Nrp2 deficiency leads to trabecular bone loss and is accompanied by enhanced osteoclast and reduced osteoblast numbers
Abstract Neuropilin 1 (Nrp1) and Nrp2 are transmembrane receptors that can bind class 3 semaphorins (Sema3A-G) in addition to VEGF family members to play important roles in axonal guidance, vascularization and angiogenesis, as well as immune responses. Moreover, recent evidence implicates Sema3A/Nrp...
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| Veröffentlicht in: | Bone (New York, N.Y.) N.Y.), 2013-08, Vol.55 (2), p.465-475 |
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| creator | Verlinden, Lieve Kriebitzsch, Carsten Beullens, Ine Tan, Biauw Keng Carmeliet, Geert Verstuyf, Annemieke |
| description | Abstract Neuropilin 1 (Nrp1) and Nrp2 are transmembrane receptors that can bind class 3 semaphorins (Sema3A-G) in addition to VEGF family members to play important roles in axonal guidance, vascularization and angiogenesis, as well as immune responses. Moreover, recent evidence implicates Sema3A/Nrp-mediated signaling in bone regulation. However, to date the expression of Nrp2 in bone has not been investigated and a possible role for Nrp2 in the maintenance of bone homeostasis in vivo remains unexplored. Here we show that Nrp2 , together with its possible coreceptors (Plexin A family members and Plexin D1) and class 3 semaphorin ligands, were expressed during in vitro osteogenic differentiation of bone marrow stromal cells. Moreover, Nrp2 transcript and protein levels were highly induced in hematopoietic bone marrow cell-derived osteoclast cultures. Osteoblastic as well as osteoclastic Nrp2 expression was confirmed by immunohistochemistry of the long bones of mice. Interestingly, Nrp2 knockout mice were characterized by a low bone mass phenotype which was accompanied by an increased number of osteoclasts and a decreased osteoblast count. Collectively, these data point to a physiological role for Nrp2 in bone homeostasis. |
| doi_str_mv | 10.1016/j.bone.2013.03.023 |
| format | Article |
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Moreover, recent evidence implicates Sema3A/Nrp-mediated signaling in bone regulation. However, to date the expression of Nrp2 in bone has not been investigated and a possible role for Nrp2 in the maintenance of bone homeostasis in vivo remains unexplored. Here we show that Nrp2 , together with its possible coreceptors (Plexin A family members and Plexin D1) and class 3 semaphorin ligands, were expressed during in vitro osteogenic differentiation of bone marrow stromal cells. Moreover, Nrp2 transcript and protein levels were highly induced in hematopoietic bone marrow cell-derived osteoclast cultures. Osteoblastic as well as osteoclastic Nrp2 expression was confirmed by immunohistochemistry of the long bones of mice. Interestingly, Nrp2 knockout mice were characterized by a low bone mass phenotype which was accompanied by an increased number of osteoclasts and a decreased osteoblast count. Collectively, these data point to a physiological role for Nrp2 in bone homeostasis.</description><identifier>ISSN: 8756-3282</identifier><identifier>EISSN: 1873-2763</identifier><identifier>DOI: 10.1016/j.bone.2013.03.023</identifier><identifier>PMID: 23598046</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Western ; Bone and Bones - cytology ; Bone and Bones - metabolism ; Bone phenotype ; Cells, Cultured ; Diseases of the osteoarticular system ; Fundamental and applied biological sciences. Psychology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neuropilin 2 ; Neuropilin-2 - genetics ; Neuropilin-2 - metabolism ; Orthopedics ; Osteoblast ; Osteoblasts - cytology ; Osteoblasts - metabolism ; Osteoclast ; Osteoclasts - cytology ; Osteoclasts - metabolism ; Osteogenesis - physiology ; Osteoporosis. Osteomalacia. Paget disease ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Semaphorin ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Bone (New York, N.Y.), 2013-08, Vol.55 (2), p.465-475</ispartof><rights>Elsevier Inc.</rights><rights>2013 Elsevier Inc.</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-bacecbc9310bf18de640bd2750fb9b5180925cefac2317e8dccd03723fd5e6433</citedby><cites>FETCH-LOGICAL-c441t-bacecbc9310bf18de640bd2750fb9b5180925cefac2317e8dccd03723fd5e6433</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bone.2013.03.023$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27512307$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23598046$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Verlinden, Lieve</creatorcontrib><creatorcontrib>Kriebitzsch, Carsten</creatorcontrib><creatorcontrib>Beullens, Ine</creatorcontrib><creatorcontrib>Tan, Biauw Keng</creatorcontrib><creatorcontrib>Carmeliet, Geert</creatorcontrib><creatorcontrib>Verstuyf, Annemieke</creatorcontrib><title>Nrp2 deficiency leads to trabecular bone loss and is accompanied by enhanced osteoclast and reduced osteoblast numbers</title><title>Bone (New York, N.Y.)</title><addtitle>Bone</addtitle><description>Abstract Neuropilin 1 (Nrp1) and Nrp2 are transmembrane receptors that can bind class 3 semaphorins (Sema3A-G) in addition to VEGF family members to play important roles in axonal guidance, vascularization and angiogenesis, as well as immune responses. Moreover, recent evidence implicates Sema3A/Nrp-mediated signaling in bone regulation. However, to date the expression of Nrp2 in bone has not been investigated and a possible role for Nrp2 in the maintenance of bone homeostasis in vivo remains unexplored. Here we show that Nrp2 , together with its possible coreceptors (Plexin A family members and Plexin D1) and class 3 semaphorin ligands, were expressed during in vitro osteogenic differentiation of bone marrow stromal cells. Moreover, Nrp2 transcript and protein levels were highly induced in hematopoietic bone marrow cell-derived osteoclast cultures. Osteoblastic as well as osteoclastic Nrp2 expression was confirmed by immunohistochemistry of the long bones of mice. Interestingly, Nrp2 knockout mice were characterized by a low bone mass phenotype which was accompanied by an increased number of osteoclasts and a decreased osteoblast count. Collectively, these data point to a physiological role for Nrp2 in bone homeostasis.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Bone and Bones - cytology</subject><subject>Bone and Bones - metabolism</subject><subject>Bone phenotype</subject><subject>Cells, Cultured</subject><subject>Diseases of the osteoarticular system</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neuropilin 2</subject><subject>Neuropilin-2 - genetics</subject><subject>Neuropilin-2 - metabolism</subject><subject>Orthopedics</subject><subject>Osteoblast</subject><subject>Osteoblasts - cytology</subject><subject>Osteoblasts - metabolism</subject><subject>Osteoclast</subject><subject>Osteoclasts - cytology</subject><subject>Osteoclasts - metabolism</subject><subject>Osteogenesis - physiology</subject><subject>Osteoporosis. Osteomalacia. Paget disease</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Semaphorin</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>8756-3282</issn><issn>1873-2763</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kk2LFDEQhoMo7rj6BzxILoKXHvPR3ekGEZZFV2HRg3oOSaUaM3YnY9K9MP_e9MzsCh6EggrFU28lb4qQl5xtOePt293WxoBbwbjcshJCPiIb3ilZCdXKx2TTqaatpOjEBXmW844xJnvFn5ILIZu-Y3W7IXdf0l5Qh4MHjwEOdETjMp0jnZOxCMtoEl3H0DHmTE1w1JcEEKe9CR4dtQeK4acJUM4xzxhhNHk-kgnd8lC2x3JYJospPydPBjNmfHHOl-THxw_frz9Vt19vPl9f3VZQ13yurAEEC73kzA68c9jWzDqhGjbY3ja8Y71oAAcDQnKFnQNwTCohB9cUVspL8uaku0_x94J51pPPgONoAsYlay7btlFKtLyg4oRCKi9NOOh98pNJB82ZXv3WO70aoVe_NSshVv1XZ_3FTugeWu4NLsDrM2AymHFIxSif_3Kq4UIyVbh3Jw6LG3cek87HD0HnE8KsXfT_v8f7f9ph9MGXib_wgHkXlxSKz5rrLDTT39bNWBeDS8Z43XXyDwVwtRw</recordid><startdate>20130801</startdate><enddate>20130801</enddate><creator>Verlinden, Lieve</creator><creator>Kriebitzsch, Carsten</creator><creator>Beullens, Ine</creator><creator>Tan, Biauw Keng</creator><creator>Carmeliet, Geert</creator><creator>Verstuyf, Annemieke</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20130801</creationdate><title>Nrp2 deficiency leads to trabecular bone loss and is accompanied by enhanced osteoclast and reduced osteoblast numbers</title><author>Verlinden, Lieve ; Kriebitzsch, Carsten ; Beullens, Ine ; Tan, Biauw Keng ; Carmeliet, Geert ; Verstuyf, Annemieke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-bacecbc9310bf18de640bd2750fb9b5180925cefac2317e8dccd03723fd5e6433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Bone and Bones - cytology</topic><topic>Bone and Bones - metabolism</topic><topic>Bone phenotype</topic><topic>Cells, Cultured</topic><topic>Diseases of the osteoarticular system</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Neuropilin 2</topic><topic>Neuropilin-2 - genetics</topic><topic>Neuropilin-2 - metabolism</topic><topic>Orthopedics</topic><topic>Osteoblast</topic><topic>Osteoblasts - cytology</topic><topic>Osteoblasts - metabolism</topic><topic>Osteoclast</topic><topic>Osteoclasts - cytology</topic><topic>Osteoclasts - metabolism</topic><topic>Osteogenesis - physiology</topic><topic>Osteoporosis. Osteomalacia. 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| subjects | Animals Biological and medical sciences Blotting, Western Bone and Bones - cytology Bone and Bones - metabolism Bone phenotype Cells, Cultured Diseases of the osteoarticular system Fundamental and applied biological sciences. Psychology Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Neuropilin 2 Neuropilin-2 - genetics Neuropilin-2 - metabolism Orthopedics Osteoblast Osteoblasts - cytology Osteoblasts - metabolism Osteoclast Osteoclasts - cytology Osteoclasts - metabolism Osteogenesis - physiology Osteoporosis. Osteomalacia. Paget disease Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Semaphorin Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Nrp2 deficiency leads to trabecular bone loss and is accompanied by enhanced osteoclast and reduced osteoblast numbers |
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