3,4-dihydroxyacetophenone inhibits hypoxia-associated human pulmonary artery smooth muscle cell proliferation by reducing [Ca.sup.2+] influx
The present study aimed to assess the effects of 3,4-dihydroxyacetophenone (DHAP) on human pulmonary artery smooth muscle cells (HPASMCs). HPASMCs were divided into the normoxia group (NG), hypoxia group (HG), and hypoxia and 0.6*[l0.sup.-4] mol/L (HD1), 1.9*[l0.sup.-4] mol/L (HD2) and 6.0*[l0.sup.-...
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| Veröffentlicht in: | Pakistan journal of pharmaceutical sciences 2020-09, Vol.33 (5), p.2153 |
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| creator | Lin, Chunlong Li, Caixia Zhao, Jianping Ni, Wang Yi, Jizu |
| description | The present study aimed to assess the effects of 3,4-dihydroxyacetophenone (DHAP) on human pulmonary artery smooth muscle cells (HPASMCs). HPASMCs were divided into the normoxia group (NG), hypoxia group (HG), and hypoxia and 0.6*[l0.sup.-4] mol/L (HD1), 1.9*[l0.sup.-4] mol/L (HD2) and 6.0*[l0.sup.-4] mol/L (HD3) DHAP treatment groups. Cell cycle was analyzed by flow-cytometrically. HPASMC growth was examined by the proliferating cell nuclear antigen (PCNA) and MTT assays. Intracellular [Ca.sup.2+] ([[[Ca.sup.2+]].sub.i]) was measured by laser scanning confocal microscopy. Compared with the NG, the HG showed significantly increased HPASMC proliferation (P |
| doi_str_mv | 10.36721/PJPS.2020.33.5.REG.2153-2159.1 |
| format | Article |
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HPASMCs were divided into the normoxia group (NG), hypoxia group (HG), and hypoxia and 0.6*[l0.sup.-4] mol/L (HD1), 1.9*[l0.sup.-4] mol/L (HD2) and 6.0*[l0.sup.-4] mol/L (HD3) DHAP treatment groups. Cell cycle was analyzed by flow-cytometrically. HPASMC growth was examined by the proliferating cell nuclear antigen (PCNA) and MTT assays. Intracellular [Ca.sup.2+] ([[[Ca.sup.2+]].sub.i]) was measured by laser scanning confocal microscopy. Compared with the NG, the HG showed significantly increased HPASMC proliferation (P<0.05); meanwhile, cells treated with DHAP showed decreased proliferation compared with the HG (P<0.05). Hypoxia enhanced cell cycle progression and DHAP partly restored cell cycle distribution toward the status of NG cells. Furthermore, CDK2 levels were markedly increased in hypoxic cells (P<0.05), while DHAP treatment starkly decreased CDK2 levels in comparison with the HG (P<0.05). Moreover, hypoxia increased intracellular [[Ca.sup.2+]] levels compared with normoxia (P<0.05); meanwhile, DHAP treatment decreased [[[Ca.sup.2+]].sub.i] compared with the HG (P<0.05). These findings suggested that DHAP inhibits hypoxia-induced proliferation of HPASMCs involving [[[Ca.sup.2+]].sub.i] reduction. Therefore, DHAP should be considered an ideal candidate for the prevention and/or treatment of hypoxia-associated pulmonary hypertension and pulmonary vascular remodeling. Keywords: 3,4-dihydroxyacetophenone, pulmonary artery smooth muscle cell, hypoxia; cell cycle, pulmonary hypertension, pulmonary vascular remodeling.]]></description><identifier>ISSN: 1011-601X</identifier><identifier>DOI: 10.36721/PJPS.2020.33.5.REG.2153-2159.1</identifier><language>eng</language><publisher>Pakistan Journal of Pharmaceutical Sciences</publisher><subject>Analysis ; Development and progression ; EDTA ; Penicillin G ; Pulmonary hypertension ; Resveratrol ; Smooth muscle</subject><ispartof>Pakistan journal of pharmaceutical sciences, 2020-09, Vol.33 (5), p.2153</ispartof><rights>COPYRIGHT 2020 Pakistan Journal of Pharmaceutical Sciences</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Lin, Chunlong</creatorcontrib><creatorcontrib>Li, Caixia</creatorcontrib><creatorcontrib>Zhao, Jianping</creatorcontrib><creatorcontrib>Ni, Wang</creatorcontrib><creatorcontrib>Yi, Jizu</creatorcontrib><title>3,4-dihydroxyacetophenone inhibits hypoxia-associated human pulmonary artery smooth muscle cell proliferation by reducing [Ca.sup.2+] influx</title><title>Pakistan journal of pharmaceutical sciences</title><description><![CDATA[The present study aimed to assess the effects of 3,4-dihydroxyacetophenone (DHAP) on human pulmonary artery smooth muscle cells (HPASMCs). HPASMCs were divided into the normoxia group (NG), hypoxia group (HG), and hypoxia and 0.6*[l0.sup.-4] mol/L (HD1), 1.9*[l0.sup.-4] mol/L (HD2) and 6.0*[l0.sup.-4] mol/L (HD3) DHAP treatment groups. Cell cycle was analyzed by flow-cytometrically. HPASMC growth was examined by the proliferating cell nuclear antigen (PCNA) and MTT assays. Intracellular [Ca.sup.2+] ([[[Ca.sup.2+]].sub.i]) was measured by laser scanning confocal microscopy. Compared with the NG, the HG showed significantly increased HPASMC proliferation (P<0.05); meanwhile, cells treated with DHAP showed decreased proliferation compared with the HG (P<0.05). Hypoxia enhanced cell cycle progression and DHAP partly restored cell cycle distribution toward the status of NG cells. Furthermore, CDK2 levels were markedly increased in hypoxic cells (P<0.05), while DHAP treatment starkly decreased CDK2 levels in comparison with the HG (P<0.05). Moreover, hypoxia increased intracellular [[Ca.sup.2+]] levels compared with normoxia (P<0.05); meanwhile, DHAP treatment decreased [[[Ca.sup.2+]].sub.i] compared with the HG (P<0.05). These findings suggested that DHAP inhibits hypoxia-induced proliferation of HPASMCs involving [[[Ca.sup.2+]].sub.i] reduction. Therefore, DHAP should be considered an ideal candidate for the prevention and/or treatment of hypoxia-associated pulmonary hypertension and pulmonary vascular remodeling. Keywords: 3,4-dihydroxyacetophenone, pulmonary artery smooth muscle cell, hypoxia; cell cycle, pulmonary hypertension, pulmonary vascular remodeling.]]></description><subject>Analysis</subject><subject>Development and progression</subject><subject>EDTA</subject><subject>Penicillin G</subject><subject>Pulmonary hypertension</subject><subject>Resveratrol</subject><subject>Smooth muscle</subject><issn>1011-601X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNptUE1LxDAQ7UHBdfU_BDx40MakH2lzXJZ1VRZcdA-CyDJNp9tI2pSmhe1_8Ecb0IMHGXiPGd4HTBBcc0ZjkUX8bvu0faURi_we05S-rNY04mkcepCUnwQzzjgPBeNvZ8G5c5-MiURKOQu-4tskLHU9lb09TqBwsF2NrW2R6LbWhR4cqafOHjWE4JxVGgYsST020JJuNI1toZ8I9AN6co21Q02a0SmDRKExpOut0RX2MGjbkmIiPZaj0u2BvC-BurGj0c2H76rMeLwITiswDi9_eR7s7le75UO4eV4_Lheb8CAyGSaikFBIAZClFbIUojzOhJIxKB5VmCshmVBlglylslCoMlkxYDISSuSYJ_E8uPqJPYDBva-2Qw-q0U7tFyKWIk1yIb2K_qPyU2KjlX9Qpf39j-EbP9d50A</recordid><startdate>20200901</startdate><enddate>20200901</enddate><creator>Lin, Chunlong</creator><creator>Li, Caixia</creator><creator>Zhao, Jianping</creator><creator>Ni, Wang</creator><creator>Yi, Jizu</creator><general>Pakistan Journal of Pharmaceutical Sciences</general><scope/></search><sort><creationdate>20200901</creationdate><title>3,4-dihydroxyacetophenone inhibits hypoxia-associated human pulmonary artery smooth muscle cell proliferation by reducing [Ca.sup.2+] influx</title><author>Lin, Chunlong ; Li, Caixia ; Zhao, Jianping ; Ni, Wang ; Yi, Jizu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g679-46b9ab96aa75fe05a28376c93ac12fe8c6906cd4e1c59bcec79f0a0926c68e843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Analysis</topic><topic>Development and progression</topic><topic>EDTA</topic><topic>Penicillin G</topic><topic>Pulmonary hypertension</topic><topic>Resveratrol</topic><topic>Smooth muscle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Chunlong</creatorcontrib><creatorcontrib>Li, Caixia</creatorcontrib><creatorcontrib>Zhao, Jianping</creatorcontrib><creatorcontrib>Ni, Wang</creatorcontrib><creatorcontrib>Yi, Jizu</creatorcontrib><jtitle>Pakistan journal of pharmaceutical sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Chunlong</au><au>Li, Caixia</au><au>Zhao, Jianping</au><au>Ni, Wang</au><au>Yi, Jizu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>3,4-dihydroxyacetophenone inhibits hypoxia-associated human pulmonary artery smooth muscle cell proliferation by reducing [Ca.sup.2+] influx</atitle><jtitle>Pakistan journal of pharmaceutical sciences</jtitle><date>2020-09-01</date><risdate>2020</risdate><volume>33</volume><issue>5</issue><spage>2153</spage><pages>2153-</pages><issn>1011-601X</issn><abstract><![CDATA[The present study aimed to assess the effects of 3,4-dihydroxyacetophenone (DHAP) on human pulmonary artery smooth muscle cells (HPASMCs). HPASMCs were divided into the normoxia group (NG), hypoxia group (HG), and hypoxia and 0.6*[l0.sup.-4] mol/L (HD1), 1.9*[l0.sup.-4] mol/L (HD2) and 6.0*[l0.sup.-4] mol/L (HD3) DHAP treatment groups. Cell cycle was analyzed by flow-cytometrically. HPASMC growth was examined by the proliferating cell nuclear antigen (PCNA) and MTT assays. Intracellular [Ca.sup.2+] ([[[Ca.sup.2+]].sub.i]) was measured by laser scanning confocal microscopy. Compared with the NG, the HG showed significantly increased HPASMC proliferation (P<0.05); meanwhile, cells treated with DHAP showed decreased proliferation compared with the HG (P<0.05). Hypoxia enhanced cell cycle progression and DHAP partly restored cell cycle distribution toward the status of NG cells. Furthermore, CDK2 levels were markedly increased in hypoxic cells (P<0.05), while DHAP treatment starkly decreased CDK2 levels in comparison with the HG (P<0.05). Moreover, hypoxia increased intracellular [[Ca.sup.2+]] levels compared with normoxia (P<0.05); meanwhile, DHAP treatment decreased [[[Ca.sup.2+]].sub.i] compared with the HG (P<0.05). These findings suggested that DHAP inhibits hypoxia-induced proliferation of HPASMCs involving [[[Ca.sup.2+]].sub.i] reduction. Therefore, DHAP should be considered an ideal candidate for the prevention and/or treatment of hypoxia-associated pulmonary hypertension and pulmonary vascular remodeling. Keywords: 3,4-dihydroxyacetophenone, pulmonary artery smooth muscle cell, hypoxia; cell cycle, pulmonary hypertension, pulmonary vascular remodeling.]]></abstract><pub>Pakistan Journal of Pharmaceutical Sciences</pub><doi>10.36721/PJPS.2020.33.5.REG.2153-2159.1</doi></addata></record> |
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| subjects | Analysis Development and progression EDTA Penicillin G Pulmonary hypertension Resveratrol Smooth muscle |
| title | 3,4-dihydroxyacetophenone inhibits hypoxia-associated human pulmonary artery smooth muscle cell proliferation by reducing [Ca.sup.2+] influx |
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