Development and characterization of a cloned rat pulmonary arterial smooth muscle cell line that maintains differentiated properties through multiple subcultures.

Rothman, Abraham; Kulik, Thomas J.; Taubman, Mark B.; Berk, B. C.; Smith, Christopher W.; Nadal‐Ginard, Bernardo

doi:10.1161/01.cir.86.6.1977

Cited by 131 publications

(104 citation statements)

References 53 publications

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“…The PAC1 (17) and A10 (18) smooth muscle cell lines were maintained in DMEM with 10% FBS and were infected with adenovirus encoding lacZ or a myocardin dominant negative mutant lacking the transcription activation domain (TAD) (13).…”

Section: Methodsmentioning

confidence: 99%

Myocardin is a master regulator of smooth muscle gene expression

Wang

Pipes

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

468

440

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Virtually all smooth muscle genes analyzed to date contain two or more essential binding sites for serum response factor (SRF) in their control regions. Because SRF is expressed in a wide range of cell types, it alone cannot account for smooth muscle-specific gene expression. We show that myocardin, a cardiac muscle-and smooth muscle-specific transcriptional coactivator of SRF, can activate smooth muscle gene expression in a variety of nonmuscle cell types via its association with SRF. Homodimerization of myocardin is required for maximal transcriptional activity and provides a mechanism for cooperative activation of smooth muscle genes by SRF-myocardin complexes bound to different SRF binding sites. These findings identify myocardin as a master regulator of smooth muscle gene expression and explain how SRF conveys smooth muscle specificity to its target genes.

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Section: Methodsmentioning

confidence: 99%

Myocardin is a master regulator of smooth muscle gene expression

Wang

Pipes

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

468

440

View full text Add to dashboard Cite

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“…After transient transfection in COS-7 cells, recombinant proteins were visualized with the aid of the EGFP tag and by staining with the fibulin-5 antibody. To examine colocalization of LOXL1 and fibulin-5 in the extracellular matrix, we cultured a rat arterial smooth muscle cell line (PAC-1) known to deposit extracellular matrix material 28 and carried out double-labeling immunofluorescence for LOXL1 and fibulin-5.…”

Section: Cell Culturesmentioning

confidence: 99%

Elastic fiber homeostasis requires lysyl oxidase–like 1 protein

et al. 2004

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“…Pulmonary artery smooth muscle cell (PASMCs) were obtained from the cleaned arteries by enzymatic digestion with collagenase (5%) using modified methods. 19,20 The PASMCs were cultured in Dulbecco's modified Eagle Medium (DMEM) and supplemental FBS (10%) in 100 mm plates in a humidified, normoxic incubator (21% O 2 , 5% CO 2 ) at 378C. PASMCs were identified by their typical elongated morphology 19 and positive staining for smooth muscle cell myosin heavy chain and a-actin.…”

Section: Pulmonary Artery Smooth Muscle Cell Isolationmentioning

confidence: 99%

Prolonged Hypoxia Augments L-Citrulline Transport By System A In The Newborn Piglet Pulmonary Circulation

Fike

Sidoryk‐Węgrzynowicz

Aschner

et al. 2012

B63. Experimental Models in Pulmonary Hypertension I

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AimsPulmonary arterial endothelial cells (PAECs) express the enzymes needed for generation of L-arginine from intracellular L-citrulline but do not express the enzymes needed for de novo L-citrulline synthesis. Hence, L-citrulline levels in PAECs are dependent on L-citrulline transport. Once generated, L-arginine can be converted to L-citrulline and nitric oxide (NO) by the enzyme NO synthase. We sought to determine whether hypoxia, a condition aetiologically linked to pulmonary hypertension, alters the transport of L-citrulline and the expression of the sodium-coupled neutral amino acid transporters (SNATs) in PAECs from newborn piglets. Methods and resultsPAECs isolated from newborn piglets were cultured under normoxic and hypoxic conditions and used to measure SNAT1, 2, 3, and 5 protein expression and 14 C-L-citrulline uptake. SNAT1 protein expression was increased, while SNAT2, SNAT3, and SNAT5 expression was unaltered in hypoxic PAECs. 14 C-L-citrulline uptake was increased in hypoxic PAECs. Studies with inhibitors of System A (SNAT1/2) and System N (SNAT3/5) revealed that the increased 14 C-L-citrulline uptake was largely due to System A-mediated transport. Additional studies were performed to evaluate SNAT protein expression and L-citrulline levels in lungs of piglets with chronic hypoxia-induced pulmonary hypertension and comparable age controls. Lungs from piglets raised in chronic hypoxia exhibited greater SNAT1 expression and higher L-citrulline levels than lungs from controls. ConclusionIncreased SNAT1 expression and the concomitant enhanced ability to transport L-citrulline in PAECs could represent an important regulatory mechanism to counteract NO signalling impairments known to occur during the development of chronic hypoxia-induced pulmonary hypertension in newborns. ----------------------------------------------------------------------- KeywordsPulmonary hypertension † Sodium-coupled neutral amino acid transporters † Nitric oxide

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Development and characterization of a cloned rat pulmonary arterial smooth muscle cell line that maintains differentiated properties through multiple subcultures.

Abstract: These cloned PASMCs retain many differentiated characteristics and should be valuable for future studies of pulmonary vascular smooth muscle cell biology.

Cited by 131 publications

References 53 publications

Myocardin is a master regulator of smooth muscle gene expression

Myocardin is a master regulator of smooth muscle gene expression

Elastic fiber homeostasis requires lysyl oxidase–like 1 protein

Prolonged Hypoxia Augments L-Citrulline Transport By System A In The Newborn Piglet Pulmonary Circulation

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