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Published on: June 8, 2014
Atorvastatin Reduces Circulating Osteoprogenitor Cells and T-Cell RANKL Expression in Osteoporotic Women:
Marcello Rattazzi1,2, Elisabetta Faggin1, Roberta Buso1,2
1Department of Medicine, University of Padova, Padova, Italy.
Insights
Atorvastatin treatment reduced circulating osteoprogenitor cells and T-cell receptor activator of nuclear factor kappa-B ligand (RANKL) expression, while increasing osteoprotegerin (OPG) levels. These findings suggest statins may protect the bone-vascular axis.
Area of Science:
- Endocrinology
- Immunology
- Cardiovascular Research
Background:
- Osteoporosis and vascular calcification share common pathways involving osteoprogenitors and receptor activator of nuclear factor kappa-B ligand (RANKL).
- The impact of statin therapy on the bone-vascular axis remains unclear.
Purpose of the Study:
- To investigate the effects of Atorvastatin on circulating osteoprogenitors and RANKL expression in immune cells.
- To explore the potential role of statins in modulating the bone-vascular axis.
Main Methods:
- Twenty postmenopausal osteoporotic hypercholesterolemic women received Atorvastatin (40 mg/day) for 3 months.
- Gene expression analysis of osteoprotegerin (OPG)/RANK/RANKL in T cells and monocytes.
- Flow cytometry to assess circulating osteoprogenitor cells.
Main Results:
- Atorvastatin reduced total cholesterol and LDL-C.
- Increased serum OPG levels and decreased osteocalcin (OCN).
- Reduced RANKL expression in T cells and circulating CD34(+) osteoprogenitor cells.
Conclusions:
- Three-month Atorvastatin treatment reduces osteoprogenitor cells and T-cell RANKL expression, increasing OPG.
- Statins may offer protective benefits for the bone-vascular axis.
Aim:
Circulating osteoprogenitors and receptor activator of nuclear factor kappa-B ligand (RANKL) expression in immune cells have been implicated in the pathogenesis of osteoporosis and vascular calcification. The role played by statin therapy in the bone-vascular axis is unknown.
Methods:
Twenty naïve postmenopausal osteoporotic hypercholesterolemic women were treated with Atorvastatin 40 mg/day for 3 months. Gene expression analysis was performed to assess modification in osteoprotegerin (OPG)/RANK/RANKL expression in isolated T cells and monocytes. A flow cytometry analysis was used to study changes in the levels of circulating osteoprogenitor cells.
Results:
After 3 months of treatment, Atorvastatin significantly reduced total cholesterol and LDL-C, without affecting HDL-C and triglycerides. Among circulating bone and phosphocalcium homeostasis markers, we found a significant increase in OPG levels (P < 0.01) and a modest reduction in osteocalcin (OCN) (P < 0.05). We also observed a significant reduction in RANKL expression in T cells (P < 0.05). No differences were found in the expression of RANK in T cells and RANKL and RANK in monocytes. OPG expression was low in both immune cell types and was not affected by the treatment. As for circulating osteoprogenitors, we found a significant reduction of CD34(+) BAP(+) (P < 0.05) and CD34(+) OCN(+) BAP(+) (P < 0.05) cells. In vitro studies showed that Atorvastatin reduced RANKL expression in activated human T-lymphoblastoid cells (Jurkat cell line).
Conclusions:
Three-month Atorvastatin treatment leads to a reduction in circulating osteoprogenitor cells and RANKL expression in T cells, as well as increase in OPG serum levels. These data suggest that statins could have protective effects in the bone-vascular axis.
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