MicroRNA‐497 elevation or LRG1 knockdown promotes osteoblast proliferation and collagen synthesis in osteoporosis via TGF‐β1/Smads signalling pathway
MicroRNAs (miRNAs) have been corroborated to engage in the process of cellular activities in osteoporosis. However, few researches have been conducted to expose the integrated role of miR‐497, leucine‐rich alpha‐2‐glycoprotein‐1 (LRG1) and transforming growth factor beta 1 (TGF‐β1)/Smads signalling...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2020-11, Vol.24 (21), p.12619-12632 |
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| creator | Gu, ZhengTao Xie, DengHui Huang, CaiQiang Ding, Rui Zhang, RongKai Li, QingChu Lin, ChuangXin Qiu, YiYan |
| description | MicroRNAs (miRNAs) have been corroborated to engage in the process of cellular activities in osteoporosis. However, few researches have been conducted to expose the integrated role of miR‐497, leucine‐rich alpha‐2‐glycoprotein‐1 (LRG1) and transforming growth factor beta 1 (TGF‐β1)/Smads signalling pathway in osteoporosis. Thereafter, the study is set out to delve into miR‐497/LRG1/TGF‐β1/Smads signalling pathway axis in osteoporosis. Osteoporosis bone tissues and normal bone tissues were collected. Rat osteoporosis models were constructed via ovariectomy. Model rats were injected with restored miR‐497 or depleted LRG1 to explore their roles in osteoporosis. Rat osteoblasts were extracted from osteoporosis rats and transfected with restored miR‐497 or depleted LRG1 for further verification. MiR‐497 and LRG1 expression in femoral head tissues and osteoblasts of osteoporosis rats were detected. TGF‐β1/Smads signalling pathway‐related factors were detected. MiR‐497 was poorly expressed while LRG1 was highly expressed and TGF‐β1/Smads signalling pathway activation was inhibited in osteoporosis. MiR‐497 up‐regulation or LRG1 down‐regulation activated TGF‐β1/Smads signalling pathway, promoted collagen type 1 synthesis and suppressed oxidative stress in femoral head tissues in osteoporosis. MiR‐497 restoration or LRG1 knockdown activated TGF‐β1/Smads signalling pathway, promoted viability and suppressed apoptosis of osteoblasts in osteoporosis. Our study suggests that miR‐497 up‐regulation or LRG1 down‐regulation promotes osteoblast viability and collagen synthesis via activating TGF‐β1/Smads signalling pathway, which may provide a novel reference for osteoporosis treatment. |
| doi_str_mv | 10.1111/jcmm.15826 |
| format | Article |
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However, few researches have been conducted to expose the integrated role of miR‐497, leucine‐rich alpha‐2‐glycoprotein‐1 (LRG1) and transforming growth factor beta 1 (TGF‐β1)/Smads signalling pathway in osteoporosis. Thereafter, the study is set out to delve into miR‐497/LRG1/TGF‐β1/Smads signalling pathway axis in osteoporosis. Osteoporosis bone tissues and normal bone tissues were collected. Rat osteoporosis models were constructed via ovariectomy. Model rats were injected with restored miR‐497 or depleted LRG1 to explore their roles in osteoporosis. Rat osteoblasts were extracted from osteoporosis rats and transfected with restored miR‐497 or depleted LRG1 for further verification. MiR‐497 and LRG1 expression in femoral head tissues and osteoblasts of osteoporosis rats were detected. TGF‐β1/Smads signalling pathway‐related factors were detected. MiR‐497 was poorly expressed while LRG1 was highly expressed and TGF‐β1/Smads signalling pathway activation was inhibited in osteoporosis. MiR‐497 up‐regulation or LRG1 down‐regulation activated TGF‐β1/Smads signalling pathway, promoted collagen type 1 synthesis and suppressed oxidative stress in femoral head tissues in osteoporosis. MiR‐497 restoration or LRG1 knockdown activated TGF‐β1/Smads signalling pathway, promoted viability and suppressed apoptosis of osteoblasts in osteoporosis. Our study suggests that miR‐497 up‐regulation or LRG1 down‐regulation promotes osteoblast viability and collagen synthesis via activating TGF‐β1/Smads signalling pathway, which may provide a novel reference for osteoporosis treatment.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.15826</identifier><identifier>PMID: 32975015</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Abdomen ; Alcohol use ; Alkaline Phosphatase - metabolism ; Angiogenesis ; Animal models ; Animals ; Apoptosis ; Bioengineering ; Biomarkers - metabolism ; Bone density ; Calcium - blood ; Calcium - urine ; Cell division ; Cell Survival ; Collagen ; Collagen (type I) ; Collagen - biosynthesis ; collagen synthesis ; Down-Regulation - genetics ; Enzymes ; Female ; Femur ; Femur Head - pathology ; Fractures ; Gene expression ; Gene Expression Regulation ; Gene Knockdown Techniques ; Glycoproteins - genetics ; Glycoproteins - metabolism ; Hydroxyproline - metabolism ; Laboratory animals ; Leucine ; leucine‐rich alpha‐2‐glycoprotein‐1 ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; microRNA‐497 ; miRNA ; Models, Biological ; Morphology ; Original ; osteoblast ; Osteoblasts ; Osteoblasts - metabolism ; Osteoblasts - pathology ; Osteoporosis ; Osteoporosis - metabolism ; Osteoporosis - pathology ; Ovariectomy ; Oxidative Stress ; Phosphatase ; Phosphorus - blood ; Phosphorus - urine ; Plasmids ; Rats, Sprague-Dawley ; Signal Transduction ; Smad Proteins - metabolism ; Software ; Transforming Growth Factor beta1 - metabolism ; transforming growth factor β1/Smads signalling pathway ; Transforming growth factor-b1 ; Up-Regulation - genetics ; viability</subject><ispartof>Journal of cellular and molecular medicine, 2020-11, Vol.24 (21), p.12619-12632</ispartof><rights>2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd</rights><rights>2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3636-fafe5f27d0b9611c525de502f3a7e2a67bcebc6fdbc8ffe0c558263cf62b08e43</citedby><cites>FETCH-LOGICAL-c3636-fafe5f27d0b9611c525de502f3a7e2a67bcebc6fdbc8ffe0c558263cf62b08e43</cites><orcidid>0000-0001-9861-0365</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7687005/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7687005/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11542,27903,27904,45553,45554,46031,46455,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32975015$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gu, ZhengTao</creatorcontrib><creatorcontrib>Xie, DengHui</creatorcontrib><creatorcontrib>Huang, CaiQiang</creatorcontrib><creatorcontrib>Ding, Rui</creatorcontrib><creatorcontrib>Zhang, RongKai</creatorcontrib><creatorcontrib>Li, QingChu</creatorcontrib><creatorcontrib>Lin, ChuangXin</creatorcontrib><creatorcontrib>Qiu, YiYan</creatorcontrib><title>MicroRNA‐497 elevation or LRG1 knockdown promotes osteoblast proliferation and collagen synthesis in osteoporosis via TGF‐β1/Smads signalling pathway</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>MicroRNAs (miRNAs) have been corroborated to engage in the process of cellular activities in osteoporosis. However, few researches have been conducted to expose the integrated role of miR‐497, leucine‐rich alpha‐2‐glycoprotein‐1 (LRG1) and transforming growth factor beta 1 (TGF‐β1)/Smads signalling pathway in osteoporosis. Thereafter, the study is set out to delve into miR‐497/LRG1/TGF‐β1/Smads signalling pathway axis in osteoporosis. Osteoporosis bone tissues and normal bone tissues were collected. Rat osteoporosis models were constructed via ovariectomy. Model rats were injected with restored miR‐497 or depleted LRG1 to explore their roles in osteoporosis. Rat osteoblasts were extracted from osteoporosis rats and transfected with restored miR‐497 or depleted LRG1 for further verification. MiR‐497 and LRG1 expression in femoral head tissues and osteoblasts of osteoporosis rats were detected. TGF‐β1/Smads signalling pathway‐related factors were detected. MiR‐497 was poorly expressed while LRG1 was highly expressed and TGF‐β1/Smads signalling pathway activation was inhibited in osteoporosis. MiR‐497 up‐regulation or LRG1 down‐regulation activated TGF‐β1/Smads signalling pathway, promoted collagen type 1 synthesis and suppressed oxidative stress in femoral head tissues in osteoporosis. MiR‐497 restoration or LRG1 knockdown activated TGF‐β1/Smads signalling pathway, promoted viability and suppressed apoptosis of osteoblasts in osteoporosis. Our study suggests that miR‐497 up‐regulation or LRG1 down‐regulation promotes osteoblast viability and collagen synthesis via activating TGF‐β1/Smads signalling pathway, which may provide a novel reference for osteoporosis treatment.</description><subject>Abdomen</subject><subject>Alcohol use</subject><subject>Alkaline Phosphatase - metabolism</subject><subject>Angiogenesis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Bioengineering</subject><subject>Biomarkers - metabolism</subject><subject>Bone density</subject><subject>Calcium - blood</subject><subject>Calcium - urine</subject><subject>Cell division</subject><subject>Cell Survival</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen - biosynthesis</subject><subject>collagen synthesis</subject><subject>Down-Regulation - genetics</subject><subject>Enzymes</subject><subject>Female</subject><subject>Femur</subject><subject>Femur Head - pathology</subject><subject>Fractures</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Gene Knockdown Techniques</subject><subject>Glycoproteins - genetics</subject><subject>Glycoproteins - metabolism</subject><subject>Hydroxyproline - metabolism</subject><subject>Laboratory animals</subject><subject>Leucine</subject><subject>leucine‐rich alpha‐2‐glycoprotein‐1</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>microRNA‐497</subject><subject>miRNA</subject><subject>Models, Biological</subject><subject>Morphology</subject><subject>Original</subject><subject>osteoblast</subject><subject>Osteoblasts</subject><subject>Osteoblasts - metabolism</subject><subject>Osteoblasts - pathology</subject><subject>Osteoporosis</subject><subject>Osteoporosis - metabolism</subject><subject>Osteoporosis - pathology</subject><subject>Ovariectomy</subject><subject>Oxidative Stress</subject><subject>Phosphatase</subject><subject>Phosphorus - blood</subject><subject>Phosphorus - urine</subject><subject>Plasmids</subject><subject>Rats, Sprague-Dawley</subject><subject>Signal Transduction</subject><subject>Smad Proteins - metabolism</subject><subject>Software</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>transforming growth factor β1/Smads signalling pathway</subject><subject>Transforming growth factor-b1</subject><subject>Up-Regulation - genetics</subject><subject>viability</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kcFu1DAQhiMEoqVw4QGQJS4IaVs7jp3kglSt6ALaBamUs-U4411vHTu1s7vaWx-hZx6DB-EheBISslTAAV_GY3_zezx_kjwn-JT062ytmuaUsCLlD5LjIU6ykmYPD3tS0OIoeRLjGmPKCS0fJ0c0LXOGCTtOvi6MCv7y4_mP27uszBFY2MrOeId8QPPLGUHXzqvr2u8caoNvfAcR-diBr6yM3XBmjYYw1khXI-WtlUtwKO5dt4JoIjJuLGl98EO-NRJdzS76J79_I2efG1lHFM3SSWuNW6JWdqud3D9NHmlpIzw7xJPky8Xbq-m7yfzT7P30fD5RlFM-0VID02le46rkhCiWshoYTjWVOaSS55WCSnFdV6rQGrBiw6So0jytcAEZPUnejLrtpmqgVuC6IK1og2lk2Asvjfj7xpmVWPqtyHmRY8x6gVcHgeBvNhA70ZiooB-DA7-JIs0yznPM8gF9-Q-69pvQf3ygOC17g4qBej1SvTUxBtD3zRAsBsvFYLn4ZXkPv_iz_Xv0t8c9QEZgZyzs_yMlPkwXi1H0Jze2vdk</recordid><startdate>202011</startdate><enddate>202011</enddate><creator>Gu, ZhengTao</creator><creator>Xie, DengHui</creator><creator>Huang, CaiQiang</creator><creator>Ding, Rui</creator><creator>Zhang, RongKai</creator><creator>Li, QingChu</creator><creator>Lin, ChuangXin</creator><creator>Qiu, YiYan</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9861-0365</orcidid></search><sort><creationdate>202011</creationdate><title>MicroRNA‐497 elevation or LRG1 knockdown promotes osteoblast proliferation and collagen synthesis in osteoporosis via TGF‐β1/Smads signalling pathway</title><author>Gu, ZhengTao ; Xie, DengHui ; Huang, CaiQiang ; Ding, Rui ; Zhang, RongKai ; Li, QingChu ; Lin, ChuangXin ; Qiu, YiYan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3636-fafe5f27d0b9611c525de502f3a7e2a67bcebc6fdbc8ffe0c558263cf62b08e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Abdomen</topic><topic>Alcohol use</topic><topic>Alkaline Phosphatase - metabolism</topic><topic>Angiogenesis</topic><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Bioengineering</topic><topic>Biomarkers - metabolism</topic><topic>Bone density</topic><topic>Calcium - blood</topic><topic>Calcium - urine</topic><topic>Cell division</topic><topic>Cell Survival</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Collagen - biosynthesis</topic><topic>collagen synthesis</topic><topic>Down-Regulation - genetics</topic><topic>Enzymes</topic><topic>Female</topic><topic>Femur</topic><topic>Femur Head - pathology</topic><topic>Fractures</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Gene Knockdown Techniques</topic><topic>Glycoproteins - genetics</topic><topic>Glycoproteins - metabolism</topic><topic>Hydroxyproline - metabolism</topic><topic>Laboratory animals</topic><topic>Leucine</topic><topic>leucine‐rich alpha‐2‐glycoprotein‐1</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>microRNA‐497</topic><topic>miRNA</topic><topic>Models, Biological</topic><topic>Morphology</topic><topic>Original</topic><topic>osteoblast</topic><topic>Osteoblasts</topic><topic>Osteoblasts - metabolism</topic><topic>Osteoblasts - pathology</topic><topic>Osteoporosis</topic><topic>Osteoporosis - metabolism</topic><topic>Osteoporosis - pathology</topic><topic>Ovariectomy</topic><topic>Oxidative Stress</topic><topic>Phosphatase</topic><topic>Phosphorus - blood</topic><topic>Phosphorus - urine</topic><topic>Plasmids</topic><topic>Rats, Sprague-Dawley</topic><topic>Signal Transduction</topic><topic>Smad Proteins - metabolism</topic><topic>Software</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>transforming growth factor β1/Smads signalling pathway</topic><topic>Transforming growth factor-b1</topic><topic>Up-Regulation - genetics</topic><topic>viability</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gu, ZhengTao</creatorcontrib><creatorcontrib>Xie, DengHui</creatorcontrib><creatorcontrib>Huang, CaiQiang</creatorcontrib><creatorcontrib>Ding, Rui</creatorcontrib><creatorcontrib>Zhang, RongKai</creatorcontrib><creatorcontrib>Li, QingChu</creatorcontrib><creatorcontrib>Lin, ChuangXin</creatorcontrib><creatorcontrib>Qiu, YiYan</creatorcontrib><collection>Wiley Open Access</collection><collection>Wiley Online Library Free Content</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>Neurosciences Abstracts</collection><collection>Health & Medical Complete (ProQuest Database)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gu, ZhengTao</au><au>Xie, DengHui</au><au>Huang, CaiQiang</au><au>Ding, Rui</au><au>Zhang, RongKai</au><au>Li, QingChu</au><au>Lin, ChuangXin</au><au>Qiu, YiYan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA‐497 elevation or LRG1 knockdown promotes osteoblast proliferation and collagen synthesis in osteoporosis via TGF‐β1/Smads signalling pathway</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-11</date><risdate>2020</risdate><volume>24</volume><issue>21</issue><spage>12619</spage><epage>12632</epage><pages>12619-12632</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>MicroRNAs (miRNAs) have been corroborated to engage in the process of cellular activities in osteoporosis. However, few researches have been conducted to expose the integrated role of miR‐497, leucine‐rich alpha‐2‐glycoprotein‐1 (LRG1) and transforming growth factor beta 1 (TGF‐β1)/Smads signalling pathway in osteoporosis. Thereafter, the study is set out to delve into miR‐497/LRG1/TGF‐β1/Smads signalling pathway axis in osteoporosis. Osteoporosis bone tissues and normal bone tissues were collected. Rat osteoporosis models were constructed via ovariectomy. Model rats were injected with restored miR‐497 or depleted LRG1 to explore their roles in osteoporosis. Rat osteoblasts were extracted from osteoporosis rats and transfected with restored miR‐497 or depleted LRG1 for further verification. MiR‐497 and LRG1 expression in femoral head tissues and osteoblasts of osteoporosis rats were detected. TGF‐β1/Smads signalling pathway‐related factors were detected. MiR‐497 was poorly expressed while LRG1 was highly expressed and TGF‐β1/Smads signalling pathway activation was inhibited in osteoporosis. MiR‐497 up‐regulation or LRG1 down‐regulation activated TGF‐β1/Smads signalling pathway, promoted collagen type 1 synthesis and suppressed oxidative stress in femoral head tissues in osteoporosis. MiR‐497 restoration or LRG1 knockdown activated TGF‐β1/Smads signalling pathway, promoted viability and suppressed apoptosis of osteoblasts in osteoporosis. Our study suggests that miR‐497 up‐regulation or LRG1 down‐regulation promotes osteoblast viability and collagen synthesis via activating TGF‐β1/Smads signalling pathway, which may provide a novel reference for osteoporosis treatment.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>32975015</pmid><doi>10.1111/jcmm.15826</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-9861-0365</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2020-11, Vol.24 (21), p.12619-12632 |
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| language | eng |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Wiley Open Access; PubMed Central; EZB Electronic Journals Library |
| subjects | Abdomen Alcohol use Alkaline Phosphatase - metabolism Angiogenesis Animal models Animals Apoptosis Bioengineering Biomarkers - metabolism Bone density Calcium - blood Calcium - urine Cell division Cell Survival Collagen Collagen (type I) Collagen - biosynthesis collagen synthesis Down-Regulation - genetics Enzymes Female Femur Femur Head - pathology Fractures Gene expression Gene Expression Regulation Gene Knockdown Techniques Glycoproteins - genetics Glycoproteins - metabolism Hydroxyproline - metabolism Laboratory animals Leucine leucine‐rich alpha‐2‐glycoprotein‐1 MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism microRNA‐497 miRNA Models, Biological Morphology Original osteoblast Osteoblasts Osteoblasts - metabolism Osteoblasts - pathology Osteoporosis Osteoporosis - metabolism Osteoporosis - pathology Ovariectomy Oxidative Stress Phosphatase Phosphorus - blood Phosphorus - urine Plasmids Rats, Sprague-Dawley Signal Transduction Smad Proteins - metabolism Software Transforming Growth Factor beta1 - metabolism transforming growth factor β1/Smads signalling pathway Transforming growth factor-b1 Up-Regulation - genetics viability |
| title | MicroRNA‐497 elevation or LRG1 knockdown promotes osteoblast proliferation and collagen synthesis in osteoporosis via TGF‐β1/Smads signalling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T17%3A37%3A05IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MicroRNA%E2%80%90497%20elevation%20or%20LRG1%20knockdown%20promotes%20osteoblast%20proliferation%20and%20collagen%20synthesis%20in%20osteoporosis%20via%20TGF%E2%80%90%CE%B21/Smads%20signalling%20pathway&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Gu,%20ZhengTao&rft.date=2020-11&rft.volume=24&rft.issue=21&rft.spage=12619&rft.epage=12632&rft.pages=12619-12632&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.15826&rft_dat=%3Cproquest_pubme%3E2463936185%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2463936185&rft_id=info:pmid/32975015&rfr_iscdi=true |