Pulmonary vascular remodeling in congenital heart disease: Enhanced expression of heat shock proteins.

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dc.contributor.authorGeiger, Ralph
dc.contributor.authorSharma, Hari S
dc.contributor.authorMooi, Wolter J
dc.contributor.authorBerger, Rolf M F
dc.date.accessioned2011-11-11T08:27:03Z
dc.date.available2011-11-11T08:27:03Z
dc.date.issued2009-12
dc.description.abstractIn congenital heart disease (CHD), mechanical wall stress by increased pulmonary artery pressure and pulmonary blood flow is believed to play a pivotal role in the pathogenesis of pulmonary plexogenic arteriopathy (PPA). The pathogenesis of this disease that involves significant pulmonary arterial remodelling, is, however, largely unknown. In the systemic circulation, upregulation of HSP-70 and HSP-27 in the arterial wall occurs in response to acute hypertension, whereas HSP-60 and increased titres of anti-HSP-60 antibodies are associated with atherosclerotic vessel disease. We looked for the involvement of HSPs in the stress response of pulmonary endothelial and vascular smooth muscle cells in different abnormal hemodynamic conditions in patients with CHDs. We analyzed the expression pattern of HSP-27, HSP-70 and HSP-60 in lung biopsies of 38 patients with CHD, using immunohistochemistry. These included 4 individuals with an essentially normal pulmonary circulation, who served as controls. Immunoreactivity against HSP-27 and also against HSP-70 was present in the pulmonary endothelium and vascular smooth muscle cells of patients and controls in a similar pattern. In contrast, expression of HSP-60 was absent in pulmonary arteries of both patients and controls. In patients with advanced PPA, cells within plexiform lesions showed strong staining for HSP-27 and HSP-70, but were again negative for HSP-60. The intensity of immunoreactivity against HSP-70 correlated inversely with medial thickness of pre-acinar arteries (r = -0.32; p = 0.04). Expression of HSP-27 and HSP-70 did not correlate with hemodynamic parameters, although immunoreactivity against HSP27 tended to be increased in cases with high pulmonary artery pressure (r = 0.37; p = 0.16) and was highest in patients with flow-associated pulmonary hypertension (p<0.01). HSP-27 and HSP-70, but not HSP-60 are engaged in the stress response of cells of small pulmonary arteries in pulmonary plexogenic arteriopathy. HSP-27 and HSP-70 are increasingly expressed in the advanced proliferative lesions of this disease.en_US
dc.identifier.citationGeiger Ralph, Sharma Hari S, Mooi Wolter J, Berger Rolf M F. Pulmonary vascular remodeling in congenital heart disease: Enhanced expression of heat shock proteins. Indian Journal of Biochemistry & Biophysics. 2009 Dec; 46(6): 482-490.en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/135231
dc.language.isoenen_US
dc.source.urihttps://nopr.niscair.res.in/bitstream/123456789/7251/1/IJBB%2046%286%29%20482-490.pdfen_US
dc.subjectHistopatholgyen_US
dc.subjectPulmonary circulationen_US
dc.subjectRemodelingen_US
dc.subjectCongenital heart diseaseen_US
dc.subjectHeat shock proteinsen_US
dc.subject.meshCase-Control Studies
dc.subject.meshChild
dc.subject.meshChild, Preschool
dc.subject.meshGene Expression Regulation
dc.subject.meshHeart Diseases --genetics
dc.subject.meshHeart Diseases --metabolism
dc.subject.meshHeat-Shock Proteins --metabolism
dc.subject.meshHemodynamics
dc.subject.meshHumans
dc.subject.meshImmunohistochemistry
dc.subject.meshInfant
dc.subject.meshInfant, Newborn
dc.subject.meshLung --blood supply
dc.subject.meshProtein Transport
dc.subject.meshPulmonary Artery --physiopathology
dc.subject.meshYoung Adult
dc.subject.otherHeart Diseases --physiopathology
dc.titlePulmonary vascular remodeling in congenital heart disease: Enhanced expression of heat shock proteins.en_US
dc.typeArticleen_US
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