Regulation of procollagen metabolism in the pressure-overloaded rat heart.

Eleftheriades, Elias G.; Durand, Jean Bernard; Ferguson, Alan; Engelmann, Gary L.; Jones, Stephen B.; Samarel, Allen M.

doi:10.1172/jci116270

Cited by 58 publications

(36 citation statements)

References 39 publications

(35 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, fibroblasts and fibroblast proliferation may also contribute to an elevation in collagen synthesis. This remodeling of collagen structure has been reported in hypertension, 16,17 heart failure, 18 stunned myocardium 19 and acute myocardial infarction. 20 In the present study, we excluded hypertensive patients accompanied by liver disease, 21 lung disease, 22 and diabetes 23 because they have other causes of the elevation of PIIIP.…”

Section: Discussionsupporting

confidence: 65%

Long-Term Effects of Delapril Hydrochloride on Procollagen Type III Amino-Terminal Peptide, Left Ventricular Mass and Left Ventricular Function in Hypertensive Patients

Matoba¹,

Asaji

Matsui

et al. 1998

Jpn Circ J

View full text Add to dashboard Cite

eft ventricular hypertrophy (LVH) is a major hazardous cardiovascular complication in patients with hypertension. 1,2 The development of LVH depends not only on the renin-angiotensin system generating angiotensin II, 3 but also on the mechanical stress, which activates the protein kinase cascade of phosphorylation in cardiac myocytes. 4 The goal of antihypertensive therapy should be prevention and regression of LVH. It is reported that angiotensin converting enzyme (ACE) inhibitors are more effective than -blockers, calcium antagonists, and diuretics in reducing left ventricular mass (LVM). 5 We therefore assessed the clinical effect of delapril hydrochloride (an ACE inhibitor) 6 from the viewpoint of echocardiographically determined cardiac function and LVH, as well as the serum concentrations of procollagen type III aminoterminal peptide (PIIIP) as reflected in the production of collagen type III. Methods Patient SelectionFifteen hypertensive patients with LVH (10 men and 5 women, mean age 77.2±7.5 years) were entered in the study. Patients were previously untreated with hypertensive drugs or had discontinued the use of these drugs for at least 4 weeks prior. Patients with hyperglycemia, liver dysfunction or pulmonary fibrosis were excluded. The 2 criteria of LVH were an interventricular septal thickness (IVST) of more than 10 mm and left ventricular posterior wall thickness (LVPWT) of more than 10 mm as measured by echocardiography. All study patients complied with these criteria. Study ProtocolAll patients were treated with an ACE inhibitor (delapril hydrochloride, 30 mg/day po) for 12 months. To evaluate the clinical effect of delapril hydrochloride, blood pressure (BP) and heart rate were measured in a supine position before administration of delapril hydrochloride and then after 6 and 12 months of administration. Blood samples were obtained from each patient. Plasma renin activity (PRA) and concentrations of serum atrial natriuretic peptide (ANP) and serum PIIIP were measured by radioimmunoassay before administration and again after 6 and 12 months of taking the drug. The normal serum concentration of PIIIP, which was 0.40±0.13 U/ml (0.25-0.70 U/ml), was obtained from 24 normal volunteers (aged 20-80 years).Jpn Circ J 1998; 62: 900 -902 (Received June 30, 1998; revised manuscript received August 20, 1998; accepted August 21, 1998

show abstract

Section: Discussionsupporting

confidence: 65%

Long-Term Effects of Delapril Hydrochloride on Procollagen Type III Amino-Terminal Peptide, Left Ventricular Mass and Left Ventricular Function in Hypertensive Patients

Matoba¹,

Asaji

Matsui

et al. 1998

Jpn Circ J

View full text Add to dashboard Cite

show abstract

“…In hypertensive myocardial fibrosis, there is an initial deposition of collagen type III, followed by type I (12,13,31). Type III collagen is also increased in many experimental cardiac diseases (7,14,(32)(33)(34)(35)(36). In human cardiac samples, the results have been controversial.…”

Section: Collagen Type Iii/i Expression Ratiomentioning

confidence: 99%

Collagen content, but not the ratios of collagen type III/I mRNAs, differs among hypertensive, alcoholic, and idiopathic dilated cardiomyopathy

Soufen

Salemi

Aneas

et al. 2008

Braz J Med Biol Res

View full text Add to dashboard Cite

Cardiac interstitial fibrosis may contribute to ventricular dysfunction and the prognosis of patients with dilated cardiomyopathy. The objective of the present study was to determine if total myocardial collagen content and collagen type III/I (III/I ratio) mRNAs differ in hypertensive, alcoholic, and idiopathic dilated cardiomyopathy subjects. Echocardiography and exercise cardiopulmonary testing were performed in patients with idiopathic (N = 22), hypertensive (N = 12), and alcoholic (N = 11) dilated cardiomyopathy. Morphometric analysis of collagen was performed in fragments obtained by endomyocardial biopsy with picrosirius red staining. The collagen III/I ratio was determined by reverse transcription polymerase chain reaction. Samples of controls (N = 10) were obtained from autopsy. Echocardiographic variables and maximal oxygen uptake were not different among dilated cardiomyopathy groups. Collagen was higher in all dilated cardiomyopathy groups (idiopathic, hypertensive and alcoholic, , , , , 7.36 ± 1.09%) versus controls (1.12 ± 0.18%), P < 0.05. Collagen was lower in idiopathic dilated cardiomyopathy (4.97 ± 0.83%) than hypertensive (8.50 ± 1.11%) and alcoholic (10.77 ± 2.09%) samples (P < 0.005 for both). The collagen III/I ratio in all samples from dilated cardiomyopathy patients was higher compared to that in controls (0.29 ± 0.04, P < 0.05) but was the same in the samples from idiopathic (0.77 ± 0.07), hypertensive (0.75 ± 0.07), and alcoholic (0.81 ± 0.16) dilated cardiomyopathy groups. Because of the different physical properties of the types of collagen, the higher III/I ratio may contribute to progressive ventricular dilation and dysfunction in dilated cardiomyopathy patients.

show abstract

“…This model of suprarenal aortic coarctation has been extensively characterized in our laboratory (5,11,20,24) and consists of three stages. During the first phase, banded animals develop concentric LVH slowly over an 8-wk period, followed by an established phase of compensatory LVH.…”

mentioning

confidence: 99%

“…Once established, LVH progresses to heart failure (16-24 wk), with the development of diastolic dysfunction and interstitial fibrosis. Characteristic alterations in LV protein content and ␤-myosin heavy chain (MHC), atrial natriuretic factor, and sarco(endo)plasmic reticulum Ca 2ϩ ATPase-2 mRNA and protein levels are evident during disease progression (5,11,20,24). Therefore, this model is ideal for examining in vivo PYK2 and FAK in relation to the induction of LVH and its transition to heart failure.…”

mentioning

confidence: 99%

PYK2 expression and phosphorylation increases in pressure overload-induced left ventricular hypertrophy

Bayer

Heidkamp

Patel

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Proline-rich tyrosine kinase 2 (PYK2) is a member of the focal adhesion kinase (FAK) family of nonreceptor protein tyrosine kinases. PYK2 has been implicated in linking G protein-coupled receptors to activation of mitogen-activated protein kinase cascades and cellular growth in a variety of cell types. To determine whether PYK2 expression and phosphorylation is altered in left ventricular (LV) myocardium undergoing LV hypertrophy (LVH) and heart failure in vivo, suprarenal abdominal aortic coarctation was performed in 160-g male Sprague-Dawley rats. Immunohistochemistry and Western blotting were performed on LV tissue 1, 8, and 24 wk after aortic banding. Aortic banding produced sustained hypertension and gradually developing LVH. PYK2 levels were increased 1.8 Ϯ 0.2-, 2.7 Ϯ 0.6-, and 2.0 Ϯ 0.2-fold in 1-, 8-, and 24-wk banded animals compared with their respective sham-operated controls. The increase in PYK2 expression was paralleled by an increase in PYK2 phosphorylation, both of which preceded the development of LVH. Immunohistochemistry revealed that enhanced PYK2 expression occurred predominantly in the cardiomyocyte population. Furthermore, there was a high degree of correlation (R ϭ 0.75; P Ͻ 0.001) between the level of PYK2 and the degree of LVH in 24-wk sham and banded animals. In contrast, FAK levels and FAK phosphorylation were not increased before the development of LVH. However, there was a high degree of correlation (R ϭ 0.68; P Ͻ 0.001) between the level of FAK and the degree of LVH in 24-wk sham and banded rats. There was also a significant increase in the ratio of phosphospecific anti-FAK to FAK at this time point. These data are consistent with a role for PYK2 in the induction of pressure overload-induced cardiomyocyte hypertrophy, and suggest that PYK2 and FAK have distinctly different roles in LVH progression. signal transduction; cytoskeleton; heart failure; focal adhesion kinase CARDIAC HYPERTROPHY is a compensatory process that leads to a heart better suited for the functional demands caused by myocyte dysfunction or loss. Because cardiac myocytes are terminally differentiated and nonproliferative, hypertrophic myocytes demonstrate an increase in protein content rather than an increase in myocyte number. Cardiac hypertrophy is also associated with sarcomeric reorganization and characteristic changes in gene expression and protein turnover. Cardiac hypertrophy, however, may independently lead to cardiac dysfunction and is also a common feature associated with the heart failure state. Despite advancements in the treatment and understanding of the pathogenesis of heart failure, the cellular and molecular mechanisms involved in hypertrophy induction are still largely unknown.Recent studies (12,17,18) have suggested that nonreceptor protein tyrosine kinases are important in transducing mechanical stimuli to biochemical pathways that lead to cardiomyocyte hypertrophy. Prolinerich tyrosine kinase 2 (PYK2) and focal adhesion kinase (FAK) are members of the FAK family of nonreceptor protein tyrosin...

show abstract

Regulation of procollagen metabolism in the pressure-overloaded rat heart.

Cited by 58 publications

References 39 publications

Long-Term Effects of Delapril Hydrochloride on Procollagen Type III Amino-Terminal Peptide, Left Ventricular Mass and Left Ventricular Function in Hypertensive Patients

Long-Term Effects of Delapril Hydrochloride on Procollagen Type III Amino-Terminal Peptide, Left Ventricular Mass and Left Ventricular Function in Hypertensive Patients

Collagen content, but not the ratios of collagen type III/I mRNAs, differs among hypertensive, alcoholic, and idiopathic dilated cardiomyopathy

PYK2 expression and phosphorylation increases in pressure overload-induced left ventricular hypertrophy

Contact Info

Product

Resources

About