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Induction of Senile Osteoporosis in Normal Mice by Intra‐Bone Marrow‐Bone Marrow Transplantation from Osteoporosis‐Prone Mice
A P6 substrain of the senescence accelerated mouse (SAMP6) spontaneously develops osteoporosis early in life. These mice show the clinical signs of osteoporosis, such as elevated levels of urinary deoxypyridinoline (Dpd), decreased bone mineral density (BMD), and a significant loss of trabecular and...
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| Published in: | Stem cells (Dayton, Ohio) Ohio), 2007-06, Vol.25 (6), p.1356-1363 |
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| cited_by | cdi_FETCH-LOGICAL-c5476-d45522eba27871f706b72b37bea3dece3166361f8ff59529ad0135d8f45055c3 |
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| container_title | Stem cells (Dayton, Ohio) |
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| creator | Ueda, Yusuke Inaba, Muneo Takada, Keizo Fukui, Junichi Sakaguchi, Yutaku Tsuda, Masanobu Omae, Mariko Kushida, Taketoshi Iida, Hirokazu Ikehara, Susumu |
| description | A P6 substrain of the senescence accelerated mouse (SAMP6) spontaneously develops osteoporosis early in life. These mice show the clinical signs of osteoporosis, such as elevated levels of urinary deoxypyridinoline (Dpd), decreased bone mineral density (BMD), and a significant loss of trabecular and cortical bone thickness at 12 months of age. Here, we describe the transfer of osteoporosis to a normal strain by the injection of bone marrow cells from SAMP6 donors directly into the bone marrow cavity (intra‐bone marrow‐bone marrow transplantation [IBM‐BMT]). More than 1 month after IBM‐BMT, hematolymphoid cells were completely reconstituted by donor‐derived cells, and bone marrow stromal cells that could differentiate into osteocytes were also found to be of donor origin. In addition, the recipient C57BL/6 mouse showed the features of osteoporosis in the trabecular bone. Decreases in BMD and increases in urinary Dpd were also observed. When the message levels of cytokines (interleukin [IL]‐11, IL‐6, receptor activator of NF‐κB ligand [RANKL], osteoprotegerin, macrophage–colony‐stimulating factor, and insulin‐like growth factor‐1) were examined by reverse transcription‐polymerase chain reaction (RT‐PCR) and real‐time RT‐PCR analysis, IL‐6 and IL‐11 were reduced to a level similar to that in SAMP6 mice, whereas that of RANKL was increased. These findings indicate that not only the hemopoietic system but also the bone marrow microenvironment are reconstituted as a result of IBM‐BMT, and suggest that the development of senile osteoporosis might be attributable to “stem cell disorders.”
Disclosure of potential conflicts of interest is found at the end of this article. |
| doi_str_mv | 10.1634/stemcells.2006-0811 |
| format | article |
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Disclosure of potential conflicts of interest is found at the end of this article.</description><identifier>ISSN: 1066-5099</identifier><identifier>EISSN: 1549-4918</identifier><identifier>DOI: 10.1634/stemcells.2006-0811</identifier><identifier>PMID: 17347492</identifier><language>eng</language><publisher>Bristol: John Wiley & Sons, Ltd</publisher><subject>Amino Acids - urine ; Animals ; Antigens, Surface - analysis ; Bone Density ; Bone Marrow Transplantation ; Cells, Cultured ; Cytokines - analysis ; Disease Models, Animal ; Female ; Infusions, Intraosseous ; Intra‐bone marrow injection ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Osteoporosis - etiology ; Osteoporosis - immunology ; Osteoporosis - metabolism ; Osteoporosis - pathology ; Senile osteoporosis Senescence accelerated mouse P6 ; Stem cell disorder</subject><ispartof>Stem cells (Dayton, Ohio), 2007-06, Vol.25 (6), p.1356-1363</ispartof><rights>Copyright © 2007 AlphaMed Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5476-d45522eba27871f706b72b37bea3dece3166361f8ff59529ad0135d8f45055c3</citedby><cites>FETCH-LOGICAL-c5476-d45522eba27871f706b72b37bea3dece3166361f8ff59529ad0135d8f45055c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1634%2Fstemcells.2006-0811$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1634%2Fstemcells.2006-0811$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17347492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ueda, Yusuke</creatorcontrib><creatorcontrib>Inaba, Muneo</creatorcontrib><creatorcontrib>Takada, Keizo</creatorcontrib><creatorcontrib>Fukui, Junichi</creatorcontrib><creatorcontrib>Sakaguchi, Yutaku</creatorcontrib><creatorcontrib>Tsuda, Masanobu</creatorcontrib><creatorcontrib>Omae, Mariko</creatorcontrib><creatorcontrib>Kushida, Taketoshi</creatorcontrib><creatorcontrib>Iida, Hirokazu</creatorcontrib><creatorcontrib>Ikehara, Susumu</creatorcontrib><title>Induction of Senile Osteoporosis in Normal Mice by Intra‐Bone Marrow‐Bone Marrow Transplantation from Osteoporosis‐Prone Mice</title><title>Stem cells (Dayton, Ohio)</title><addtitle>Stem Cells</addtitle><description>A P6 substrain of the senescence accelerated mouse (SAMP6) spontaneously develops osteoporosis early in life. These mice show the clinical signs of osteoporosis, such as elevated levels of urinary deoxypyridinoline (Dpd), decreased bone mineral density (BMD), and a significant loss of trabecular and cortical bone thickness at 12 months of age. Here, we describe the transfer of osteoporosis to a normal strain by the injection of bone marrow cells from SAMP6 donors directly into the bone marrow cavity (intra‐bone marrow‐bone marrow transplantation [IBM‐BMT]). More than 1 month after IBM‐BMT, hematolymphoid cells were completely reconstituted by donor‐derived cells, and bone marrow stromal cells that could differentiate into osteocytes were also found to be of donor origin. In addition, the recipient C57BL/6 mouse showed the features of osteoporosis in the trabecular bone. Decreases in BMD and increases in urinary Dpd were also observed. When the message levels of cytokines (interleukin [IL]‐11, IL‐6, receptor activator of NF‐κB ligand [RANKL], osteoprotegerin, macrophage–colony‐stimulating factor, and insulin‐like growth factor‐1) were examined by reverse transcription‐polymerase chain reaction (RT‐PCR) and real‐time RT‐PCR analysis, IL‐6 and IL‐11 were reduced to a level similar to that in SAMP6 mice, whereas that of RANKL was increased. These findings indicate that not only the hemopoietic system but also the bone marrow microenvironment are reconstituted as a result of IBM‐BMT, and suggest that the development of senile osteoporosis might be attributable to “stem cell disorders.”
Disclosure of potential conflicts of interest is found at the end of this article.</description><subject>Amino Acids - urine</subject><subject>Animals</subject><subject>Antigens, Surface - analysis</subject><subject>Bone Density</subject><subject>Bone Marrow Transplantation</subject><subject>Cells, Cultured</subject><subject>Cytokines - analysis</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Infusions, Intraosseous</subject><subject>Intra‐bone marrow injection</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Osteoporosis - etiology</subject><subject>Osteoporosis - immunology</subject><subject>Osteoporosis - metabolism</subject><subject>Osteoporosis - pathology</subject><subject>Senile osteoporosis Senescence accelerated mouse P6</subject><subject>Stem cell disorder</subject><issn>1066-5099</issn><issn>1549-4918</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNqNkctKxDAUQIMovr9AkKzcVZPmjSsVHwOOCs4-pG0ClTYZkw4yO8Ef8Bv9EjPOoLjSVRI498DNAeAAo2PMCT1Jg-1r23XpuESIF0hivAa2MaOqoArL9XxHnBcMKbUFdlJ6QghTJuUm2MKCUEFVuQ3eRr6Z1UMbPAwOPlrfdhbeZ3WYhhhSm2Dr4V2IvenguK0trOZw5IdoPl7fz4O3cGxiDC-_X3ASjU_TzvjBfKldDP0va-Yf4tdAdu6BDWe6ZPdX5y6YXF1OLm6K2_vr0cXZbVEzKnjRUMbK0lamFFJgJxCvRFkRUVlDGltbgjknHDvpHFOsVKZBmLBGOsoQYzXZBUdL7TSG55lNg-7btPhA422YJS0QExwh-SeIlZJYcJVBsgTrvFSK1ulpbHsT5xojvWikvxvpRSO9aJSnDlf6WdXb5mdmFSUDp0vgJceY_8epHyeX45LldTn5BM4ap1k</recordid><startdate>200706</startdate><enddate>200706</enddate><creator>Ueda, Yusuke</creator><creator>Inaba, Muneo</creator><creator>Takada, Keizo</creator><creator>Fukui, Junichi</creator><creator>Sakaguchi, Yutaku</creator><creator>Tsuda, Masanobu</creator><creator>Omae, Mariko</creator><creator>Kushida, Taketoshi</creator><creator>Iida, Hirokazu</creator><creator>Ikehara, Susumu</creator><general>John Wiley & Sons, Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7QP</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200706</creationdate><title>Induction of Senile Osteoporosis in Normal Mice by Intra‐Bone Marrow‐Bone Marrow Transplantation from Osteoporosis‐Prone Mice</title><author>Ueda, Yusuke ; 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These mice show the clinical signs of osteoporosis, such as elevated levels of urinary deoxypyridinoline (Dpd), decreased bone mineral density (BMD), and a significant loss of trabecular and cortical bone thickness at 12 months of age. Here, we describe the transfer of osteoporosis to a normal strain by the injection of bone marrow cells from SAMP6 donors directly into the bone marrow cavity (intra‐bone marrow‐bone marrow transplantation [IBM‐BMT]). More than 1 month after IBM‐BMT, hematolymphoid cells were completely reconstituted by donor‐derived cells, and bone marrow stromal cells that could differentiate into osteocytes were also found to be of donor origin. In addition, the recipient C57BL/6 mouse showed the features of osteoporosis in the trabecular bone. Decreases in BMD and increases in urinary Dpd were also observed. When the message levels of cytokines (interleukin [IL]‐11, IL‐6, receptor activator of NF‐κB ligand [RANKL], osteoprotegerin, macrophage–colony‐stimulating factor, and insulin‐like growth factor‐1) were examined by reverse transcription‐polymerase chain reaction (RT‐PCR) and real‐time RT‐PCR analysis, IL‐6 and IL‐11 were reduced to a level similar to that in SAMP6 mice, whereas that of RANKL was increased. These findings indicate that not only the hemopoietic system but also the bone marrow microenvironment are reconstituted as a result of IBM‐BMT, and suggest that the development of senile osteoporosis might be attributable to “stem cell disorders.”
Disclosure of potential conflicts of interest is found at the end of this article.</abstract><cop>Bristol</cop><pub>John Wiley & Sons, Ltd</pub><pmid>17347492</pmid><doi>10.1634/stemcells.2006-0811</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Stem cells (Dayton, Ohio), 2007-06, Vol.25 (6), p.1356-1363 |
| issn | 1066-5099 1549-4918 |
| language | eng |
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| source | Wiley-Blackwell Journals; Oxford Journals Online |
| subjects | Amino Acids - urine Animals Antigens, Surface - analysis Bone Density Bone Marrow Transplantation Cells, Cultured Cytokines - analysis Disease Models, Animal Female Infusions, Intraosseous Intra‐bone marrow injection Mice Mice, Inbred C3H Mice, Inbred C57BL Osteoporosis - etiology Osteoporosis - immunology Osteoporosis - metabolism Osteoporosis - pathology Senile osteoporosis Senescence accelerated mouse P6 Stem cell disorder |
| title | Induction of Senile Osteoporosis in Normal Mice by Intra‐Bone Marrow‐Bone Marrow Transplantation from Osteoporosis‐Prone Mice |
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