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Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease
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| Zeitschriftentitel: | Hepatology Communications |
|---|---|
| Personen und Körperschaften: | , , , , , , , , |
| In: | Hepatology Communications, 2, 2018, 1, S. 84-98 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Magdaleno, Fernando Ge, Xiaodong Fey, Holger Lu, Yongke Gaskell, Harriet Blajszczak, Chuck C. Aloman, Costica Fiel, M. Isabel Nieto, Natalia Magdaleno, Fernando Ge, Xiaodong Fey, Holger Lu, Yongke Gaskell, Harriet Blajszczak, Chuck C. Aloman, Costica Fiel, M. Isabel Nieto, Natalia |
|---|---|
| author |
Magdaleno, Fernando Ge, Xiaodong Fey, Holger Lu, Yongke Gaskell, Harriet Blajszczak, Chuck C. Aloman, Costica Fiel, M. Isabel Nieto, Natalia |
| spellingShingle |
Magdaleno, Fernando Ge, Xiaodong Fey, Holger Lu, Yongke Gaskell, Harriet Blajszczak, Chuck C. Aloman, Costica Fiel, M. Isabel Nieto, Natalia Hepatology Communications Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease Hepatology |
| author_sort |
magdaleno, fernando |
| spelling |
Magdaleno, Fernando Ge, Xiaodong Fey, Holger Lu, Yongke Gaskell, Harriet Blajszczak, Chuck C. Aloman, Costica Fiel, M. Isabel Nieto, Natalia 2471-254X 2471-254X Ovid Technologies (Wolters Kluwer Health) Hepatology http://dx.doi.org/10.1002/hep4.1116 <jats:p>The aim of this study was to investigate the role of osteopontin (OPN) in hematopoietic stem cell (HPSC) mobilization to the liver and its contribution to alcoholic liver disease (ALD). We analyzed young (14‐16 weeks) and old (>1.5 years) wild‐type (WT) littermates and global <jats:italic toggle="yes">Opn</jats:italic> knockout (<jats:italic toggle="yes">Opn−/− </jats:italic>) mice for HPSC mobilization to the liver. In addition, WT and <jats:italic toggle="yes">Opn−/− </jats:italic> mice were chronically fed the Lieber–DeCarli diet for 7 weeks. Bone marrow (BM), blood, spleen, and liver were analyzed by flow cytometry for HPSC progenitors and polymorphonuclear neutrophils (PMNs). Chemokines, growth factors, and cytokines were measured in serum and liver. Prussian blue staining for iron deposits and naphthol AS‐D chloroacetate esterase staining for PMNs were performed on liver sections. Hematopoietic progenitors were lower in liver and BM of young compared to old <jats:italic toggle="yes">Opn−/− </jats:italic> mice. Granulocyte colony‐stimulating factor and macrophage colony‐stimulating factor were increased in <jats:italic toggle="yes">Opn−/− </jats:italic> mice, suggesting potential migration of HPSCs from the BM to the liver. Furthermore, ethanol‐fed <jats:italic toggle="yes">Opn−/− </jats:italic> mice showed significant hepatic PMN infiltration and hemosiderin compared to WT mice. As a result, ethanol feeding caused greater liver injury in <jats:italic toggle="yes">Opn−/− </jats:italic> compared to WT mice. <jats:italic toggle="yes">Conclusion: Opn</jats:italic> deletion promotes HPSC mobilization, PMN infiltration, and iron deposits in the liver and thereby enhances the severity of ALD. The age‐associated contribution of OPN to HPSC mobilization to the liver, the prevalence of PMNs, and accumulation of hepatic iron, which potentiates oxidant stress, reveal novel signaling mechanisms that could be targeted for therapeutic benefit in patients with ALD. (<jats:italic toggle="yes">Hepatology Communications</jats:italic> 2018;2:84–98)</jats:p> Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease Hepatology Communications |
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10.1002/hep4.1116 |
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Ovid Technologies (Wolters Kluwer Health), 2018 |
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Ovid Technologies (Wolters Kluwer Health), 2018 |
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2471-254X |
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Ovid Technologies (Wolters Kluwer Health) |
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Hepatology Communications |
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| title |
Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_unstemmed |
Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_full |
Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_fullStr |
Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_full_unstemmed |
Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_short |
Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_sort |
osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| topic |
Hepatology |
| url |
http://dx.doi.org/10.1002/hep4.1116 |
| publishDate |
2018 |
| physical |
84-98 |
| description |
<jats:p>The aim of this study was to investigate the role of osteopontin (OPN) in hematopoietic stem cell (HPSC) mobilization to the liver and its contribution to alcoholic liver disease (ALD). We analyzed young (14‐16 weeks) and old (>1.5 years) wild‐type (WT) littermates and global <jats:italic toggle="yes">Opn</jats:italic> knockout (<jats:italic toggle="yes">Opn−/−
</jats:italic>) mice for HPSC mobilization to the liver. In addition, WT and <jats:italic toggle="yes">Opn−/−
</jats:italic> mice were chronically fed the Lieber–DeCarli diet for 7 weeks. Bone marrow (BM), blood, spleen, and liver were analyzed by flow cytometry for HPSC progenitors and polymorphonuclear neutrophils (PMNs). Chemokines, growth factors, and cytokines were measured in serum and liver. Prussian blue staining for iron deposits and naphthol AS‐D chloroacetate esterase staining for PMNs were performed on liver sections. Hematopoietic progenitors were lower in liver and BM of young compared to old <jats:italic toggle="yes">Opn−/−
</jats:italic> mice. Granulocyte colony‐stimulating factor and macrophage colony‐stimulating factor were increased in <jats:italic toggle="yes">Opn−/−
</jats:italic> mice, suggesting potential migration of HPSCs from the BM to the liver. Furthermore, ethanol‐fed <jats:italic toggle="yes">Opn−/−
</jats:italic> mice showed significant hepatic PMN infiltration and hemosiderin compared to WT mice. As a result, ethanol feeding caused greater liver injury in <jats:italic toggle="yes">Opn−/−
</jats:italic> compared to WT mice. <jats:italic toggle="yes">Conclusion: Opn</jats:italic> deletion promotes HPSC mobilization, PMN infiltration, and iron deposits in the liver and thereby enhances the severity of ALD. The age‐associated contribution of OPN to HPSC mobilization to the liver, the prevalence of PMNs, and accumulation of hepatic iron, which potentiates oxidant stress, reveal novel signaling mechanisms that could be targeted for therapeutic benefit in patients with ALD. (<jats:italic toggle="yes">Hepatology Communications</jats:italic> 2018;2:84–98)</jats:p> |
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| author | Magdaleno, Fernando, Ge, Xiaodong, Fey, Holger, Lu, Yongke, Gaskell, Harriet, Blajszczak, Chuck C., Aloman, Costica, Fiel, M. Isabel, Nieto, Natalia |
| author_facet | Magdaleno, Fernando, Ge, Xiaodong, Fey, Holger, Lu, Yongke, Gaskell, Harriet, Blajszczak, Chuck C., Aloman, Costica, Fiel, M. Isabel, Nieto, Natalia, Magdaleno, Fernando, Ge, Xiaodong, Fey, Holger, Lu, Yongke, Gaskell, Harriet, Blajszczak, Chuck C., Aloman, Costica, Fiel, M. Isabel, Nieto, Natalia |
| author_sort | magdaleno, fernando |
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| description | <jats:p>The aim of this study was to investigate the role of osteopontin (OPN) in hematopoietic stem cell (HPSC) mobilization to the liver and its contribution to alcoholic liver disease (ALD). We analyzed young (14‐16 weeks) and old (>1.5 years) wild‐type (WT) littermates and global <jats:italic toggle="yes">Opn</jats:italic> knockout (<jats:italic toggle="yes">Opn−/− </jats:italic>) mice for HPSC mobilization to the liver. In addition, WT and <jats:italic toggle="yes">Opn−/− </jats:italic> mice were chronically fed the Lieber–DeCarli diet for 7 weeks. Bone marrow (BM), blood, spleen, and liver were analyzed by flow cytometry for HPSC progenitors and polymorphonuclear neutrophils (PMNs). Chemokines, growth factors, and cytokines were measured in serum and liver. Prussian blue staining for iron deposits and naphthol AS‐D chloroacetate esterase staining for PMNs were performed on liver sections. Hematopoietic progenitors were lower in liver and BM of young compared to old <jats:italic toggle="yes">Opn−/− </jats:italic> mice. Granulocyte colony‐stimulating factor and macrophage colony‐stimulating factor were increased in <jats:italic toggle="yes">Opn−/− </jats:italic> mice, suggesting potential migration of HPSCs from the BM to the liver. Furthermore, ethanol‐fed <jats:italic toggle="yes">Opn−/− </jats:italic> mice showed significant hepatic PMN infiltration and hemosiderin compared to WT mice. As a result, ethanol feeding caused greater liver injury in <jats:italic toggle="yes">Opn−/− </jats:italic> compared to WT mice. <jats:italic toggle="yes">Conclusion: Opn</jats:italic> deletion promotes HPSC mobilization, PMN infiltration, and iron deposits in the liver and thereby enhances the severity of ALD. The age‐associated contribution of OPN to HPSC mobilization to the liver, the prevalence of PMNs, and accumulation of hepatic iron, which potentiates oxidant stress, reveal novel signaling mechanisms that could be targeted for therapeutic benefit in patients with ALD. (<jats:italic toggle="yes">Hepatology Communications</jats:italic> 2018;2:84–98)</jats:p> |
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| imprint | Ovid Technologies (Wolters Kluwer Health), 2018 |
| imprint_str_mv | Ovid Technologies (Wolters Kluwer Health), 2018 |
| institution | DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1 |
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| physical | 84-98 |
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| spelling | Magdaleno, Fernando Ge, Xiaodong Fey, Holger Lu, Yongke Gaskell, Harriet Blajszczak, Chuck C. Aloman, Costica Fiel, M. Isabel Nieto, Natalia 2471-254X 2471-254X Ovid Technologies (Wolters Kluwer Health) Hepatology http://dx.doi.org/10.1002/hep4.1116 <jats:p>The aim of this study was to investigate the role of osteopontin (OPN) in hematopoietic stem cell (HPSC) mobilization to the liver and its contribution to alcoholic liver disease (ALD). We analyzed young (14‐16 weeks) and old (>1.5 years) wild‐type (WT) littermates and global <jats:italic toggle="yes">Opn</jats:italic> knockout (<jats:italic toggle="yes">Opn−/− </jats:italic>) mice for HPSC mobilization to the liver. In addition, WT and <jats:italic toggle="yes">Opn−/− </jats:italic> mice were chronically fed the Lieber–DeCarli diet for 7 weeks. Bone marrow (BM), blood, spleen, and liver were analyzed by flow cytometry for HPSC progenitors and polymorphonuclear neutrophils (PMNs). Chemokines, growth factors, and cytokines were measured in serum and liver. Prussian blue staining for iron deposits and naphthol AS‐D chloroacetate esterase staining for PMNs were performed on liver sections. Hematopoietic progenitors were lower in liver and BM of young compared to old <jats:italic toggle="yes">Opn−/− </jats:italic> mice. Granulocyte colony‐stimulating factor and macrophage colony‐stimulating factor were increased in <jats:italic toggle="yes">Opn−/− </jats:italic> mice, suggesting potential migration of HPSCs from the BM to the liver. Furthermore, ethanol‐fed <jats:italic toggle="yes">Opn−/− </jats:italic> mice showed significant hepatic PMN infiltration and hemosiderin compared to WT mice. As a result, ethanol feeding caused greater liver injury in <jats:italic toggle="yes">Opn−/− </jats:italic> compared to WT mice. <jats:italic toggle="yes">Conclusion: Opn</jats:italic> deletion promotes HPSC mobilization, PMN infiltration, and iron deposits in the liver and thereby enhances the severity of ALD. The age‐associated contribution of OPN to HPSC mobilization to the liver, the prevalence of PMNs, and accumulation of hepatic iron, which potentiates oxidant stress, reveal novel signaling mechanisms that could be targeted for therapeutic benefit in patients with ALD. (<jats:italic toggle="yes">Hepatology Communications</jats:italic> 2018;2:84–98)</jats:p> Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease Hepatology Communications |
| spellingShingle | Magdaleno, Fernando, Ge, Xiaodong, Fey, Holger, Lu, Yongke, Gaskell, Harriet, Blajszczak, Chuck C., Aloman, Costica, Fiel, M. Isabel, Nieto, Natalia, Hepatology Communications, Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease, Hepatology |
| title | Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_full | Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_fullStr | Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_full_unstemmed | Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_short | Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_sort | osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| title_unstemmed | Osteopontin deletion drives hematopoietic stem cell mobilization to the liver and increases hepatic iron contributing to alcoholic liver disease |
| topic | Hepatology |
| url | http://dx.doi.org/10.1002/hep4.1116 |