Chronic TGF-β1 Signaling in Pulmonary Arterial Hypertension Induces Sustained Canonical Smad3 Pathways in Vascular Smooth Muscle Cells
(A) The mRNA and microRNA (miR) expression of TGF-β1 targets was evaluated by qPCR in starved (48 h) human pulmonary artery smooth muscle cells (HPASMCs) stimulated with TGF-β1 (5 ng/ml, 8 hours, n = 3), as well as in the main pulmonary artery (PA) and total lung of transgenic mice overexpressing TG...
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2019-07, Vol.61 (1), p.121-123 |
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| creator | Calvier, Laurent Chouvarine, Philippe Legchenko, Ekaterina Kokeny, Gabor Mozes, Miklos M Hansmann, Georg |
| description | (A) The mRNA and microRNA (miR) expression of TGF-β1 targets was evaluated by qPCR in starved (48 h) human pulmonary artery smooth muscle cells (HPASMCs) stimulated with TGF-β1 (5 ng/ml, 8 hours, n = 3), as well as in the main pulmonary artery (PA) and total lung of transgenic mice overexpressing TGF-β1 in the circulation (TG-TGFβ1) versus wild-type control (males, n = 8–16). (C) Adult male Sprague Dawley rats (∼200 g body weight) were divided into three age-matched groups: control normoxia, control hypoxia (i.e., rats injected once s.c. with vehicle [DMSO; vol/vol] and then exposed to hypoxia [FiO2 = 0.1] for 3 weeks, followed by 6 weeks in room air [FiO2 = 0.21]), and Sugen hypoxia (SuHx, i.e., rats injected with SU5416 20 mg/kg/dose s.c. and then exposed to hypoxia [3 wk], followed by 6 weeks in room air). mRNA expression was evaluated in total lungs (n = 6–11). Here, we found that the TGF-β1 pathway was indeed activated in the hypertensive SuHx rat lung (increased TGF-β1 mRNA expression; Figure 1C), whereas Smad3 mRNA expression remained unchanged (Figure 1C). [...]based on our SuHx data, the canonical TGF-β1/Smad3 pathway is not decreased in the rat lung with severe PAH. Smad3 mRNA (trend, statistically not significant) and miR-130a/301b (P < 0.01) expression was higher in the PAs and plexiform lesions of patients with idiopathic PAH compared with control subjects (Figure 1E). [...]our human data support the notion that boosted signaling of TGF-β1 and its canonical downstream effector Smad3 in human PAs is crucial for PAH development and severity. |
| doi_str_mv | 10.1165/rcmb.2018-0275LE |
| format | Article |
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(C) Adult male Sprague Dawley rats (∼200 g body weight) were divided into three age-matched groups: control normoxia, control hypoxia (i.e., rats injected once s.c. with vehicle [DMSO; vol/vol] and then exposed to hypoxia [FiO2 = 0.1] for 3 weeks, followed by 6 weeks in room air [FiO2 = 0.21]), and Sugen hypoxia (SuHx, i.e., rats injected with SU5416 20 mg/kg/dose s.c. and then exposed to hypoxia [3 wk], followed by 6 weeks in room air). mRNA expression was evaluated in total lungs (n = 6–11). Here, we found that the TGF-β1 pathway was indeed activated in the hypertensive SuHx rat lung (increased TGF-β1 mRNA expression; Figure 1C), whereas Smad3 mRNA expression remained unchanged (Figure 1C). [...]based on our SuHx data, the canonical TGF-β1/Smad3 pathway is not decreased in the rat lung with severe PAH. Smad3 mRNA (trend, statistically not significant) and miR-130a/301b (P < 0.01) expression was higher in the PAs and plexiform lesions of patients with idiopathic PAH compared with control subjects (Figure 1E). [...]our human data support the notion that boosted signaling of TGF-β1 and its canonical downstream effector Smad3 in human PAs is crucial for PAH development and severity.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2018-0275LE</identifier><identifier>PMID: 31259625</identifier><language>eng</language><publisher>United States: American Thoracic Society</publisher><subject>Animals ; Body weight ; Chronic obstructive pulmonary disease ; Gene expression ; Genotype & phenotype ; Growth factors ; Heart failure ; Hemodynamics ; Humans ; Hypoxia ; Lungs ; Male ; Mice, Transgenic ; MicroRNAs ; miRNA ; Morphology ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - metabolism ; Phosphorylation ; Protein expression ; Proteins ; Pulmonary Arterial Hypertension - metabolism ; Pulmonary arteries ; Pulmonary artery ; Pulmonary hypertension ; Rats, Sprague-Dawley ; Rodents ; Signal Transduction ; Smad3 protein ; Smad3 Protein - metabolism ; Smooth muscle ; Statistical analysis ; Transforming Growth Factor beta1 - metabolism ; Transforming growth factor-b1 ; Transgenic mice ; Veins & arteries</subject><ispartof>American journal of respiratory cell and molecular biology, 2019-07, Vol.61 (1), p.121-123</ispartof><rights>Copyright American Thoracic Society Jul 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1725-84ee48b4a68345fcc20d5f437599c41fcb31019c8f1a2eb59bffdea6f888b8ac3</citedby><cites>FETCH-LOGICAL-c1725-84ee48b4a68345fcc20d5f437599c41fcb31019c8f1a2eb59bffdea6f888b8ac3</cites><orcidid>0000-0003-0709-3935</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31259625$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Calvier, Laurent</creatorcontrib><creatorcontrib>Chouvarine, Philippe</creatorcontrib><creatorcontrib>Legchenko, Ekaterina</creatorcontrib><creatorcontrib>Kokeny, Gabor</creatorcontrib><creatorcontrib>Mozes, Miklos M</creatorcontrib><creatorcontrib>Hansmann, Georg</creatorcontrib><title>Chronic TGF-β1 Signaling in Pulmonary Arterial Hypertension Induces Sustained Canonical Smad3 Pathways in Vascular Smooth Muscle Cells</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>(A) The mRNA and microRNA (miR) expression of TGF-β1 targets was evaluated by qPCR in starved (48 h) human pulmonary artery smooth muscle cells (HPASMCs) stimulated with TGF-β1 (5 ng/ml, 8 hours, n = 3), as well as in the main pulmonary artery (PA) and total lung of transgenic mice overexpressing TGF-β1 in the circulation (TG-TGFβ1) versus wild-type control (males, n = 8–16). (C) Adult male Sprague Dawley rats (∼200 g body weight) were divided into three age-matched groups: control normoxia, control hypoxia (i.e., rats injected once s.c. with vehicle [DMSO; vol/vol] and then exposed to hypoxia [FiO2 = 0.1] for 3 weeks, followed by 6 weeks in room air [FiO2 = 0.21]), and Sugen hypoxia (SuHx, i.e., rats injected with SU5416 20 mg/kg/dose s.c. and then exposed to hypoxia [3 wk], followed by 6 weeks in room air). mRNA expression was evaluated in total lungs (n = 6–11). Here, we found that the TGF-β1 pathway was indeed activated in the hypertensive SuHx rat lung (increased TGF-β1 mRNA expression; Figure 1C), whereas Smad3 mRNA expression remained unchanged (Figure 1C). [...]based on our SuHx data, the canonical TGF-β1/Smad3 pathway is not decreased in the rat lung with severe PAH. Smad3 mRNA (trend, statistically not significant) and miR-130a/301b (P < 0.01) expression was higher in the PAs and plexiform lesions of patients with idiopathic PAH compared with control subjects (Figure 1E). [...]our human data support the notion that boosted signaling of TGF-β1 and its canonical downstream effector Smad3 in human PAs is crucial for PAH development and severity.</description><subject>Animals</subject><subject>Body weight</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Gene expression</subject><subject>Genotype & phenotype</subject><subject>Growth factors</subject><subject>Heart failure</subject><subject>Hemodynamics</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Lungs</subject><subject>Male</subject><subject>Mice, Transgenic</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Morphology</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Phosphorylation</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Pulmonary Arterial Hypertension - metabolism</subject><subject>Pulmonary arteries</subject><subject>Pulmonary artery</subject><subject>Pulmonary hypertension</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Smad3 protein</subject><subject>Smad3 Protein - metabolism</subject><subject>Smooth muscle</subject><subject>Statistical analysis</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming growth factor-b1</subject><subject>Transgenic mice</subject><subject>Veins & arteries</subject><issn>1044-1549</issn><issn>1535-4989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkc9u1DAQhy0EoqVw54QsceGS4nHsxD5WUf9Ji6i0hWvkOHbXVWIvdqxqn4D34UF4Jhxt4cBpRppvfhrNh9B7IOcADf8c9TycUwKiIrTlm8sX6BR4zSsmhXxZesJYBZzJE_QmpUdCgAqA1-ikBsplQ_kp-tntYvBO4_vrq-r3L8Bb9-DV5PwDdh7f5WkOXsUDvoiLiU5N-OawN6X3yQWPb_2YtUl4m9OinDcj7pRf4wq4ndVY4zu17J7UIa1p31XSeVKxjEJYdvhLTnoyuDPTlN6iV1ZNybx7rmfo29XlfXdTbb5e33YXm0pDS3klmDFMDEw1ombcak3JyC2rWy6lZmD1UAMBqYUFRc3A5WDtaFRjhRCDULo-Q5-OufsYfmSTln52SZcLlDchp55SThpKSEMK-vE_9DHkWJ6zUkI2LSGsLRQ5UjqGlKKx_T66ubysB9KvkvpVUr9K6o-SysqH5-A8zGb8t_DXSv0HhOiPlQ</recordid><startdate>201907</startdate><enddate>201907</enddate><creator>Calvier, Laurent</creator><creator>Chouvarine, Philippe</creator><creator>Legchenko, Ekaterina</creator><creator>Kokeny, Gabor</creator><creator>Mozes, Miklos M</creator><creator>Hansmann, Georg</creator><general>American Thoracic Society</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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</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>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>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0709-3935</orcidid></search><sort><creationdate>201907</creationdate><title>Chronic TGF-β1 Signaling in Pulmonary Arterial Hypertension Induces Sustained Canonical Smad3 Pathways in Vascular Smooth Muscle Cells</title><author>Calvier, Laurent ; Chouvarine, Philippe ; Legchenko, Ekaterina ; Kokeny, Gabor ; Mozes, Miklos M ; Hansmann, Georg</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1725-84ee48b4a68345fcc20d5f437599c41fcb31019c8f1a2eb59bffdea6f888b8ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Body weight</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Gene expression</topic><topic>Genotype & phenotype</topic><topic>Growth factors</topic><topic>Heart failure</topic><topic>Hemodynamics</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Lungs</topic><topic>Male</topic><topic>Mice, Transgenic</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Morphology</topic><topic>Muscle, Smooth, Vascular - 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Academic</collection><jtitle>American journal of respiratory cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Calvier, Laurent</au><au>Chouvarine, Philippe</au><au>Legchenko, Ekaterina</au><au>Kokeny, Gabor</au><au>Mozes, Miklos M</au><au>Hansmann, Georg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic TGF-β1 Signaling in Pulmonary Arterial Hypertension Induces Sustained Canonical Smad3 Pathways in Vascular Smooth Muscle Cells</atitle><jtitle>American journal of respiratory cell and molecular biology</jtitle><addtitle>Am J Respir Cell Mol Biol</addtitle><date>2019-07</date><risdate>2019</risdate><volume>61</volume><issue>1</issue><spage>121</spage><epage>123</epage><pages>121-123</pages><issn>1044-1549</issn><eissn>1535-4989</eissn><abstract>(A) The mRNA and microRNA (miR) expression of TGF-β1 targets was evaluated by qPCR in starved (48 h) human pulmonary artery smooth muscle cells (HPASMCs) stimulated with TGF-β1 (5 ng/ml, 8 hours, n = 3), as well as in the main pulmonary artery (PA) and total lung of transgenic mice overexpressing TGF-β1 in the circulation (TG-TGFβ1) versus wild-type control (males, n = 8–16). (C) Adult male Sprague Dawley rats (∼200 g body weight) were divided into three age-matched groups: control normoxia, control hypoxia (i.e., rats injected once s.c. with vehicle [DMSO; vol/vol] and then exposed to hypoxia [FiO2 = 0.1] for 3 weeks, followed by 6 weeks in room air [FiO2 = 0.21]), and Sugen hypoxia (SuHx, i.e., rats injected with SU5416 20 mg/kg/dose s.c. and then exposed to hypoxia [3 wk], followed by 6 weeks in room air). mRNA expression was evaluated in total lungs (n = 6–11). Here, we found that the TGF-β1 pathway was indeed activated in the hypertensive SuHx rat lung (increased TGF-β1 mRNA expression; Figure 1C), whereas Smad3 mRNA expression remained unchanged (Figure 1C). [...]based on our SuHx data, the canonical TGF-β1/Smad3 pathway is not decreased in the rat lung with severe PAH. Smad3 mRNA (trend, statistically not significant) and miR-130a/301b (P < 0.01) expression was higher in the PAs and plexiform lesions of patients with idiopathic PAH compared with control subjects (Figure 1E). [...]our human data support the notion that boosted signaling of TGF-β1 and its canonical downstream effector Smad3 in human PAs is crucial for PAH development and severity.</abstract><cop>United States</cop><pub>American Thoracic Society</pub><pmid>31259625</pmid><doi>10.1165/rcmb.2018-0275LE</doi><tpages>3</tpages><orcidid>https://orcid.org/0000-0003-0709-3935</orcidid></addata></record> |
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| subjects | Animals Body weight Chronic obstructive pulmonary disease Gene expression Genotype & phenotype Growth factors Heart failure Hemodynamics Humans Hypoxia Lungs Male Mice, Transgenic MicroRNAs miRNA Morphology Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - metabolism Phosphorylation Protein expression Proteins Pulmonary Arterial Hypertension - metabolism Pulmonary arteries Pulmonary artery Pulmonary hypertension Rats, Sprague-Dawley Rodents Signal Transduction Smad3 protein Smad3 Protein - metabolism Smooth muscle Statistical analysis Transforming Growth Factor beta1 - metabolism Transforming growth factor-b1 Transgenic mice Veins & arteries |
| title | Chronic TGF-β1 Signaling in Pulmonary Arterial Hypertension Induces Sustained Canonical Smad3 Pathways in Vascular Smooth Muscle Cells |
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