Hypoxia-induced pulmonary vascular remodeling: Contribution of the adventitial fibroblasts

Physiological Research

Volumn 49, Issue 5, 2000, Pages 503-517

  Stenmark, Kurt R ^a,b   Bouchey, D ^a   Nemenoff, R ^b   Dempsey, E C ^c   Das, M ^a  

^a Box B131   (United States)

^b UNIVERSITY OF COLORADO   (United States)

^c VETERANS AFFAIRS MEDICAL CENTER   (United States)

Author keywords

Extracellular matrix; Growth factors; Hypoxia; Mitogen activated protein kinase; Protein kinase C; Pulmonary hypertension; Smooth muscle cells; Tyrosine kinase; Vascular remodeling

Indexed keywords

CALCIUM ION; MITOGEN ACTIVATED PROTEIN KINASE; PHORBOL 13 ACETATE 12 MYRISTATE; PROTEIN KINASE C;

BLOOD VESSEL INJURY; CELL MIGRATION; CELL PROLIFERATION; CONFERENCE PAPER; CONTROLLED STUDY; CORONARY ARTERY DILATATION; ENDOTHELIUM CELL; HUMAN; HUMAN CELL; HUMAN TISSUE; PULMONARY HYPERTENSION; VEIN GRAFT;

ANIMALS; ANOXIA; BLOOD VESSELS; CELL DEATH; CELL DIVISION; FIBROBLASTS; HUMANS; PULMONARY CIRCULATION;

EID: 0033678883     PISSN: 08628408     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Conference Paper

References (71)

1. Remodeling rather than neointimal formation explains luminal narrowing after deep vessel wall injury
2. Normal fibroblasts responding to anoxia exhibit features of the malignant phenotype
3. The anoxic fibroblast response is an early stage wound healing program
4. Regulation of c-jun expression during hypoxic and low-glucose stress
5. Hypoxia increases bromodeoxyuridine labeling indices in bovine neonatal pulmonary arteries
6. Rapid development of atherosclerotic lesions in the rabbit carotid artery induced by perivascular manipulation
7. Hypoxia activates extracellular-signal regulated kinase (Erk) and induces proliferation in adventitial fibroblasts from the neonatal bovine main pulmonary artery (MPA-Fibs)
8. Transcription factors and pattern formation in the developing lung
9. Increased DNA replication in the arterial adventitia after aortic ligation
10. Mesenchymal cells isolated after acute lung injury manifest an enhanced proliferative phenotype
11. Enhanced growth of fetal and neonatal pulmonary artery adventitial fibroblasts is dependent on protein kinase C
12. Hypoxia stimulates growth of selective subsets of pulmonary artery adventitial fibroblasts
13. Selected isozymes of PKC contribute to augmented growth of fetal and neonatal bovine pulmonary artery fibroblasts
14. Selective subpopulations of pulmonary artery adventitial fibroblasts exhibit unique proliferative and apoptotic capabilities
15. Chronic hypoxia induces exaggerated growth responses in pulmonary artery adventitial fibroblasts: Potential contribution of specific protein kinase C isozymes
16. Enhanced growth capacity of neonatal pulmonary artery smooth muscle cells in vitro: Dependence on cell size, time from birth, insulin like growth factor I, and auto-activation of protein kinase C
17. Paracrine role of adventitial superoxide anion in mediating spontaneous tone of the isolated rat aorta in angiotensin II-induced hypertension
18. Progressive loss of vasodilator responsive component of pulmonary hypertension in neonatal calves exposed to 4,570m
19. Persistence, re-expression, and induction of pulmonary arterial fibronectin, tropoelastin and type I procollagen mRNA expression in neonatal hypoxic pulmonary hypertension
20. Anoxic induction of a sarcoma virus-related VL30 retrotransposon is mediated by a cis-acting element which binds hypoxia-inducible factor 1 and an anoxia inducible factor
21. Normal fibroblasts induce the c/EBPβ and ATF-4 bZIP transcription factors in response to anoxia
22. Smooth muscle cells isolated from discrete compartments of the mature vascular media exhibit unique phenotypes and distinct growth capabilities
23. Evidence of fibroblast heterogeneity and the role of fibroblast subpopulations in fibrosis
24. Chronic hypoxia induces the appearance of myofibroblast-like cells with enhanced proliferative and migratory properties in the distal pulmonary artery media
25. 1-phase checkpoint by low-oxygen conditions is independent of p53 status
26. Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours
27. Adventitia-dependent influences on vascular function
28. Evidence for apoptosis in human atherogenesis and in a rat vascular injury model
29. Nitric oxide, prostacyclin and cyclic nucleotide formation in externally stented procine vein grafts
30. Characterization of activators and inhibitors of protein kinase C-μ
31. Vascular remodelling in clinical and experimental pulmonary hypertensions
32. Heterogeneity of human lung fibroblast proliferation in relation to disease expression
33. Heterogeneous proliferative characteristics of human adult lung fibroblast lines and clonally derived fibroblasts from control and fibrotic tissue
34. Significance of adventitial inflammation of the coronary artery in patients with unstable angina: Results at autopsy
35. Increase in atherosclerosis and adventitial mast cells in cocaine abusers: An alternative mechanism of cocaine-associated coronary vasospasm and thrombosis
36. Hypoxia causes the activation of nuclear factor kappa B through the phosphorylation of I kappa B alpha on tyrosine residues
37. Systemic scleroderma
38. Production of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha by inflammatory granuloma fibroblasts
39. 3H]-thymidine by cells of the rat pulmonary arteries and alveolar wall
40. Epithelial-mesenchymal interactions in lung development
41. The structural basis of persistent pulmonary hypertension of the newborn infant
42. Intracellular signaling by hydrolysis of phospholipids and activation of protein kinase C
43. Localization of a constitutively active, phagocyte-like NADPH oxidase in rabbit aortic adventitia: Enhancement by Angiotensin II
44. Prazosin administration enhances proliferation of arteriolar adventitial fibroblasts
45. Differential proliferation of fibroblasts cultured from normal and fibrotic human lungs
46. Abnormal growth and clonal proliferation of fibroblasts derived from kidneys with interstitial fbrosis
47. Inhibition of experimental neointimal hyperplasia and thrombosis depends on the type of vascular injury and the site of drug administration
48. Clonal heterogeneity in fibroblast phenotype: Implications for the control of epithelial-mesenchymal interactions
49. Identification of a potential role for the adventitia in vascular lesion formation after balloon overstretch injury of porcine coronary arteries
50. Hypoxic stimulation of the stress-activated protein kinases in pulmonary artery fibroblasts
51. A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation
52. Mechanisms of myofibroblast activity and phenotypic modulation
53. Epithelial-mesenchymal interactions in lung development
54. Adventitial myofibroblasts contribute to neointimal formation in injured porcine coronary arteries
55. Transforming growth factor β 1 expression and myofibroblast formation during arterial repair
56. Adventitial remodeling following coronary arterial injury
57. Origin of extracellular matrix synthesis during coronary repair
58. Remodeling of autologous saphenous vein grafts: The role of perivascular myofibroblasts
59. Chronic treatment with interleukin-1β induces coronary intimal lesions and vasopastic responses in pigs in vivo
60. Subacute infantile mountain sickness
61. Cellular and molecular mechanisms of pulmonary vascular remodeling
62. Modulation of vascular wall cell phenotype in pulmonary hypertension
63. Anchorage-independent colony growth of pulmonary fibroblasts derived from fibrotic human lung tissue
64. Superoxide anion from the adventitia of the rat thoracic aorta inactivates nitric oxide
65. Hypoxia enhances cellular proliferation and inositol 1, 4, 5-triphosphate generation in fibroblasts from bovine pulmonary artery but not from mesenteric artery
66. Pulmonary artery smooth muscle cells from chronically hypoxic neonatal calves retain fetal-like and acquire new growth properties
67. The roles of protein kinase C beta I and beta II in vascular smooth muscle cell proliferation
68. Activation of AP-1 and of a nuclear redox factor, Ref-1, in the response of HT29 colon cancer cells to hypoxia
69. Regulation of atypical ζ-protein kinase C in cellular signaling