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    <subfield code="2">doi</subfield>
    <subfield code="a">10.1161/ATVBAHA.106.132266</subfield>
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  <datafield tag="024" ind1="8" ind2=" ">
    <subfield code="2">sideral</subfield>
    <subfield code="a">66931</subfield>
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  <datafield tag="037" ind1=" " ind2=" ">
    <subfield code="a">ART-2007-66931</subfield>
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  <datafield tag="041" ind1=" " ind2=" ">
    <subfield code="a">eng</subfield>
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  <datafield tag="100" ind1=" " ind2=" ">
    <subfield code="a">Villa-Bellosta, Ricardo</subfield>
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  <datafield tag="245" ind1=" " ind2=" ">
    <subfield code="a">Characterization of Phosphate Transport in Rat Vascular Smooth Muscle Cells: Implication for Vascular Calcification</subfield>
  </datafield>
  <datafield tag="260" ind1=" " ind2=" ">
    <subfield code="c">2007</subfield>
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  <datafield tag="520" ind1="3" ind2=" ">
    <subfield code="a">Objective— Hyperphosphatemia and inorganic phosphate (Pi) transport by vascular smooth muscle cells (VSMCs) have been implicated in the pathogenesis of vascular calcification. The aim of this work has been to characterize Pi transport in VSMCs.
Methods and Results— Primary cultures of VSMCs express both high affinity Na-dependent and Na-independent components of Pi transport. Under physiological conditions both transport systems are saturated, show similar activity, and are inhibited by increasing pH. The Na-dependent transport is also weakly inhibited by phosphonoformic acid (PFA) (3.9 mmol/L IC50 at 0.05 mmol/L Pi). Real-time polymerase chain reaction shows that Pit1 and Pit2 are expressed to the same degree, and no other Pi transporters are significantly expressed. When expressed in Xenopus oocytes they are strictly Na-dependent, with high affinities for Pi, and are inhibited by increasing pH, but only weakly inhibited by PFA. We have used RNA interference to demonstrate that Pit1 and Pit2 are the transporters responsible for Na-dependent Pi transport in VSMCs.
Conclusions— Taken together these novel findings suggest new roles of Pi transport in the pathogenesis of VC and have implications as potential future clinical targets.</subfield>
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    <subfield code="a">Access copy available to the general public</subfield>
    <subfield code="f">Unrestricted</subfield>
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  <datafield tag="536" ind1=" " ind2=" ">
    <subfield code="9">info:eu-repo/grantAgreement/ES/MEC/BFU2016-06284-BFI</subfield>
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    <subfield code="9">info:eu-repo/semantics/openAccess</subfield>
    <subfield code="a">All rights reserved</subfield>
    <subfield code="u">http://www.europeana.eu/rights/rr-f/</subfield>
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  <datafield tag="590" ind1=" " ind2=" ">
    <subfield code="a">7.221</subfield>
    <subfield code="b">2007</subfield>
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  <datafield tag="591" ind1=" " ind2=" ">
    <subfield code="a">PERIPHERAL VASCULAR DISEASE</subfield>
    <subfield code="b">3 / 54 = 0.056</subfield>
    <subfield code="c">2007</subfield>
    <subfield code="d">Q1</subfield>
    <subfield code="e">T1</subfield>
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    <subfield code="a">HEMATOLOGY</subfield>
    <subfield code="b">5 / 62 = 0.081</subfield>
    <subfield code="c">2007</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Bogaert, Yolanda E.</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Levi, Moshe</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Sorribas, Víctor</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0003-3457-323X</subfield>
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    <subfield code="1">1000</subfield>
    <subfield code="2">807</subfield>
    <subfield code="a">Universidad de Zaragoza</subfield>
    <subfield code="b">Dpto. Anat.Pat.Med.Leg.For.To.</subfield>
    <subfield code="c">Area Toxicología</subfield>
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  <datafield tag="773" ind1=" " ind2=" ">
    <subfield code="g">27, 5 (2007), 1030-1036</subfield>
    <subfield code="p">Arterioscler. thromb. vasc. biol.</subfield>
    <subfield code="t">Arteriosclerosis, Thrombosis, and Vascular Biology</subfield>
    <subfield code="x">1079-5642</subfield>
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