Radiation-induced changes in gene expression and distribution of atrial natriuretic peptide (ANP) in different anatomical regions of the rat heart

Kruse, Jacqueline J C M; Strootman, Erwin G; Bart, Cindy I.; Visser, Anke; Leer, Jan-Willem H.; Wondergem, J.

doi:10.1080/09553000110102021

Cited by 13 publications

(9 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, ANP is synthesized by fibroblasts infiltrating the infarct (2). Interestingly, irradiation of the left ventricle induces ANP gene expression in the proximity of injured areas with degenerated myocytes and fibrosis (12). In the present study, NT-proANP, BNP, and NT-proBNP correlated with PIIINP, suggesting that ANP and BNP modulate collagen scar formation after AMI.…”

Section: Discussionsupporting

confidence: 58%

“…Serum samples for mass of the myocardial isoform of creatine kinase (CK-MBm) assays were taken before treatment (when feasible), at 1. 5,3,6,9,12,15,18,21,24,48,72,96, and 120 h after thrombolysis, and at discharge (day 9 or 10 after AMI) from the hospital. Troponin T (TnT) was assayed before treatment (when feasible), at 6, 48, 72, 96, and 120 h after thrombolysis, and at discharge from the hospital.…”

Section: Patientsmentioning

confidence: 99%

“…ANP and collagen I and III mRNA levels are increased in the adjacent noninfarcted myocardium as well as in the remote noninfarcted myocardium (44). Furthermore, radiation of the left ventricle induces ANP gene expression in the proximity of injured areas with degenerated myocytes and fibrosis (12). The main goal of the present study was to investigate the role of ANP and BNP in collagen formation and degradation and left ventricular remodeling in humans suffering acute myocardial infarction (AMI).…”

mentioning

confidence: 95%

See 2 more Smart Citations

Atrial natriuretic peptide, B-type natriuretic peptide, and serum collagen markers after acute myocardial infarction

Magga

Puhakka²,

Hietakorpi³

et al. 2004

Journal of Applied Physiology

View full text Add to dashboard Cite

Experimental data suggest that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) act locally as antifibrotic factors in heart. We investigated the interrelationships of natriuretic peptides and collagen markers in 93 patients receiving thrombolytic treatment for their first acute myocardial infarction (AMI). Collagen formation following AMI, evaluated as serum levels of amino terminal propeptide of type III procollagen, correlated with NH(2)-terminal proANP (r = 0.45, P < 0.001), BNP (r = 0.55, P < 0.001) and NH(2)-terminal proBNP (r = 0.50, P < 0.01) on day 4 after thrombolysis. Levels of intact amino terminal propeptide of type I procollagen decreased by 34% (P < 0.001), and levels of carboxy terminal cross-linked telopeptide of type I collagen (ICTP) increased by 65% (P < 0.001). ICTP levels correlated with NH(2)-terminal proBNP (r = 0.25, P < 0.05) and BNP (r = 0.28, P < 0.05) on day 4. Our results suggest that ANP and BNP may act as regulators of collagen scar formation and left ventricular remodeling after AMI in humans. Furthermore, degradation of type I collagen is increased after AMI and may be regulated by BNP.

show abstract

Section: Discussionsupporting

confidence: 58%

Section: Patientsmentioning

confidence: 99%

mentioning

confidence: 95%

See 1 more Smart Citation

Atrial natriuretic peptide, B-type natriuretic peptide, and serum collagen markers after acute myocardial infarction

Magga

Puhakka²,

Hietakorpi³

et al. 2004

Journal of Applied Physiology

View full text Add to dashboard Cite

show abstract

“…Together, these associations suggest that ␤-MHC reexpression does not develop without fibrosis. A similar statement can be made with respect to ventricular reexpression of ANP; increased ANP levels do not invariably correlate with cardiac hypertrophy but are observed always in the presence of cardiac pathology and accompanied by fibrosis (interstitial and parivascular) (37)(38)(39).…”

Section: Discussionmentioning

confidence: 83%

Fibrosis, not cell size, delineates β-myosin heavy chain reexpression during cardiac hypertrophy and normal aging in vivo

Pandya

Kim

Smithies

2006

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

117

View full text Add to dashboard Cite

Reexpression of the fetally expressed ␤-myosin heavy chain (␤-MHC) gene is a well documented marker of pathological cardiac hypertrophy and normal aging in many experimental models. To gain insights into factors affecting this reexpression of ␤-MHC within the complex anatomical structure of the heart, we investigated the spatial pattern of its expression at the level of single cells during aging and hypertrophy. We generated mice that express yellow fluorescent protein fused to the N terminus of the ␤-MHC and examined its expression pattern during normal aging and in mice with hypertrophy induced by constitutive expression of a renin transgene. The localization of fibrosis within the hearts also was determined by using a fluorescent lectin. The results show that reexpression of ␤-MHC occurs in discrete subsets of myocytes within the subendocardium rather than uniformly throughout the heart, that ␤-MHC induction is not an obligatory consequence of cellular hypertrophy, and that ␤-MHC-expressing cells in the normal aging heart and the hypertrophic heart are distributed predominantly in clusters within and surrounding foci of fibrosis. We conclude that ␤-MHC gene expression in the normal aging adult and hypertrophic mouse heart is a marker of fibrosis rather than of cellular hypertrophy. genetic reprogramming T he adult myocardium responds to extrinsic forms of stress, such as hypertension, myocardial infarction, and pressure overload, by a hypertrophic growth response (reviewed in ref.

show abstract

“…The human and animal data indicate the important role of vascular injury and endothelial dysfunction [ 25 ], but also of myocardial remodeling, degeneration and dysfunction [ 31 , 61 – 63 ] in the pathogenesis of radiation-induced CD. Endothelial dysfunction (loss of thromboresistance and increased expression of adhesion molecules and cytokines) contributes to pro-fibrotic and pro-inflammatory environments, which are common aspects of radiation-induced tissue injury [ 64 , 65 ].…”

Section: Biology Of Radiation-induced CDmentioning

confidence: 99%

Pathology and biology of radiation-induced cardiac disease

Tapio

2016

Journal of Radiation Research

151

148

View full text Add to dashboard Cite

Heart disease is the leading global cause of death. The risk for this disease is significantly increased in populations exposed to ionizing radiation, but the mechanisms are not fully elucidated yet. This review aims to gather and discuss the latest data about pathological and biological consequences in the radiation-exposed heart in a comprehensive manner. A better understanding of the molecular and cellular mechanisms underlying radiation-induced damage in heart tissue and cardiac vasculature will provide novel targets for therapeutic interventions. These may be valuable for individuals clinically or occupationally exposed to varying doses of ionizing radiation.

show abstract

Radiation-induced changes in gene expression and distribution of atrial natriuretic peptide (ANP) in different anatomical regions of the rat heart

Cited by 13 publications

References 30 publications

Atrial natriuretic peptide, B-type natriuretic peptide, and serum collagen markers after acute myocardial infarction

Atrial natriuretic peptide, B-type natriuretic peptide, and serum collagen markers after acute myocardial infarction

Fibrosis, not cell size, delineates β-myosin heavy chain reexpression during cardiac hypertrophy and normal aging in vivo

Pathology and biology of radiation-induced cardiac disease

Contact Info

Product

Resources

About