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Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Hu...
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| Zeitschriftentitel: | Circulation |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , |
| In: | Circulation, 128, 2013, 22, S. 2351-2363 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Hutter, Randolph Huang, Li Speidl, Walter S. Giannarelli, Chiara Trubin, Paul Bauriedel, Gerhard Klotman, Mary E. Fuster, Valentin Badimon, Juan J. Klotman, Paul E. Hutter, Randolph Huang, Li Speidl, Walter S. Giannarelli, Chiara Trubin, Paul Bauriedel, Gerhard Klotman, Mary E. Fuster, Valentin Badimon, Juan J. Klotman, Paul E. |
|---|---|
| author |
Hutter, Randolph Huang, Li Speidl, Walter S. Giannarelli, Chiara Trubin, Paul Bauriedel, Gerhard Klotman, Mary E. Fuster, Valentin Badimon, Juan J. Klotman, Paul E. |
| spellingShingle |
Hutter, Randolph Huang, Li Speidl, Walter S. Giannarelli, Chiara Trubin, Paul Bauriedel, Gerhard Klotman, Mary E. Fuster, Valentin Badimon, Juan J. Klotman, Paul E. Circulation Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma Physiology (medical) Cardiology and Cardiovascular Medicine |
| author_sort |
hutter, randolph |
| spelling |
Hutter, Randolph Huang, Li Speidl, Walter S. Giannarelli, Chiara Trubin, Paul Bauriedel, Gerhard Klotman, Mary E. Fuster, Valentin Badimon, Juan J. Klotman, Paul E. 0009-7322 1524-4539 Ovid Technologies (Wolters Kluwer Health) Physiology (medical) Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1161/circulationaha.113.004634 <jats:sec> <jats:title>Background—</jats:title> <jats:p>Smooth muscle cell (SMC) migration and proliferation critically influence the clinical course of vascular disease. We tested the effect of the novel small leucine-rich repeat protein podocan on SMC migration and proliferation using a podocan-deficient mouse in combination with a model of arterial injury and aortic explant SMC culture. In addition, we examined the effect of overexpression of the human form of podocan on human SMCs and tested for podocan expression in human atherosclerosis. In all these conditions, we concomitantly evaluated the Wnt-TCF (T-cell factor) pathway.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods and Results—</jats:title> <jats:p> Podocan was strongly and selectively expressed in arteries of wild-type mice after injury. Podocan-deficient mice showed increased arterial lesion formation compared with wild-type littermates in response to injury ( <jats:italic>P</jats:italic> <0.05). Also, SMC proliferation was increased in arteries of podocan-deficient mice compared with wild-type ( <jats:italic>P</jats:italic> <0.05). In vitro, migration and proliferation were increased in podocan-deficient SMCs and were normalized by transfection with the wild-type podocan gene ( <jats:italic>P</jats:italic> <0.05). In addition, upregulation of the Wnt-TCF pathway was found in SMCs of podocan-deficient mice both in vitro and in vivo. On the other hand, podocan overexpression in human SMCs significantly reduced SMC migration and proliferation, inhibiting the Wnt-TCF pathway. Podocan and a Wnt-TCF pathway marker were differently expressed in human coronary restenotic versus primary lesions. </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions—</jats:title> <jats:p>Podocan appears to be a potent negative regulator of the migration and proliferation of both murine and human SMCs. The lack of podocan results in excessive arterial repair and prolonged SMC proliferation, which likely is mediated by the Wnt-TCF pathway.</jats:p> </jats:sec> Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma Circulation |
| doi_str_mv |
10.1161/circulationaha.113.004634 |
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Online Free |
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Medizin Biologie |
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Ovid Technologies (Wolters Kluwer Health), 2013 |
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Ovid Technologies (Wolters Kluwer Health), 2013 |
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0009-7322 1524-4539 |
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Circulation |
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49 |
| title |
Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_unstemmed |
Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_full |
Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_fullStr |
Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_full_unstemmed |
Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_short |
Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_sort |
novel small leucine-rich repeat protein podocan is a negative regulator of migration and proliferation of smooth muscle cells, modulates neointima formation, and is expressed in human atheroma |
| topic |
Physiology (medical) Cardiology and Cardiovascular Medicine |
| url |
http://dx.doi.org/10.1161/circulationaha.113.004634 |
| publishDate |
2013 |
| physical |
2351-2363 |
| description |
<jats:sec>
<jats:title>Background—</jats:title>
<jats:p>Smooth muscle cell (SMC) migration and proliferation critically influence the clinical course of vascular disease. We tested the effect of the novel small leucine-rich repeat protein podocan on SMC migration and proliferation using a podocan-deficient mouse in combination with a model of arterial injury and aortic explant SMC culture. In addition, we examined the effect of overexpression of the human form of podocan on human SMCs and tested for podocan expression in human atherosclerosis. In all these conditions, we concomitantly evaluated the Wnt-TCF (T-cell factor) pathway.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Methods and Results—</jats:title>
<jats:p>
Podocan was strongly and selectively expressed in arteries of wild-type mice after injury. Podocan-deficient mice showed increased arterial lesion formation compared with wild-type littermates in response to injury (
<jats:italic>P</jats:italic>
<0.05). Also, SMC proliferation was increased in arteries of podocan-deficient mice compared with wild-type (
<jats:italic>P</jats:italic>
<0.05). In vitro, migration and proliferation were increased in podocan-deficient SMCs and were normalized by transfection with the wild-type podocan gene (
<jats:italic>P</jats:italic>
<0.05). In addition, upregulation of the Wnt-TCF pathway was found in SMCs of podocan-deficient mice both in vitro and in vivo. On the other hand, podocan overexpression in human SMCs significantly reduced SMC migration and proliferation, inhibiting the Wnt-TCF pathway. Podocan and a Wnt-TCF pathway marker were differently expressed in human coronary restenotic versus primary lesions.
</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Conclusions—</jats:title>
<jats:p>Podocan appears to be a potent negative regulator of the migration and proliferation of both murine and human SMCs. The lack of podocan results in excessive arterial repair and prolonged SMC proliferation, which likely is mediated by the Wnt-TCF pathway.</jats:p>
</jats:sec> |
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| author | Hutter, Randolph, Huang, Li, Speidl, Walter S., Giannarelli, Chiara, Trubin, Paul, Bauriedel, Gerhard, Klotman, Mary E., Fuster, Valentin, Badimon, Juan J., Klotman, Paul E. |
| author_facet | Hutter, Randolph, Huang, Li, Speidl, Walter S., Giannarelli, Chiara, Trubin, Paul, Bauriedel, Gerhard, Klotman, Mary E., Fuster, Valentin, Badimon, Juan J., Klotman, Paul E., Hutter, Randolph, Huang, Li, Speidl, Walter S., Giannarelli, Chiara, Trubin, Paul, Bauriedel, Gerhard, Klotman, Mary E., Fuster, Valentin, Badimon, Juan J., Klotman, Paul E. |
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| description | <jats:sec> <jats:title>Background—</jats:title> <jats:p>Smooth muscle cell (SMC) migration and proliferation critically influence the clinical course of vascular disease. We tested the effect of the novel small leucine-rich repeat protein podocan on SMC migration and proliferation using a podocan-deficient mouse in combination with a model of arterial injury and aortic explant SMC culture. In addition, we examined the effect of overexpression of the human form of podocan on human SMCs and tested for podocan expression in human atherosclerosis. In all these conditions, we concomitantly evaluated the Wnt-TCF (T-cell factor) pathway.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods and Results—</jats:title> <jats:p> Podocan was strongly and selectively expressed in arteries of wild-type mice after injury. Podocan-deficient mice showed increased arterial lesion formation compared with wild-type littermates in response to injury ( <jats:italic>P</jats:italic> <0.05). Also, SMC proliferation was increased in arteries of podocan-deficient mice compared with wild-type ( <jats:italic>P</jats:italic> <0.05). In vitro, migration and proliferation were increased in podocan-deficient SMCs and were normalized by transfection with the wild-type podocan gene ( <jats:italic>P</jats:italic> <0.05). In addition, upregulation of the Wnt-TCF pathway was found in SMCs of podocan-deficient mice both in vitro and in vivo. On the other hand, podocan overexpression in human SMCs significantly reduced SMC migration and proliferation, inhibiting the Wnt-TCF pathway. Podocan and a Wnt-TCF pathway marker were differently expressed in human coronary restenotic versus primary lesions. </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions—</jats:title> <jats:p>Podocan appears to be a potent negative regulator of the migration and proliferation of both murine and human SMCs. The lack of podocan results in excessive arterial repair and prolonged SMC proliferation, which likely is mediated by the Wnt-TCF pathway.</jats:p> </jats:sec> |
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| imprint_str_mv | Ovid Technologies (Wolters Kluwer Health), 2013 |
| institution | DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1 |
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| spelling | Hutter, Randolph Huang, Li Speidl, Walter S. Giannarelli, Chiara Trubin, Paul Bauriedel, Gerhard Klotman, Mary E. Fuster, Valentin Badimon, Juan J. Klotman, Paul E. 0009-7322 1524-4539 Ovid Technologies (Wolters Kluwer Health) Physiology (medical) Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1161/circulationaha.113.004634 <jats:sec> <jats:title>Background—</jats:title> <jats:p>Smooth muscle cell (SMC) migration and proliferation critically influence the clinical course of vascular disease. We tested the effect of the novel small leucine-rich repeat protein podocan on SMC migration and proliferation using a podocan-deficient mouse in combination with a model of arterial injury and aortic explant SMC culture. In addition, we examined the effect of overexpression of the human form of podocan on human SMCs and tested for podocan expression in human atherosclerosis. In all these conditions, we concomitantly evaluated the Wnt-TCF (T-cell factor) pathway.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods and Results—</jats:title> <jats:p> Podocan was strongly and selectively expressed in arteries of wild-type mice after injury. Podocan-deficient mice showed increased arterial lesion formation compared with wild-type littermates in response to injury ( <jats:italic>P</jats:italic> <0.05). Also, SMC proliferation was increased in arteries of podocan-deficient mice compared with wild-type ( <jats:italic>P</jats:italic> <0.05). In vitro, migration and proliferation were increased in podocan-deficient SMCs and were normalized by transfection with the wild-type podocan gene ( <jats:italic>P</jats:italic> <0.05). In addition, upregulation of the Wnt-TCF pathway was found in SMCs of podocan-deficient mice both in vitro and in vivo. On the other hand, podocan overexpression in human SMCs significantly reduced SMC migration and proliferation, inhibiting the Wnt-TCF pathway. Podocan and a Wnt-TCF pathway marker were differently expressed in human coronary restenotic versus primary lesions. </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions—</jats:title> <jats:p>Podocan appears to be a potent negative regulator of the migration and proliferation of both murine and human SMCs. The lack of podocan results in excessive arterial repair and prolonged SMC proliferation, which likely is mediated by the Wnt-TCF pathway.</jats:p> </jats:sec> Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma Circulation |
| spellingShingle | Hutter, Randolph, Huang, Li, Speidl, Walter S., Giannarelli, Chiara, Trubin, Paul, Bauriedel, Gerhard, Klotman, Mary E., Fuster, Valentin, Badimon, Juan J., Klotman, Paul E., Circulation, Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma, Physiology (medical), Cardiology and Cardiovascular Medicine |
| title | Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_full | Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_fullStr | Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_full_unstemmed | Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_short | Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| title_sort | novel small leucine-rich repeat protein podocan is a negative regulator of migration and proliferation of smooth muscle cells, modulates neointima formation, and is expressed in human atheroma |
| title_unstemmed | Novel Small Leucine-Rich Repeat Protein Podocan Is a Negative Regulator of Migration and Proliferation of Smooth Muscle Cells, Modulates Neointima Formation, and Is Expressed in Human Atheroma |
| topic | Physiology (medical), Cardiology and Cardiovascular Medicine |
| url | http://dx.doi.org/10.1161/circulationaha.113.004634 |