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Originally published In Press as doi:10.1074/jbc.M308825200 on September 22, 2003

J. Biol. Chem., Vol. 278, Issue 50, 50195-50202, December 12, 2003
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Teriparatide (Human Parathyroid Hormone (1–34)) Inhibits Osteogenic Vascular Calcification in Diabetic Low Density Lipoprotein Receptor-deficient Mice*

Jian-Su Shao, Su-Li Cheng, Nichole Charlton-Kachigian, Arleen P. Loewy, and Dwight A. Towler{ddagger}

From the Department of Medicine, Division of Bone and Mineral Diseases, Washington University School of Medicine, Barnes-Jewish Hospital North Campus, St. Louis, Missouri 63110

Cardiovascular calcification is a common consequence of diabetes. High fat diets induce diabetes and arterial calcification in male low density lipoprotein receptor (LDLR) –/– mice; calcification occurs via Msx2 signaling that promotes the osteogenic differentiation of arterial myofibroblasts. We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1–34) (also called teriparatide) in LDLR –/– mice fed diabetogenic diets for 4 weeks. LDLR –/– mice were treated with vehicle or 0.4 mg/kg of PTH(1–34) subcutaneously five times/week. Gene expression was determined from single aortas and hind limb RNA by fluorescence reverse transcription-PCR. Valve calcification was determined by histological staining of cardiac sections using image analysis to quantify valve leaflet mineralization. PTH(1–34) increased bone mineral content (by dual energy x-ray absorptiometry) in LDLR –/– mice, with induction of osseous osteopontin (OPN) expression and serum OPN levels (>150 nM); PTH(1–34) did not significantly change serum glucose, lipids, body weight, or fat mass. PTH(1–34) suppressed aortic OPN and Msx2 expression >50% and decreased cardiac valve calcification 80% (8.3 ± 1.5% versus 1.4 ± 0.5%; p < 0.001). Of the known circulating regulators of vascular calcification (OPN, osteoprotegerin, and leptin), PTH(1–34) regulated only serum OPN. We therefore studied actions of PTH(1–34) and OPN in vitro on cells induced to mineralize with Msx2. OPN (5–50 nM) reversed Msx2-induced mineralization. PTH(1–34) inhibited mineralization by 40% and down-regulated Msx2 in aortic myofibroblasts. PTH(1–34) inhibits vascular calcification and aortic osteogenic differentiation via direct actions and potentially via circulating OPN. PTH(1–34) exerts beneficial actions at early stages of macrovascular disease responses to diabetes and dyslipidemia.

Received for publication, August 11, 2003 , and in revised form, September 14, 2003.

* This work was supported by National Institutes of Health Grant HL69229 (to D. A. T.) and by funds from the American Diabetes Association (to D. A. T.) and the Barnes-Jewish Hospital Research Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

{ddagger} To whom correspondence should be addressed: Div. of Bone and Mineral Diseases, Washington University School of Medicine, Barnes-Jewish Hospital North Campus, Box 8301, 7th Floor Steinberg, 216 South Kingshighway Blvd., St. Louis, MO 63110. Fax: 314-454-5047; E-mail: dtowler{at}im.wustl.edu.


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