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UBE2E3 regulates cellular senescence and osteogenic differentiation of BMSCs during aging
Osteoporosis has gradually become a public health problem in the world. However, the exact molecular mechanism of osteoporosis still remains unclear. Senescence and osteogenic differentiation inhibition of bone marrow mesenchymal stem cells (BMSCs ) are supposed to play an important part in osteopor...
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Published in: | PeerJ (San Francisco, CA) CA), 2021-11, Vol.9, p.e12253-e12253, Article e12253 |
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description | Osteoporosis has gradually become a public health problem in the world. However, the exact molecular mechanism of osteoporosis still remains unclear. Senescence and osteogenic differentiation inhibition of bone marrow mesenchymal stem cells (BMSCs ) are supposed to play an important part in osteoporosis.
We used two gene expression profiles (GSE35956 and GSE35958) associated with osteoporosis and selected the promising gene Ubiquitin-conjugating enzyme E2 E3 (UBE2E3). We then verified its function and mechanism by
experiments.
UBE2E3 was highly expressed in the bone marrow and positively associated with osteogenesis related genes. Besides, UBE2E3 expression reduced in old BMSCs compared with that in young BMSCs. In
experiments, knockdown of UBE2E3 accelerated cellular senescence and inhibited osteogenic differentiation of young BMSCs. On the other hand, overexpression of UBE2E3 attenuated cellular senescence as well as enhanced osteogenic differentiation of old BMSCs. Mechanistically, UBE2E3 might regulate the nuclear factor erythroid 2-related factor (Nrf2) and control its function, thus affecting the senescence and osteogenic differentiation of BMSCs.
UBE2E3 may be potentially involved in the pathogenesis of osteoporosis by regulating cellular senescence and osteogenic differentiation of BMSCs. |
doi_str_mv | 10.7717/peerj.12253 |
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We used two gene expression profiles (GSE35956 and GSE35958) associated with osteoporosis and selected the promising gene Ubiquitin-conjugating enzyme E2 E3 (UBE2E3). We then verified its function and mechanism by
experiments.
UBE2E3 was highly expressed in the bone marrow and positively associated with osteogenesis related genes. Besides, UBE2E3 expression reduced in old BMSCs compared with that in young BMSCs. In
experiments, knockdown of UBE2E3 accelerated cellular senescence and inhibited osteogenic differentiation of young BMSCs. On the other hand, overexpression of UBE2E3 attenuated cellular senescence as well as enhanced osteogenic differentiation of old BMSCs. Mechanistically, UBE2E3 might regulate the nuclear factor erythroid 2-related factor (Nrf2) and control its function, thus affecting the senescence and osteogenic differentiation of BMSCs.
UBE2E3 may be potentially involved in the pathogenesis of osteoporosis by regulating cellular senescence and osteogenic differentiation of BMSCs.</description><identifier>ISSN: 2167-8359</identifier><identifier>EISSN: 2167-8359</identifier><identifier>DOI: 10.7717/peerj.12253</identifier><identifier>PMID: 34820159</identifier><language>eng</language><publisher>United States: PeerJ. Ltd</publisher><subject>Aging ; Bioinformatics ; Biotechnology ; Bone marrow ; Cell differentiation ; Data Mining and Machine Learning ; Enzymes ; Fractures ; Gene expression ; Genes ; Genetic aspects ; Genomes ; Geriatrics ; Laboratory animals ; Membranes ; Mesenchyme ; Metabolic Sciences ; Nrf2 ; Older people ; Orthopedics ; Osteogenesis ; Osteogenic differentiation ; Osteoporosis ; Proteins ; Public health ; Senescence ; Stem cells ; UBE2E3 ; Ubiquitin ; Ubiquitin-conjugating enzyme ; Ubiquitin-protein ligase</subject><ispartof>PeerJ (San Francisco, CA), 2021-11, Vol.9, p.e12253-e12253, Article e12253</ispartof><rights>2021 Liu et al.</rights><rights>COPYRIGHT 2021 PeerJ. Ltd.</rights><rights>2021 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 Liu et al. 2021 Liu et al.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c573t-4b63ede455f80c151c67fe3424a64d45f90efdae420af68d689a55b6a17ea1813</citedby><cites>FETCH-LOGICAL-c573t-4b63ede455f80c151c67fe3424a64d45f90efdae420af68d689a55b6a17ea1813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2598831376/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2598831376?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34820159$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Yalin</creatorcontrib><creatorcontrib>Cai, Guangping</creatorcontrib><creatorcontrib>Chen, Peng</creatorcontrib><creatorcontrib>Jiang, Tiejian</creatorcontrib><creatorcontrib>Xia, Zhuying</creatorcontrib><title>UBE2E3 regulates cellular senescence and osteogenic differentiation of BMSCs during aging</title><title>PeerJ (San Francisco, CA)</title><addtitle>PeerJ</addtitle><description>Osteoporosis has gradually become a public health problem in the world. However, the exact molecular mechanism of osteoporosis still remains unclear. Senescence and osteogenic differentiation inhibition of bone marrow mesenchymal stem cells (BMSCs ) are supposed to play an important part in osteoporosis.
We used two gene expression profiles (GSE35956 and GSE35958) associated with osteoporosis and selected the promising gene Ubiquitin-conjugating enzyme E2 E3 (UBE2E3). We then verified its function and mechanism by
experiments.
UBE2E3 was highly expressed in the bone marrow and positively associated with osteogenesis related genes. Besides, UBE2E3 expression reduced in old BMSCs compared with that in young BMSCs. In
experiments, knockdown of UBE2E3 accelerated cellular senescence and inhibited osteogenic differentiation of young BMSCs. On the other hand, overexpression of UBE2E3 attenuated cellular senescence as well as enhanced osteogenic differentiation of old BMSCs. Mechanistically, UBE2E3 might regulate the nuclear factor erythroid 2-related factor (Nrf2) and control its function, thus affecting the senescence and osteogenic differentiation of BMSCs.
UBE2E3 may be potentially involved in the pathogenesis of osteoporosis by regulating cellular senescence and osteogenic differentiation of BMSCs.</description><subject>Aging</subject><subject>Bioinformatics</subject><subject>Biotechnology</subject><subject>Bone marrow</subject><subject>Cell differentiation</subject><subject>Data Mining and Machine Learning</subject><subject>Enzymes</subject><subject>Fractures</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Geriatrics</subject><subject>Laboratory animals</subject><subject>Membranes</subject><subject>Mesenchyme</subject><subject>Metabolic Sciences</subject><subject>Nrf2</subject><subject>Older people</subject><subject>Orthopedics</subject><subject>Osteogenesis</subject><subject>Osteogenic differentiation</subject><subject>Osteoporosis</subject><subject>Proteins</subject><subject>Public health</subject><subject>Senescence</subject><subject>Stem cells</subject><subject>UBE2E3</subject><subject>Ubiquitin</subject><subject>Ubiquitin-conjugating enzyme</subject><subject>Ubiquitin-protein ligase</subject><issn>2167-8359</issn><issn>2167-8359</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUl2LEzEUHURxl3WffJcBQRakNR-Tj3kRdkvVhRUfdB98CmlyM02ZJjWZEfz3Ztp1bcUEksvNuSfcc09VvcRoLgQW73YAaTPHhDD6pDonmIuZpKx9ehSfVZc5b1BZknAk6fPqjDaSIMza8-r7_c2SLGmdoBt7PUCuDfR9CVOdIUA2EAzUOtg65gFiB8Gb2nrnIEEYvB58DHV09c3nr4tc2zH50NW6K-eL6pnTfYbLh_uiuv-w_Lb4NLv78vF2cX03M0zQYdasOAULDWNOIoMZNlw4oA1pNG9sw1yLwFkNDUHacWm5bDVjK66xAI0lphfV7YHXRr1Ru-S3Ov1SUXu1T8TUKZ0Gb3pQEiGmrWs1yKJAi1YrpnGLLROttJK2hev9gWs3rrZgS_ND0v0J6elL8GvVxZ9KcsQxJ4Xg6oEgxR8j5EFtfZ4U1QHimFUZAOENQoIV6Ot_oJs4plCkUoS1UlJMBf-L6nRpwAcXy79mIlXXAjeiFRRPXPP_oMq2sPUmBnC-5E8K3hwVrEH3wzrHfpzGmU-Bbw9Ak2LOCdyjGBipyYFq70C1d2BBvzrW7xH7x2_0NzM11Ek</recordid><startdate>20211118</startdate><enddate>20211118</enddate><creator>Liu, Yalin</creator><creator>Cai, Guangping</creator><creator>Chen, Peng</creator><creator>Jiang, Tiejian</creator><creator>Xia, Zhuying</creator><general>PeerJ. 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However, the exact molecular mechanism of osteoporosis still remains unclear. Senescence and osteogenic differentiation inhibition of bone marrow mesenchymal stem cells (BMSCs ) are supposed to play an important part in osteoporosis.
We used two gene expression profiles (GSE35956 and GSE35958) associated with osteoporosis and selected the promising gene Ubiquitin-conjugating enzyme E2 E3 (UBE2E3). We then verified its function and mechanism by
experiments.
UBE2E3 was highly expressed in the bone marrow and positively associated with osteogenesis related genes. Besides, UBE2E3 expression reduced in old BMSCs compared with that in young BMSCs. In
experiments, knockdown of UBE2E3 accelerated cellular senescence and inhibited osteogenic differentiation of young BMSCs. On the other hand, overexpression of UBE2E3 attenuated cellular senescence as well as enhanced osteogenic differentiation of old BMSCs. Mechanistically, UBE2E3 might regulate the nuclear factor erythroid 2-related factor (Nrf2) and control its function, thus affecting the senescence and osteogenic differentiation of BMSCs.
UBE2E3 may be potentially involved in the pathogenesis of osteoporosis by regulating cellular senescence and osteogenic differentiation of BMSCs.</abstract><cop>United States</cop><pub>PeerJ. Ltd</pub><pmid>34820159</pmid><doi>10.7717/peerj.12253</doi><oa>free_for_read</oa></addata></record> |
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subjects | Aging Bioinformatics Biotechnology Bone marrow Cell differentiation Data Mining and Machine Learning Enzymes Fractures Gene expression Genes Genetic aspects Genomes Geriatrics Laboratory animals Membranes Mesenchyme Metabolic Sciences Nrf2 Older people Orthopedics Osteogenesis Osteogenic differentiation Osteoporosis Proteins Public health Senescence Stem cells UBE2E3 Ubiquitin Ubiquitin-conjugating enzyme Ubiquitin-protein ligase |
title | UBE2E3 regulates cellular senescence and osteogenic differentiation of BMSCs during aging |
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