary osteoblasts. Methods: Primary human osteoblasts (hOBs) were obtained by the primary explant technique from bone tissue of patients undergoing hip replacement surgery for hip fractures (n=28) or osteoarthritis (n=26). Patients with secondary osteoporosis, fractures due to high-energy trauma or secondary osteoarthritis were excluded. RANKL and OPG gene expression was explored by real time quantitative PCR. Results: No statistical differences in RANKL and OPG gene expression were found along the in vitro mineralization of hOBs. Interestingly, OPG transcriptional levels were markedly higher than RANKL levels. However, no differences in the transcriptional levels of RANKL and OPG were observed between both groups. Conclusions: Overall, our data confirm that osteoblasts produce RANKL and OPG. However, our results suggest that the gene expression differences found in the osteoporotic and osteoarthritic bone tissue are not explained by the intrinsic characteristics of osteoblasts.

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What this paper is about

Summary Objective: Osteoblasts are specialized cells responsible for bone formation. Furthermore, these cells modulate osteoclast formation and maturation, mainly by the production of RANKL and OPG. We previously reported that the bone tissue of osteoporotic patients showed increased RANKL expression and RANKL/OPG ratio when compared to osteoarthritic patients. Thus we decided to explore whether this aberrant expression may be related to an abnormal expression of these genes by osteoblasts. The aim of this study was to explore the transcriptional levels of these factors in primary osteoblasts. Methods: Primary human osteoblasts (hOBs) were obtained by the primary explant technique from bone tissue of patients undergoing hip replacement surgery for hip fractures (n=28) or osteoarthritis (n=26). Patients with secondary osteoporosis, fractures due to high-energy trauma or secondary osteoarthritis were excluded. RANKL and OPG gene expression was explored by real time quantitative PCR. Results: No statistical differences in RANKL and OPG gene expression were found along the in vitro mineralization of hOBs. Interestingly, OPG transcriptional levels were markedly higher than RANKL levels. However, no differences in the transcriptional levels of RANKL and OPG were observed between both groups. Conclusions: Overall, our data confirm that osteoblasts produce RANKL and OPG. However, our results suggest that the gene expression differences found in the osteoporotic and osteoarthritic bone tissue are not explained by the intrinsic characteristics of osteoblasts.

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Available abstract

Summary Objective: Osteoblasts are specialized cells responsible for bone formation. Furthermore, these cells modulate osteoclast formation and maturation, mainly by the production of RANKL and OPG. We previously reported that the bone tissue of osteoporotic patients showed increased RANKL expression and RANKL/OPG ratio when compared to osteoarthritic patients. Thus we decided to explore whether this aberrant expression may be related to an abnormal expression of these genes by osteoblasts. The aim of this study was to explore the transcriptional levels of these factors in primary osteoblasts. Methods: Primary human osteoblasts (hOBs) were obtained by the primary explant technique from bone tissue of patients undergoing hip replacement surgery for hip fractures (n=28) or osteoarthritis (n=26). Patients with secondary osteoporosis, fractures due to high-energy trauma or secondary osteoarthritis were excluded. RANKL and OPG gene expression was explored by real time quantitative PCR. Results: No statistical differences in RANKL and OPG gene expression were found along the in vitro mineralization of hOBs. Interestingly, OPG transcriptional levels were markedly higher than RANKL levels. However, no differences in the transcriptional levels of RANKL and OPG were observed between both groups. Conclusions: Overall, our data confirm that osteoblasts produce RANKL and OPG. However, our results suggest that the gene expression differences found in the osteoporotic and osteoarthritic bone tissue are not explained by the intrinsic characteristics of osteoblasts.

Key concepts: RANKL, Osteoprotegerin, Osteoporosis, Osteoarthritis, Osteoclast, Osteoblast, Internal medicine, Bone remodeling

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