Role of Adenylyl Cyclase in Proliferation of Neonatal Pulmonary Artery Smooth Muscle Cells

Guldemeester, H.A.; Stenmark, Kurt R.; Brough, George H.; Tuder, Rubin M.; Stevens, Troy

doi:10.1378/chest.114.1_supplement.38s

Cited by 6 publications

(3 citation statements)

References 2 publications

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“…Previous studies on arterial smooth muscle from different species have demonstrated expression of multiple AC isoforms. AC2, AC4, AC5/6, and AC7, but not AC3, have been found in bovine pulmonary artery SMCs (30,31). Rat aortic SMCs have been shown to express AC3 and possibly AC8 but not the neuronal AC1 (32).…”

Section: Ac3 Mediates the Growth-inhibitory Effects Of Pge 2 Inmentioning

confidence: 96%

Adenylyl Cyclase 3 Mediates Prostaglandin E2-induced Growth Inhibition in Arterial Smooth Muscle Cells

Wong¹,

Baker²,

Trinh³

et al. 2001

Journal of Biological Chemistry

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Arterial smooth muscle cell (SMC) proliferation contributes to a number of vascular pathologies. Prostaglandin E 2 (PGE 2 ), produced by the endothelium and by SMCs themselves, acts as a potent SMC growth inhibitor. The growth-inhibitory effects of PGE 2 are mediated through activation of G-protein-coupled membrane receptors, activation of adenylyl cyclases (ACs), formation of cAMP, and subsequent inhibition of mitogenic signal transduction pathways in SMCs. Of the 10 different mammalian AC isoforms known today, seven isoforms (AC2-7 and AC9) are expressed in SMCs from various species. We show that, despite the presence of several different AC isoforms, the principal AC isoform activated by PGE 2 in human arterial SMCs is a calmodulin kinase II-inhibited AC with characteristics similar to those of AC3. AC3 is expressed in isolated human arterial SMCs and in intact aorta. We further show that arterial SMCs isolated from AC3-deficient mice are resistant to PGE 2 -induced growth inhibition. In summary, AC3 is the principal AC isoform activated by PGE 2 in arterial SMCs, and AC3 mediates the growth-inhibitory effects of PGE 2 . Because AC3 activity is inhibited by intracellular calcium through calmodulin kinase II, AC3 may serve as an important integrator of growth-inhibitory signals that stimulate cAMP formation and growth factors that increase intracellular calcium.

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Section: Ac3 Mediates the Growth-inhibitory Effects Of Pge 2 Inmentioning

confidence: 96%

Adenylyl Cyclase 3 Mediates Prostaglandin E2-induced Growth Inhibition in Arterial Smooth Muscle Cells

Wong¹,

Baker²,

Trinh³

et al. 2001

Journal of Biological Chemistry

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“…ACs are activated by ligands that bind to trimeric G-protein-coupled receptors, such as b-adrenergic agents and prostaglandin E 2 (Ishikawa and Homcy, 1997). Expression of AC2-7 has been demonstrated in different studies of arterial SMCs (Zhang et al, 1997;Guldemeester et al, 1998), but the function of speci®c AC isoforms remains to be elucidated. All known ACs, with the exception of AC9, are activated by forskolin, a diterpene derivate isolated from the Indian plant Coleus forskohli.…”

Section: Formation Of Camp and Cgmp Is Regulated By Adenylyl-and Guanmentioning

confidence: 99%

Molecular pathways of cyclic nucleotide‐induced inhibition of arterial smooth muscle cell proliferation

et al. 2001

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Cyclic adenosine 3',5'-monophosphate (cAMP) and cyclic guanosine 3',5'-monophosphate (cGMP) are second messengers involved in the intracellular signal transduction of a wide variety of extracellular stimuli. These signals regulate many biological processes including cell proliferation, differentiation, migration, and apoptosis. Recently, significant progress has been achieved in the molecular basis underlying cyclic nucleotide regulation of cell proliferation. This review summarizes our knowledge of the signaling pathways regulated by cyclic nucleotides in arterial smooth muscle cells.

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“…All known ACs, with the exception of AC9, are activated by forskolin, a diterpene derivate isolated from the Indian plant Coleus forskohli . Expression of AC2‐7 has been demonstrated in different studies of arterial SMCs (Zhang et al, 1997; Guldemeester et al, 1998), but the function of specific AC isoforms remains to be elucidated.…”

Section: Formation Of Camp and Cgmp Is Regulated By Adenylyl‐ And Guamentioning

confidence: 99%

Molecular pathways of cyclic nucleotide-induced inhibition of arterial smooth muscle cell proliferation

et al. 2000

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Role of Adenylyl Cyclase in Proliferation of Neonatal Pulmonary Artery Smooth Muscle Cells

Cited by 6 publications

References 2 publications

Adenylyl Cyclase 3 Mediates Prostaglandin E2-induced Growth Inhibition in Arterial Smooth Muscle Cells

Adenylyl Cyclase 3 Mediates Prostaglandin E2-induced Growth Inhibition in Arterial Smooth Muscle Cells

Molecular pathways of cyclic nucleotide‐induced inhibition of arterial smooth muscle cell proliferation

Molecular pathways of cyclic nucleotide-induced inhibition of arterial smooth muscle cell proliferation

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