Osteoblastic differentiation of bone marrow mesenchymal stem cells in uremic rats
Severe secondary hyperparathyroidism (SHPT) represents a high turnover bone disease, osteitis fibrosa, but the pathogenesis of osteitis fibrosa remains to be fully elucidated. We examined the characteristics of the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteoblasts in ure...
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creator | Kato, Tadashi Mizobuchi, Masahide Sasa, Kiyohito Yamada, Atsushi Ogata, Hiroaki Honda, Hirokazu Sakashita, Akiko Kamijo, Ryutaro |
description | Severe secondary hyperparathyroidism (SHPT) represents a high turnover bone disease, osteitis fibrosa, but the pathogenesis of osteitis fibrosa remains to be fully elucidated. We examined the characteristics of the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteoblasts in uremic rats.
We bred 5/6 nephrectomized (Nx) rats with a high phosphorus (P) diet to induce SHPT (Nx + HP), or Nx (Nx + ND) and normal rats (Nc + ND) fed a standard diet (ND). After 8 weeks, BMSCs were isolated from the femur and serum were analyzed. BMSCs underwent flow cytometric examination for the expression patterns of cell surface markers (CD90+, CD29+, CD45−, and CD31−).
Serum creatinine (Cre) levels were significantly elevated in the Nx + NP rats compared with the Nc + NP rats. Cre levels in the Nx + HP rats were levels to those in the Nx + ND rats. Serum P and PTH levels were significantly elevated in the Nx + HP rats compared with the Nx + ND rats. Bone morphometrical analysis showed increases in both osteoid volume and eroded surfaces in the Nx + HP but not in the Nx + ND rats. The populations of harvested BMSCs were similar between all three groups. Alp, Runx2, Pth1r and Cyclin D1 mRNA expression in the BMSCs from the Nx + ND rats were significantly suppressed compared with those isolated from the Nc + ND groups. Alizarin red staining tended to be similar to the expression of these mRNA. These results suggest that the BMSCs differentiation into osteoblasts was disturbed in the uremic rats.
•Osteoblastic differentiation of mesenchymal stem cell from chronic kidney disease rat.•Secondary hyperparathyroidism represents a high turnover bone disease in vivo.•Parathyroid hormone little affect differentiation of mesenchymal stem cell in vitro.•Chronic kidney disease may affect differentiation potential of mesenchymal stem cells. |
doi_str_mv | 10.1016/j.bbrc.2020.05.096 |
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We bred 5/6 nephrectomized (Nx) rats with a high phosphorus (P) diet to induce SHPT (Nx + HP), or Nx (Nx + ND) and normal rats (Nc + ND) fed a standard diet (ND). After 8 weeks, BMSCs were isolated from the femur and serum were analyzed. BMSCs underwent flow cytometric examination for the expression patterns of cell surface markers (CD90+, CD29+, CD45−, and CD31−).
Serum creatinine (Cre) levels were significantly elevated in the Nx + NP rats compared with the Nc + NP rats. Cre levels in the Nx + HP rats were levels to those in the Nx + ND rats. Serum P and PTH levels were significantly elevated in the Nx + HP rats compared with the Nx + ND rats. Bone morphometrical analysis showed increases in both osteoid volume and eroded surfaces in the Nx + HP but not in the Nx + ND rats. The populations of harvested BMSCs were similar between all three groups. Alp, Runx2, Pth1r and Cyclin D1 mRNA expression in the BMSCs from the Nx + ND rats were significantly suppressed compared with those isolated from the Nc + ND groups. Alizarin red staining tended to be similar to the expression of these mRNA. These results suggest that the BMSCs differentiation into osteoblasts was disturbed in the uremic rats.
•Osteoblastic differentiation of mesenchymal stem cell from chronic kidney disease rat.•Secondary hyperparathyroidism represents a high turnover bone disease in vivo.•Parathyroid hormone little affect differentiation of mesenchymal stem cell in vitro.•Chronic kidney disease may affect differentiation potential of mesenchymal stem cells.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2020.05.096</identifier><identifier>PMID: 32826057</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alkaline Phosphatase - genetics ; Alkaline Phosphatase - metabolism ; Animals ; Calcification, Physiologic ; Cell Differentiation - genetics ; Cell Differentiation - physiology ; CKD-MBD ; Creatinine - blood ; Disease Models, Animal ; Hyperparathyroidism, Secondary - etiology ; Hyperparathyroidism, Secondary - pathology ; Hyperparathyroidism, Secondary - physiopathology ; Male ; Mesenchymal Stem Cells - metabolism ; Mesenchymal Stem Cells - pathology ; MSC ; Osteoblasts - metabolism ; Osteoblasts - pathology ; Phosphate ; Rats ; Rats, Sprague-Dawley ; Renal Insufficiency, Chronic - complications ; Renal Insufficiency, Chronic - pathology ; Renal Insufficiency, Chronic - physiopathology ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; SHPT ; Uremia - complications ; Uremia - pathology ; Uremia - physiopathology</subject><ispartof>Biochemical and biophysical research communications, 2020-10, Vol.532 (1), p.11-18</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-8047b82b4a86d3a7f62b00e97ba7bf42225374dfe2a603c1028d562bed13fb693</citedby><cites>FETCH-LOGICAL-c422t-8047b82b4a86d3a7f62b00e97ba7bf42225374dfe2a603c1028d562bed13fb693</cites><orcidid>0000-0002-6949-9773 ; 0000-0002-5634-6145 ; 0000-0002-6117-8414 ; 0000-0002-0046-5575</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X20310172$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32826057$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kato, Tadashi</creatorcontrib><creatorcontrib>Mizobuchi, Masahide</creatorcontrib><creatorcontrib>Sasa, Kiyohito</creatorcontrib><creatorcontrib>Yamada, Atsushi</creatorcontrib><creatorcontrib>Ogata, Hiroaki</creatorcontrib><creatorcontrib>Honda, Hirokazu</creatorcontrib><creatorcontrib>Sakashita, Akiko</creatorcontrib><creatorcontrib>Kamijo, Ryutaro</creatorcontrib><title>Osteoblastic differentiation of bone marrow mesenchymal stem cells in uremic rats</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Severe secondary hyperparathyroidism (SHPT) represents a high turnover bone disease, osteitis fibrosa, but the pathogenesis of osteitis fibrosa remains to be fully elucidated. We examined the characteristics of the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteoblasts in uremic rats.
We bred 5/6 nephrectomized (Nx) rats with a high phosphorus (P) diet to induce SHPT (Nx + HP), or Nx (Nx + ND) and normal rats (Nc + ND) fed a standard diet (ND). After 8 weeks, BMSCs were isolated from the femur and serum were analyzed. BMSCs underwent flow cytometric examination for the expression patterns of cell surface markers (CD90+, CD29+, CD45−, and CD31−).
Serum creatinine (Cre) levels were significantly elevated in the Nx + NP rats compared with the Nc + NP rats. Cre levels in the Nx + HP rats were levels to those in the Nx + ND rats. Serum P and PTH levels were significantly elevated in the Nx + HP rats compared with the Nx + ND rats. Bone morphometrical analysis showed increases in both osteoid volume and eroded surfaces in the Nx + HP but not in the Nx + ND rats. The populations of harvested BMSCs were similar between all three groups. Alp, Runx2, Pth1r and Cyclin D1 mRNA expression in the BMSCs from the Nx + ND rats were significantly suppressed compared with those isolated from the Nc + ND groups. Alizarin red staining tended to be similar to the expression of these mRNA. These results suggest that the BMSCs differentiation into osteoblasts was disturbed in the uremic rats.
•Osteoblastic differentiation of mesenchymal stem cell from chronic kidney disease rat.•Secondary hyperparathyroidism represents a high turnover bone disease in vivo.•Parathyroid hormone little affect differentiation of mesenchymal stem cell in vitro.•Chronic kidney disease may affect differentiation potential of mesenchymal stem cells.</description><subject>Alkaline Phosphatase - genetics</subject><subject>Alkaline Phosphatase - metabolism</subject><subject>Animals</subject><subject>Calcification, Physiologic</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Differentiation - physiology</subject><subject>CKD-MBD</subject><subject>Creatinine - blood</subject><subject>Disease Models, Animal</subject><subject>Hyperparathyroidism, Secondary - etiology</subject><subject>Hyperparathyroidism, Secondary - pathology</subject><subject>Hyperparathyroidism, Secondary - physiopathology</subject><subject>Male</subject><subject>Mesenchymal Stem Cells - metabolism</subject><subject>Mesenchymal Stem Cells - pathology</subject><subject>MSC</subject><subject>Osteoblasts - metabolism</subject><subject>Osteoblasts - pathology</subject><subject>Phosphate</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renal Insufficiency, Chronic - complications</subject><subject>Renal Insufficiency, Chronic - pathology</subject><subject>Renal Insufficiency, Chronic - physiopathology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>SHPT</subject><subject>Uremia - complications</subject><subject>Uremia - pathology</subject><subject>Uremia - physiopathology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLxDAUhYMoOj7-gAvJ0k3rTdKmLbgR8QWCCAruQpLeYIa20aSj-O_NMOrS1d1853DPR8gxg5IBk2fL0phoSw4cSqhL6OQWWTDooOAMqm2yAABZ8I697JH9lJYAjFWy2yV7grdcQt0syONDmjGYQafZW9p75zDiNHs9-zDR4KgJE9JRxxg-6YgJJ_v6NeqB5thILQ5Don6iq4hjzkc9p0Oy4_SQ8OjnHpDn66uny9vi_uHm7vLivrAV53PRQtWYlptKt7IXunGSGwDsGqMb4zLCa9FUvUOuJQjLgLd9nRnsmXBGduKAnG5632J4X2Ga1ejT-iE9YVglxSshRVdJKTLKN6iNIaWITr1Fnzd9KQZqrVIt1VqlWqtUUKusModOfvpXZsT-L_LrLgPnGwDzyg-PUSXrsx_sfUQ7qz74__q_AbHChU0</recordid><startdate>20201029</startdate><enddate>20201029</enddate><creator>Kato, Tadashi</creator><creator>Mizobuchi, Masahide</creator><creator>Sasa, Kiyohito</creator><creator>Yamada, Atsushi</creator><creator>Ogata, Hiroaki</creator><creator>Honda, Hirokazu</creator><creator>Sakashita, Akiko</creator><creator>Kamijo, Ryutaro</creator><general>Elsevier Inc</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>7X8</scope><orcidid>https://orcid.org/0000-0002-6949-9773</orcidid><orcidid>https://orcid.org/0000-0002-5634-6145</orcidid><orcidid>https://orcid.org/0000-0002-6117-8414</orcidid><orcidid>https://orcid.org/0000-0002-0046-5575</orcidid></search><sort><creationdate>20201029</creationdate><title>Osteoblastic differentiation of bone marrow mesenchymal stem cells in uremic rats</title><author>Kato, Tadashi ; Mizobuchi, Masahide ; Sasa, Kiyohito ; Yamada, Atsushi ; Ogata, Hiroaki ; Honda, Hirokazu ; Sakashita, Akiko ; Kamijo, Ryutaro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-8047b82b4a86d3a7f62b00e97ba7bf42225374dfe2a603c1028d562bed13fb693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Alkaline Phosphatase - genetics</topic><topic>Alkaline Phosphatase - metabolism</topic><topic>Animals</topic><topic>Calcification, Physiologic</topic><topic>Cell Differentiation - genetics</topic><topic>Cell Differentiation - physiology</topic><topic>CKD-MBD</topic><topic>Creatinine - blood</topic><topic>Disease Models, Animal</topic><topic>Hyperparathyroidism, Secondary - etiology</topic><topic>Hyperparathyroidism, Secondary - pathology</topic><topic>Hyperparathyroidism, Secondary - physiopathology</topic><topic>Male</topic><topic>Mesenchymal Stem Cells - metabolism</topic><topic>Mesenchymal Stem Cells - pathology</topic><topic>MSC</topic><topic>Osteoblasts - metabolism</topic><topic>Osteoblasts - pathology</topic><topic>Phosphate</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renal Insufficiency, Chronic - complications</topic><topic>Renal Insufficiency, Chronic - pathology</topic><topic>Renal Insufficiency, Chronic - physiopathology</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>SHPT</topic><topic>Uremia - complications</topic><topic>Uremia - pathology</topic><topic>Uremia - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kato, Tadashi</creatorcontrib><creatorcontrib>Mizobuchi, Masahide</creatorcontrib><creatorcontrib>Sasa, Kiyohito</creatorcontrib><creatorcontrib>Yamada, Atsushi</creatorcontrib><creatorcontrib>Ogata, Hiroaki</creatorcontrib><creatorcontrib>Honda, Hirokazu</creatorcontrib><creatorcontrib>Sakashita, Akiko</creatorcontrib><creatorcontrib>Kamijo, Ryutaro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kato, Tadashi</au><au>Mizobuchi, Masahide</au><au>Sasa, Kiyohito</au><au>Yamada, Atsushi</au><au>Ogata, Hiroaki</au><au>Honda, Hirokazu</au><au>Sakashita, Akiko</au><au>Kamijo, Ryutaro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Osteoblastic differentiation of bone marrow mesenchymal stem cells in uremic rats</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2020-10-29</date><risdate>2020</risdate><volume>532</volume><issue>1</issue><spage>11</spage><epage>18</epage><pages>11-18</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Severe secondary hyperparathyroidism (SHPT) represents a high turnover bone disease, osteitis fibrosa, but the pathogenesis of osteitis fibrosa remains to be fully elucidated. We examined the characteristics of the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteoblasts in uremic rats.
We bred 5/6 nephrectomized (Nx) rats with a high phosphorus (P) diet to induce SHPT (Nx + HP), or Nx (Nx + ND) and normal rats (Nc + ND) fed a standard diet (ND). After 8 weeks, BMSCs were isolated from the femur and serum were analyzed. BMSCs underwent flow cytometric examination for the expression patterns of cell surface markers (CD90+, CD29+, CD45−, and CD31−).
Serum creatinine (Cre) levels were significantly elevated in the Nx + NP rats compared with the Nc + NP rats. Cre levels in the Nx + HP rats were levels to those in the Nx + ND rats. Serum P and PTH levels were significantly elevated in the Nx + HP rats compared with the Nx + ND rats. Bone morphometrical analysis showed increases in both osteoid volume and eroded surfaces in the Nx + HP but not in the Nx + ND rats. The populations of harvested BMSCs were similar between all three groups. Alp, Runx2, Pth1r and Cyclin D1 mRNA expression in the BMSCs from the Nx + ND rats were significantly suppressed compared with those isolated from the Nc + ND groups. Alizarin red staining tended to be similar to the expression of these mRNA. These results suggest that the BMSCs differentiation into osteoblasts was disturbed in the uremic rats.
•Osteoblastic differentiation of mesenchymal stem cell from chronic kidney disease rat.•Secondary hyperparathyroidism represents a high turnover bone disease in vivo.•Parathyroid hormone little affect differentiation of mesenchymal stem cell in vitro.•Chronic kidney disease may affect differentiation potential of mesenchymal stem cells.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>32826057</pmid><doi>10.1016/j.bbrc.2020.05.096</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-6949-9773</orcidid><orcidid>https://orcid.org/0000-0002-5634-6145</orcidid><orcidid>https://orcid.org/0000-0002-6117-8414</orcidid><orcidid>https://orcid.org/0000-0002-0046-5575</orcidid></addata></record> |
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subjects | Alkaline Phosphatase - genetics Alkaline Phosphatase - metabolism Animals Calcification, Physiologic Cell Differentiation - genetics Cell Differentiation - physiology CKD-MBD Creatinine - blood Disease Models, Animal Hyperparathyroidism, Secondary - etiology Hyperparathyroidism, Secondary - pathology Hyperparathyroidism, Secondary - physiopathology Male Mesenchymal Stem Cells - metabolism Mesenchymal Stem Cells - pathology MSC Osteoblasts - metabolism Osteoblasts - pathology Phosphate Rats Rats, Sprague-Dawley Renal Insufficiency, Chronic - complications Renal Insufficiency, Chronic - pathology Renal Insufficiency, Chronic - physiopathology RNA, Messenger - genetics RNA, Messenger - metabolism SHPT Uremia - complications Uremia - pathology Uremia - physiopathology |
title | Osteoblastic differentiation of bone marrow mesenchymal stem cells in uremic rats |
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