ACY‑1215, a HDAC6 inhibitor, decreases the dexamethasone‑induced suppression of osteogenesis in MC3T3‑E1 cells
Glucocorticoid‑induced osteoporosis is the commonest form of drug‑induced osteoporosis. Histone deacetylase 6 (HDAC6) is involved in the differentiation from mesenchymal stem cells to osteoblasts. However, the role of ricolinostat (ACY‑1215, HDAC6 inhibitor) in the dexamethasone (Dex)‑induced prolif...
Gespeichert in:
| Veröffentlicht in: | Molecular medicine reports 2020-09, Vol.22 (3), p.2451-2459 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2459 |
|---|---|
| container_issue | 3 |
| container_start_page | 2451 |
| container_title | Molecular medicine reports |
| container_volume | 22 |
| creator | Wang, Na Wang, Hua Chen, Jianming Wang, Fubin Wang, Shuaiyi Zhou, Qiang Ying, Jichong Huang, Shanzhao Wang, Pu Yuan, Fangfang |
| description | Glucocorticoid‑induced osteoporosis is the commonest form of drug‑induced osteoporosis. Histone deacetylase 6 (HDAC6) is involved in the differentiation from mesenchymal stem cells to osteoblasts. However, the role of ricolinostat (ACY‑1215, HDAC6 inhibitor) in the dexamethasone (Dex)‑induced proliferation and differentiation of preosteoblasts remains to be elucidated. The protein expression and mRNA expression levels of HDAC6, osteopontin (OPN), runt‑related transcription factor 2 (Runx2), osterix (Osx), collagen I (COL1A1) and glucocorticoid receptor (GR) in MC3T3‑E1 cells were analyzed by western blot analysis and reverse transcription‑quantitative PCR analysis. The cell viability was detected by CCK‑8 assay. The alkaline phosphatase (ALP) activity and capacity of mineralization was determined by ALP assay kit and alizarin red staining. HDAC6 expression was increased in patient serum and Dex‑induced MC3T3‑E1 cells at a certain concentration range; 1 µM Dex was selected for further experimentation. Cell viability was decreased after Dex induction and restored following ACY‑1215 treatment. The ALP activity and capability for mineralization was decreased when MC3T3‑E1 cells were induced by 1 µM Dex and was gradually improved by the treatment of ACY‑1215 at 1, 5 and 10 mM. The expression of OPN, Runx2, Osx and COL1A1 was similar, with the changes of capability for mineralization. Furthermore, GR expression was increased in Dex‑induced MC3T3‑E1 cells. ACY‑1215 promoted the GR expression in MC3T3‑E1 cells from 1‑5 mM while GR receptor expression was increased with 10 mM ACY‑1215 treatment. In conclusion, ACY‑1215 reversed the Dex‑induced suppression of proliferation and differentiation of MC3T3‑E1 cells. |
| doi_str_mv | 10.3892/mmr.2020.11319 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmed_primary_32705192</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A633845432</galeid><sourcerecordid>A633845432</sourcerecordid><originalsourceid>FETCH-LOGICAL-c485t-189787a84f47cd0aa755b50a7435726759ff27340845e9463e5cc21d3b3871363</originalsourceid><addsrcrecordid>eNptUUFvFCEYJUZja_Xq0ZB47a7AB8NwMdlMqzVp00s9eCIs880uzcywwoyxt_6F_kV_iVTXpiYNB_jgvZfHe4S85WwJtREfhiEtBRNsyTlw84wccm34AhiTz_dnYYw-IK9yvmasUkKZl-QAhGaKG3FIplXz7dftHRdcHVNHz05WTUXDuA3rMMV0TFv0CV3GTKctlumnG3DauhxHLLQwtrPHluZ5t0uYc4gjjR2NecK4wRFzyEWMXjRwBQV-yqnHvs-vyYvO9Rnf7Pcj8vXT6VVztji__PylWZ0vvKzVtOC10bV2teyk9i1zTiu1VsxpCUqLSivTdUKDZLVUaGQFqLwXvIU11JpDBUfk41_d3bwesPU4Tsn1dpfC4NKNjS7Y_1_GsLWb-MNqWeI0vAi83wuk-H3GPNnrOKexeLZCAteq5PYItXE92jB2sYj5IWRvVxVAcSdBFNTyCVRZLQ7Blzy7UO6fIvgUc07YPRjnzN6Xb0v59r58-6f8Qnj3-LsP8H9tw28OAqpP</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2431751211</pqid></control><display><type>article</type><title>ACY‑1215, a HDAC6 inhibitor, decreases the dexamethasone‑induced suppression of osteogenesis in MC3T3‑E1 cells</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Wang, Na ; Wang, Hua ; Chen, Jianming ; Wang, Fubin ; Wang, Shuaiyi ; Zhou, Qiang ; Ying, Jichong ; Huang, Shanzhao ; Wang, Pu ; Yuan, Fangfang</creator><creatorcontrib>Wang, Na ; Wang, Hua ; Chen, Jianming ; Wang, Fubin ; Wang, Shuaiyi ; Zhou, Qiang ; Ying, Jichong ; Huang, Shanzhao ; Wang, Pu ; Yuan, Fangfang</creatorcontrib><description>Glucocorticoid‑induced osteoporosis is the commonest form of drug‑induced osteoporosis. Histone deacetylase 6 (HDAC6) is involved in the differentiation from mesenchymal stem cells to osteoblasts. However, the role of ricolinostat (ACY‑1215, HDAC6 inhibitor) in the dexamethasone (Dex)‑induced proliferation and differentiation of preosteoblasts remains to be elucidated. The protein expression and mRNA expression levels of HDAC6, osteopontin (OPN), runt‑related transcription factor 2 (Runx2), osterix (Osx), collagen I (COL1A1) and glucocorticoid receptor (GR) in MC3T3‑E1 cells were analyzed by western blot analysis and reverse transcription‑quantitative PCR analysis. The cell viability was detected by CCK‑8 assay. The alkaline phosphatase (ALP) activity and capacity of mineralization was determined by ALP assay kit and alizarin red staining. HDAC6 expression was increased in patient serum and Dex‑induced MC3T3‑E1 cells at a certain concentration range; 1 µM Dex was selected for further experimentation. Cell viability was decreased after Dex induction and restored following ACY‑1215 treatment. The ALP activity and capability for mineralization was decreased when MC3T3‑E1 cells were induced by 1 µM Dex and was gradually improved by the treatment of ACY‑1215 at 1, 5 and 10 mM. The expression of OPN, Runx2, Osx and COL1A1 was similar, with the changes of capability for mineralization. Furthermore, GR expression was increased in Dex‑induced MC3T3‑E1 cells. ACY‑1215 promoted the GR expression in MC3T3‑E1 cells from 1‑5 mM while GR receptor expression was increased with 10 mM ACY‑1215 treatment. In conclusion, ACY‑1215 reversed the Dex‑induced suppression of proliferation and differentiation of MC3T3‑E1 cells.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2020.11319</identifier><identifier>PMID: 32705192</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Adult ; Alkaline phosphatase ; Analysis ; Animals ; Biotechnology ; Bone density ; Case-Control Studies ; Cbfa-1 protein ; Cell culture ; Cell differentiation ; Cell Differentiation - drug effects ; Cell Line ; Cell proliferation ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cell viability ; Cholecystokinin ; Clinical medicine ; Collagen ; Collagen (type I) ; Dexamethasone ; Dexamethasone - adverse effects ; Disease Models, Animal ; Drug therapy ; Female ; Gene expression ; Gene Expression Regulation - drug effects ; Glucocorticoids ; Histone deacetylase ; Histone Deacetylase 6 - genetics ; Histone Deacetylase 6 - metabolism ; Humans ; Hydroxamic Acids - pharmacology ; Male ; Mediation ; Mesenchyme ; Mice ; Middle Aged ; Mineralization ; Osteoblastogenesis ; Osteoblasts ; Osteogenesis ; Osteogenesis - drug effects ; Osteopontin ; Osteoporosis ; Osteoporosis - chemically induced ; Osteoporosis - drug therapy ; Osteoporosis - genetics ; Osteoporosis - metabolism ; Phosphatases ; Proteins ; Pyrimidines - pharmacology ; Receptors, Glucocorticoid - genetics ; Receptors, Glucocorticoid - metabolism ; Reverse transcription ; Software ; Stem cells ; Steroids</subject><ispartof>Molecular medicine reports, 2020-09, Vol.22 (3), p.2451-2459</ispartof><rights>COPYRIGHT 2020 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2020</rights><rights>Copyright: © Wang et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-189787a84f47cd0aa755b50a7435726759ff27340845e9463e5cc21d3b3871363</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32705192$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Na</creatorcontrib><creatorcontrib>Wang, Hua</creatorcontrib><creatorcontrib>Chen, Jianming</creatorcontrib><creatorcontrib>Wang, Fubin</creatorcontrib><creatorcontrib>Wang, Shuaiyi</creatorcontrib><creatorcontrib>Zhou, Qiang</creatorcontrib><creatorcontrib>Ying, Jichong</creatorcontrib><creatorcontrib>Huang, Shanzhao</creatorcontrib><creatorcontrib>Wang, Pu</creatorcontrib><creatorcontrib>Yuan, Fangfang</creatorcontrib><title>ACY‑1215, a HDAC6 inhibitor, decreases the dexamethasone‑induced suppression of osteogenesis in MC3T3‑E1 cells</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Glucocorticoid‑induced osteoporosis is the commonest form of drug‑induced osteoporosis. Histone deacetylase 6 (HDAC6) is involved in the differentiation from mesenchymal stem cells to osteoblasts. However, the role of ricolinostat (ACY‑1215, HDAC6 inhibitor) in the dexamethasone (Dex)‑induced proliferation and differentiation of preosteoblasts remains to be elucidated. The protein expression and mRNA expression levels of HDAC6, osteopontin (OPN), runt‑related transcription factor 2 (Runx2), osterix (Osx), collagen I (COL1A1) and glucocorticoid receptor (GR) in MC3T3‑E1 cells were analyzed by western blot analysis and reverse transcription‑quantitative PCR analysis. The cell viability was detected by CCK‑8 assay. The alkaline phosphatase (ALP) activity and capacity of mineralization was determined by ALP assay kit and alizarin red staining. HDAC6 expression was increased in patient serum and Dex‑induced MC3T3‑E1 cells at a certain concentration range; 1 µM Dex was selected for further experimentation. Cell viability was decreased after Dex induction and restored following ACY‑1215 treatment. The ALP activity and capability for mineralization was decreased when MC3T3‑E1 cells were induced by 1 µM Dex and was gradually improved by the treatment of ACY‑1215 at 1, 5 and 10 mM. The expression of OPN, Runx2, Osx and COL1A1 was similar, with the changes of capability for mineralization. Furthermore, GR expression was increased in Dex‑induced MC3T3‑E1 cells. ACY‑1215 promoted the GR expression in MC3T3‑E1 cells from 1‑5 mM while GR receptor expression was increased with 10 mM ACY‑1215 treatment. In conclusion, ACY‑1215 reversed the Dex‑induced suppression of proliferation and differentiation of MC3T3‑E1 cells.</description><subject>Adult</subject><subject>Alkaline phosphatase</subject><subject>Analysis</subject><subject>Animals</subject><subject>Biotechnology</subject><subject>Bone density</subject><subject>Case-Control Studies</subject><subject>Cbfa-1 protein</subject><subject>Cell culture</subject><subject>Cell differentiation</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Line</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Cholecystokinin</subject><subject>Clinical medicine</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Dexamethasone</subject><subject>Dexamethasone - adverse effects</subject><subject>Disease Models, Animal</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glucocorticoids</subject><subject>Histone deacetylase</subject><subject>Histone Deacetylase 6 - genetics</subject><subject>Histone Deacetylase 6 - metabolism</subject><subject>Humans</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Male</subject><subject>Mediation</subject><subject>Mesenchyme</subject><subject>Mice</subject><subject>Middle Aged</subject><subject>Mineralization</subject><subject>Osteoblastogenesis</subject><subject>Osteoblasts</subject><subject>Osteogenesis</subject><subject>Osteogenesis - drug effects</subject><subject>Osteopontin</subject><subject>Osteoporosis</subject><subject>Osteoporosis - chemically induced</subject><subject>Osteoporosis - drug therapy</subject><subject>Osteoporosis - genetics</subject><subject>Osteoporosis - metabolism</subject><subject>Phosphatases</subject><subject>Proteins</subject><subject>Pyrimidines - pharmacology</subject><subject>Receptors, Glucocorticoid - genetics</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>Reverse transcription</subject><subject>Software</subject><subject>Stem cells</subject><subject>Steroids</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><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>eNptUUFvFCEYJUZja_Xq0ZB47a7AB8NwMdlMqzVp00s9eCIs880uzcywwoyxt_6F_kV_iVTXpiYNB_jgvZfHe4S85WwJtREfhiEtBRNsyTlw84wccm34AhiTz_dnYYw-IK9yvmasUkKZl-QAhGaKG3FIplXz7dftHRdcHVNHz05WTUXDuA3rMMV0TFv0CV3GTKctlumnG3DauhxHLLQwtrPHluZ5t0uYc4gjjR2NecK4wRFzyEWMXjRwBQV-yqnHvs-vyYvO9Rnf7Pcj8vXT6VVztji__PylWZ0vvKzVtOC10bV2teyk9i1zTiu1VsxpCUqLSivTdUKDZLVUaGQFqLwXvIU11JpDBUfk41_d3bwesPU4Tsn1dpfC4NKNjS7Y_1_GsLWb-MNqWeI0vAi83wuk-H3GPNnrOKexeLZCAteq5PYItXE92jB2sYj5IWRvVxVAcSdBFNTyCVRZLQ7Blzy7UO6fIvgUc07YPRjnzN6Xb0v59r58-6f8Qnj3-LsP8H9tw28OAqpP</recordid><startdate>20200901</startdate><enddate>20200901</enddate><creator>Wang, Na</creator><creator>Wang, Hua</creator><creator>Chen, Jianming</creator><creator>Wang, Fubin</creator><creator>Wang, Shuaiyi</creator><creator>Zhou, Qiang</creator><creator>Ying, Jichong</creator><creator>Huang, Shanzhao</creator><creator>Wang, Pu</creator><creator>Yuan, Fangfang</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</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>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20200901</creationdate><title>ACY‑1215, a HDAC6 inhibitor, decreases the dexamethasone‑induced suppression of osteogenesis in MC3T3‑E1 cells</title><author>Wang, Na ; Wang, Hua ; Chen, Jianming ; Wang, Fubin ; Wang, Shuaiyi ; Zhou, Qiang ; Ying, Jichong ; Huang, Shanzhao ; Wang, Pu ; Yuan, Fangfang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-189787a84f47cd0aa755b50a7435726759ff27340845e9463e5cc21d3b3871363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>Alkaline phosphatase</topic><topic>Analysis</topic><topic>Animals</topic><topic>Biotechnology</topic><topic>Bone density</topic><topic>Case-Control Studies</topic><topic>Cbfa-1 protein</topic><topic>Cell culture</topic><topic>Cell differentiation</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Line</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Cholecystokinin</topic><topic>Clinical medicine</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Dexamethasone</topic><topic>Dexamethasone - adverse effects</topic><topic>Disease Models, Animal</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glucocorticoids</topic><topic>Histone deacetylase</topic><topic>Histone Deacetylase 6 - genetics</topic><topic>Histone Deacetylase 6 - metabolism</topic><topic>Humans</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Male</topic><topic>Mediation</topic><topic>Mesenchyme</topic><topic>Mice</topic><topic>Middle Aged</topic><topic>Mineralization</topic><topic>Osteoblastogenesis</topic><topic>Osteoblasts</topic><topic>Osteogenesis</topic><topic>Osteogenesis - drug effects</topic><topic>Osteopontin</topic><topic>Osteoporosis</topic><topic>Osteoporosis - chemically induced</topic><topic>Osteoporosis - drug therapy</topic><topic>Osteoporosis - genetics</topic><topic>Osteoporosis - metabolism</topic><topic>Phosphatases</topic><topic>Proteins</topic><topic>Pyrimidines - pharmacology</topic><topic>Receptors, Glucocorticoid - genetics</topic><topic>Receptors, Glucocorticoid - metabolism</topic><topic>Reverse transcription</topic><topic>Software</topic><topic>Stem cells</topic><topic>Steroids</topic><toplevel>online_resources</toplevel><creatorcontrib>Wang, Na</creatorcontrib><creatorcontrib>Wang, Hua</creatorcontrib><creatorcontrib>Chen, Jianming</creatorcontrib><creatorcontrib>Wang, Fubin</creatorcontrib><creatorcontrib>Wang, Shuaiyi</creatorcontrib><creatorcontrib>Zhou, Qiang</creatorcontrib><creatorcontrib>Ying, Jichong</creatorcontrib><creatorcontrib>Huang, Shanzhao</creatorcontrib><creatorcontrib>Wang, Pu</creatorcontrib><creatorcontrib>Yuan, Fangfang</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Na</au><au>Wang, Hua</au><au>Chen, Jianming</au><au>Wang, Fubin</au><au>Wang, Shuaiyi</au><au>Zhou, Qiang</au><au>Ying, Jichong</au><au>Huang, Shanzhao</au><au>Wang, Pu</au><au>Yuan, Fangfang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ACY‑1215, a HDAC6 inhibitor, decreases the dexamethasone‑induced suppression of osteogenesis in MC3T3‑E1 cells</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2020-09-01</date><risdate>2020</risdate><volume>22</volume><issue>3</issue><spage>2451</spage><epage>2459</epage><pages>2451-2459</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Glucocorticoid‑induced osteoporosis is the commonest form of drug‑induced osteoporosis. Histone deacetylase 6 (HDAC6) is involved in the differentiation from mesenchymal stem cells to osteoblasts. However, the role of ricolinostat (ACY‑1215, HDAC6 inhibitor) in the dexamethasone (Dex)‑induced proliferation and differentiation of preosteoblasts remains to be elucidated. The protein expression and mRNA expression levels of HDAC6, osteopontin (OPN), runt‑related transcription factor 2 (Runx2), osterix (Osx), collagen I (COL1A1) and glucocorticoid receptor (GR) in MC3T3‑E1 cells were analyzed by western blot analysis and reverse transcription‑quantitative PCR analysis. The cell viability was detected by CCK‑8 assay. The alkaline phosphatase (ALP) activity and capacity of mineralization was determined by ALP assay kit and alizarin red staining. HDAC6 expression was increased in patient serum and Dex‑induced MC3T3‑E1 cells at a certain concentration range; 1 µM Dex was selected for further experimentation. Cell viability was decreased after Dex induction and restored following ACY‑1215 treatment. The ALP activity and capability for mineralization was decreased when MC3T3‑E1 cells were induced by 1 µM Dex and was gradually improved by the treatment of ACY‑1215 at 1, 5 and 10 mM. The expression of OPN, Runx2, Osx and COL1A1 was similar, with the changes of capability for mineralization. Furthermore, GR expression was increased in Dex‑induced MC3T3‑E1 cells. ACY‑1215 promoted the GR expression in MC3T3‑E1 cells from 1‑5 mM while GR receptor expression was increased with 10 mM ACY‑1215 treatment. In conclusion, ACY‑1215 reversed the Dex‑induced suppression of proliferation and differentiation of MC3T3‑E1 cells.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>32705192</pmid><doi>10.3892/mmr.2020.11319</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1791-2997 |
| ispartof | Molecular medicine reports, 2020-09, Vol.22 (3), p.2451-2459 |
| issn | 1791-2997 1791-3004 |
| language | eng |
| recordid | cdi_pubmed_primary_32705192 |
| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Alkaline phosphatase Analysis Animals Biotechnology Bone density Case-Control Studies Cbfa-1 protein Cell culture Cell differentiation Cell Differentiation - drug effects Cell Line Cell proliferation Cell Proliferation - drug effects Cell Survival - drug effects Cell viability Cholecystokinin Clinical medicine Collagen Collagen (type I) Dexamethasone Dexamethasone - adverse effects Disease Models, Animal Drug therapy Female Gene expression Gene Expression Regulation - drug effects Glucocorticoids Histone deacetylase Histone Deacetylase 6 - genetics Histone Deacetylase 6 - metabolism Humans Hydroxamic Acids - pharmacology Male Mediation Mesenchyme Mice Middle Aged Mineralization Osteoblastogenesis Osteoblasts Osteogenesis Osteogenesis - drug effects Osteopontin Osteoporosis Osteoporosis - chemically induced Osteoporosis - drug therapy Osteoporosis - genetics Osteoporosis - metabolism Phosphatases Proteins Pyrimidines - pharmacology Receptors, Glucocorticoid - genetics Receptors, Glucocorticoid - metabolism Reverse transcription Software Stem cells Steroids |
| title | ACY‑1215, a HDAC6 inhibitor, decreases the dexamethasone‑induced suppression of osteogenesis in MC3T3‑E1 cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T13%3A20%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ACY%E2%80%911215,%20a%20HDAC6%20inhibitor,%20decreases%20the%20dexamethasone%E2%80%91induced%20suppression%20of%20osteogenesis%20in%20MC3T3%E2%80%91E1%20cells&rft.jtitle=Molecular%20medicine%20reports&rft.au=Wang,%20Na&rft.date=2020-09-01&rft.volume=22&rft.issue=3&rft.spage=2451&rft.epage=2459&rft.pages=2451-2459&rft.issn=1791-2997&rft.eissn=1791-3004&rft_id=info:doi/10.3892/mmr.2020.11319&rft_dat=%3Cgale_pubme%3EA633845432%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2431751211&rft_id=info:pmid/32705192&rft_galeid=A633845432&rfr_iscdi=true |