Human PTH (1-34) induces longitudinal bone growth in rats
The growth plate is a specialized structure that is responsible for longitudinal bone growth (LGR). Growth plate organization is altered with loading in rats. Parathyroid hormone (PTH) is known to induce mitogenic effect on chondrocytes in vitro. Type I PTH/PTH related peptide (rP) receptor is expre...
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Veröffentlicht in: | Journal of bone and mineral metabolism 2002-01, Vol.20 (2), p.83-90 |
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container_title | Journal of bone and mineral metabolism |
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creator | OGAWA, Taishi YAMAGIWA, Hiroshi HAYAMI, Tadashi LIU, Zhang HUANG, Kuan-Yu TOKUNAGA, Kunihiko MURAI, Takehiro ENDO, Naoto |
description | The growth plate is a specialized structure that is responsible for longitudinal bone growth (LGR). Growth plate organization is altered with loading in rats. Parathyroid hormone (PTH) is known to induce mitogenic effect on chondrocytes in vitro. Type I PTH/PTH related peptide (rP) receptor is expressed in growth plate cartilage in rats. We therefore investigated the effect of PTH administration on the organization and longitudinal growth rate of the growth plate in rats. We also investigated the effect of PTH on the changes induced by unloading in the organization and growth of the growth plate. Thirty 6-week-old and 30 15-week-old male Sprague-Dawley rats were randomly assigned to five groups (n = 6 per group), i.e., basal controls, control (i.e., normally loaded), PTH-treated control (i.e., PTH-treated under normal loading), unloaded, and PTH-treated under unloading. PTH-treated animals received human PTH (1-34) at a dose of 80 microg/kg per day five times per week for 3 weeks, for the duration of unloading. In young loaded rats treated with the systemic administration of PTH, growth plate thickness, chondrocyte number, and LGR were increased in the proximal tibiae compared with findings in young loaded rats without PTH administration. Hindlimb unloading induced a reduction in growth plate thickness, chondrocyte number, and LGR. In young rats, systemic administration of PTH partly prevented these changes induced by unloading. These preventive effects of PTH were observed only in young rats; not in adult rats. These results show that the systemic administration of PTH stimulates longitudinal bone growth, and diminishes the reduction in growth plate growth induced by unloading in young rats. |
doi_str_mv | 10.1007/s007740200011 |
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Growth plate organization is altered with loading in rats. Parathyroid hormone (PTH) is known to induce mitogenic effect on chondrocytes in vitro. Type I PTH/PTH related peptide (rP) receptor is expressed in growth plate cartilage in rats. We therefore investigated the effect of PTH administration on the organization and longitudinal growth rate of the growth plate in rats. We also investigated the effect of PTH on the changes induced by unloading in the organization and growth of the growth plate. Thirty 6-week-old and 30 15-week-old male Sprague-Dawley rats were randomly assigned to five groups (n = 6 per group), i.e., basal controls, control (i.e., normally loaded), PTH-treated control (i.e., PTH-treated under normal loading), unloaded, and PTH-treated under unloading. PTH-treated animals received human PTH (1-34) at a dose of 80 microg/kg per day five times per week for 3 weeks, for the duration of unloading. In young loaded rats treated with the systemic administration of PTH, growth plate thickness, chondrocyte number, and LGR were increased in the proximal tibiae compared with findings in young loaded rats without PTH administration. Hindlimb unloading induced a reduction in growth plate thickness, chondrocyte number, and LGR. In young rats, systemic administration of PTH partly prevented these changes induced by unloading. These preventive effects of PTH were observed only in young rats; not in adult rats. These results show that the systemic administration of PTH stimulates longitudinal bone growth, and diminishes the reduction in growth plate growth induced by unloading in young rats.</description><identifier>ISSN: 0914-8779</identifier><identifier>EISSN: 1435-5604</identifier><identifier>DOI: 10.1007/s007740200011</identifier><identifier>PMID: 11862529</identifier><language>eng</language><publisher>Tokyo: Springer</publisher><subject>Animals ; Biological and medical sciences ; Bone Development - drug effects ; Cartilage ; Cartilage - cytology ; Cartilage - metabolism ; Growth Plate - cytology ; Growth Plate - metabolism ; Hindlimb Suspension ; Hormones. Endocrine system ; Humans ; Male ; Medical sciences ; Pharmacology. Drug treatments ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Rodents ; Skeletal system ; Space life sciences ; Teriparatide - pharmacology ; Tibia - anatomy & histology ; Tibia - drug effects ; Tibia - metabolism</subject><ispartof>Journal of bone and mineral metabolism, 2002-01, Vol.20 (2), p.83-90</ispartof><rights>2002 INIST-CNRS</rights><rights>Springer-Verlag Tokyo 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-46279b73bad0294aff4a6427bc8fd98499a45495d443d61b1c60edee63003f683</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13474022$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11862529$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OGAWA, Taishi</creatorcontrib><creatorcontrib>YAMAGIWA, Hiroshi</creatorcontrib><creatorcontrib>HAYAMI, Tadashi</creatorcontrib><creatorcontrib>LIU, Zhang</creatorcontrib><creatorcontrib>HUANG, Kuan-Yu</creatorcontrib><creatorcontrib>TOKUNAGA, Kunihiko</creatorcontrib><creatorcontrib>MURAI, Takehiro</creatorcontrib><creatorcontrib>ENDO, Naoto</creatorcontrib><title>Human PTH (1-34) induces longitudinal bone growth in rats</title><title>Journal of bone and mineral metabolism</title><addtitle>J Bone Miner Metab</addtitle><description>The growth plate is a specialized structure that is responsible for longitudinal bone growth (LGR). Growth plate organization is altered with loading in rats. Parathyroid hormone (PTH) is known to induce mitogenic effect on chondrocytes in vitro. Type I PTH/PTH related peptide (rP) receptor is expressed in growth plate cartilage in rats. We therefore investigated the effect of PTH administration on the organization and longitudinal growth rate of the growth plate in rats. We also investigated the effect of PTH on the changes induced by unloading in the organization and growth of the growth plate. Thirty 6-week-old and 30 15-week-old male Sprague-Dawley rats were randomly assigned to five groups (n = 6 per group), i.e., basal controls, control (i.e., normally loaded), PTH-treated control (i.e., PTH-treated under normal loading), unloaded, and PTH-treated under unloading. PTH-treated animals received human PTH (1-34) at a dose of 80 microg/kg per day five times per week for 3 weeks, for the duration of unloading. In young loaded rats treated with the systemic administration of PTH, growth plate thickness, chondrocyte number, and LGR were increased in the proximal tibiae compared with findings in young loaded rats without PTH administration. Hindlimb unloading induced a reduction in growth plate thickness, chondrocyte number, and LGR. In young rats, systemic administration of PTH partly prevented these changes induced by unloading. These preventive effects of PTH were observed only in young rats; not in adult rats. These results show that the systemic administration of PTH stimulates longitudinal bone growth, and diminishes the reduction in growth plate growth induced by unloading in young rats.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone Development - drug effects</subject><subject>Cartilage</subject><subject>Cartilage - cytology</subject><subject>Cartilage - metabolism</subject><subject>Growth Plate - cytology</subject><subject>Growth Plate - metabolism</subject><subject>Hindlimb Suspension</subject><subject>Hormones. Endocrine system</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Skeletal system</subject><subject>Space life sciences</subject><subject>Teriparatide - pharmacology</subject><subject>Tibia - anatomy & histology</subject><subject>Tibia - drug effects</subject><subject>Tibia - metabolism</subject><issn>0914-8779</issn><issn>1435-5604</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqF0MFLwzAUx_EgipvTo1cpiKKHal7zkjRHGeqEgR7muaRNOju6diYt4n9vxgpDL16Sy4cfvC8h50DvgFJ578MjkSaUUoADMgZkPOaC4iEZUwUYp1KqETnxfhWE5BKOyQggFQlP1JioWb_WTfS2mEU3EDO8jarG9IX1Ud02y6rrTdXoOsrbxkZL1351HwFETnf-lByVuvb2bPgn5P3pcTGdxfPX55fpwzwuUMkuRpFIlUuWa0MThbosUQtMZF6kpVEpKqWRo-IGkRkBORSCWmOtYJSyUqRsQq53uxvXfvbWd9m68oWta93YtveZBJ6kDOFfCKlkEEoFePkHrtrehTODAWCcAaM8qHinCtd672yZbVy11u47A5pt02e_0gd_Maz2-dqavR5aB3A1AO0LXZdON0Xl947hdixhP-9KhpY</recordid><startdate>20020101</startdate><enddate>20020101</enddate><creator>OGAWA, Taishi</creator><creator>YAMAGIWA, Hiroshi</creator><creator>HAYAMI, Tadashi</creator><creator>LIU, Zhang</creator><creator>HUANG, Kuan-Yu</creator><creator>TOKUNAGA, Kunihiko</creator><creator>MURAI, Takehiro</creator><creator>ENDO, Naoto</creator><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20020101</creationdate><title>Human PTH (1-34) induces longitudinal bone growth in rats</title><author>OGAWA, Taishi ; YAMAGIWA, Hiroshi ; HAYAMI, Tadashi ; LIU, Zhang ; HUANG, Kuan-Yu ; TOKUNAGA, Kunihiko ; MURAI, Takehiro ; ENDO, Naoto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-46279b73bad0294aff4a6427bc8fd98499a45495d443d61b1c60edee63003f683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone Development - drug effects</topic><topic>Cartilage</topic><topic>Cartilage - cytology</topic><topic>Cartilage - metabolism</topic><topic>Growth Plate - cytology</topic><topic>Growth Plate - metabolism</topic><topic>Hindlimb Suspension</topic><topic>Hormones. Endocrine system</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Skeletal system</topic><topic>Space life sciences</topic><topic>Teriparatide - pharmacology</topic><topic>Tibia - anatomy & histology</topic><topic>Tibia - drug effects</topic><topic>Tibia - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>OGAWA, Taishi</creatorcontrib><creatorcontrib>YAMAGIWA, Hiroshi</creatorcontrib><creatorcontrib>HAYAMI, Tadashi</creatorcontrib><creatorcontrib>LIU, Zhang</creatorcontrib><creatorcontrib>HUANG, Kuan-Yu</creatorcontrib><creatorcontrib>TOKUNAGA, Kunihiko</creatorcontrib><creatorcontrib>MURAI, Takehiro</creatorcontrib><creatorcontrib>ENDO, Naoto</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database (ProQuest)</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of bone and mineral metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OGAWA, Taishi</au><au>YAMAGIWA, Hiroshi</au><au>HAYAMI, Tadashi</au><au>LIU, Zhang</au><au>HUANG, Kuan-Yu</au><au>TOKUNAGA, Kunihiko</au><au>MURAI, Takehiro</au><au>ENDO, Naoto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human PTH (1-34) induces longitudinal bone growth in rats</atitle><jtitle>Journal of bone and mineral metabolism</jtitle><addtitle>J Bone Miner Metab</addtitle><date>2002-01-01</date><risdate>2002</risdate><volume>20</volume><issue>2</issue><spage>83</spage><epage>90</epage><pages>83-90</pages><issn>0914-8779</issn><eissn>1435-5604</eissn><abstract>The growth plate is a specialized structure that is responsible for longitudinal bone growth (LGR). Growth plate organization is altered with loading in rats. Parathyroid hormone (PTH) is known to induce mitogenic effect on chondrocytes in vitro. Type I PTH/PTH related peptide (rP) receptor is expressed in growth plate cartilage in rats. We therefore investigated the effect of PTH administration on the organization and longitudinal growth rate of the growth plate in rats. We also investigated the effect of PTH on the changes induced by unloading in the organization and growth of the growth plate. Thirty 6-week-old and 30 15-week-old male Sprague-Dawley rats were randomly assigned to five groups (n = 6 per group), i.e., basal controls, control (i.e., normally loaded), PTH-treated control (i.e., PTH-treated under normal loading), unloaded, and PTH-treated under unloading. PTH-treated animals received human PTH (1-34) at a dose of 80 microg/kg per day five times per week for 3 weeks, for the duration of unloading. In young loaded rats treated with the systemic administration of PTH, growth plate thickness, chondrocyte number, and LGR were increased in the proximal tibiae compared with findings in young loaded rats without PTH administration. Hindlimb unloading induced a reduction in growth plate thickness, chondrocyte number, and LGR. In young rats, systemic administration of PTH partly prevented these changes induced by unloading. These preventive effects of PTH were observed only in young rats; not in adult rats. These results show that the systemic administration of PTH stimulates longitudinal bone growth, and diminishes the reduction in growth plate growth induced by unloading in young rats.</abstract><cop>Tokyo</cop><pub>Springer</pub><pmid>11862529</pmid><doi>10.1007/s007740200011</doi><tpages>8</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Bone Development - drug effects Cartilage Cartilage - cytology Cartilage - metabolism Growth Plate - cytology Growth Plate - metabolism Hindlimb Suspension Hormones. Endocrine system Humans Male Medical sciences Pharmacology. Drug treatments Random Allocation Rats Rats, Sprague-Dawley Rodents Skeletal system Space life sciences Teriparatide - pharmacology Tibia - anatomy & histology Tibia - drug effects Tibia - metabolism |
title | Human PTH (1-34) induces longitudinal bone growth in rats |
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