Atrial Natriuretic Peptide Helps Prevent Late Remodeling After Left Ventricular Aneurysm Repair

Tsuneyoshi, Hiroshi; Nishina, Tomohiro; Nomoto, Takuya; Kanemitsu, Hideo; Kawakami, Rika; Unimonh, Oriyanhan; Nishimura, Kazunobu; Komeda, Masashi

doi:10.1161/01.cir.0000138348.77856.ef

Cited by 35 publications

(27 citation statements)

References 28 publications

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“…Therefore, ILK overexpression is likely to enhance cardiomyocyte contractility as well as atrial natriuretic peptide and vascular endothelial growth factor expression after infarct, and atrial natriuretic peptide could in turn reduce LV remodeling. 16 Moreover, ILK has been reported to contribute to angiogenesis as well as cell growth, proliferation, survival, and differentiation in noncardiological studies, 5 which could also contribute to the therapeutic effect of ILK in postinfarct remodeling. Our results bear out the cardioprotective, proangiogenic, proliferative, and antiapoptotic effects of ILK.…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Integrin-Linked Kinase Attenuates Left Ventricular Remodeling and Improves Cardiac Function After Myocardial Infarction

Ding

Chen

et al. 2009

Circulation

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Background-Left ventricular (LV) remodeling is associated with the development of heart failure after myocardial infarction. Here we investigated whether integrin-linked kinase (ILK) may regulate LV remodeling and function after myocardial infarction. Methods and Results-Adenoviral vector expressing ILK (nϭ25) or empty adeno-null (nϭ25) was injected into rat peri-infarct myocardium after left anterior descending coronary artery ligation. ILK expression was confirmed by Western blotting and immunofluorescence. Echocardiographic and hemodynamic analyses demonstrated relatively preserved cardiac function in adeno-ILK animals. ILK treatment was associated with reduced infarct scar size, increased scar thinning ratio, and preserved LV diameter, wall thickness, cardiomyocyte size, and myofilament density. Enhanced angiogenesis and reduced fibrosis were observed in the adeno-ILK group, along with reduced apoptosis as demonstrated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling analysis. Moreover, increased cardiomyocyte proliferation was found in adeno-ILK animals, as measured by proliferating cell nuclear antigen, Ki-67, and phosphohistone-H3 staining. At long-term follow-up, most indices of cardiac function and hemodynamics showed no difference between adeno-ILK and control animals by 9 weeks, although LV end-systolic diameter and infarct scar size were reduced in the adeno-ILK group at this time point. Additionally, ILK overexpression was found to exert a rescue effect on remodeling when administered in a delayed fashion 1 week after coronary artery ligation. Conclusions-ILK gene therapy improves cardiac remodeling and function in rats after myocardial infarction and is associated with increased angiogenesis, reduced apoptosis, and increased cardiomyocyte proliferation. This may represent a new approach to the treatment of postinfarct remodeling and subsequent heart failure. Key Words: angiogenesis Ⅲ apoptosis Ⅲ gene therapy Ⅲ myocardial infarction Ⅲ remodeling H eart failure is an increasing public health problem worldwide, with the most common cause currently being cardiac remodeling after myocardial infarction (MI). 1,2 Cardiomyocyte death in the context of MI in combination with increased preload and afterload triggers a cascade of biochemical intracellular signaling processes that modulate cardiac remodeling (which includes dilatation, hypertrophy, and fibrosis), 3 and prevention or attenuation of these signaling processes is an important therapeutic goal. Clinical Perspective on p 773Integrin-linked kinase (ILK), a widely expressed serine/ threonine protein kinase, is highly expressed in the heart. 4 Previous studies have shown that ILK plays an important role in transducing cell-matrix interaction-induced biomechanical signals via binding to the cytoplasmic domain of ␤-integrins, which regulate cytoskeletal remodeling and angiogenesis, as well as cell growth, proliferation, survival, and differentiation. 4,5 Recently, ILK has been reported to be an important factor regulating car...

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Section: Discussionmentioning

confidence: 99%

Increased Expression of Integrin-Linked Kinase Attenuates Left Ventricular Remodeling and Improves Cardiac Function After Myocardial Infarction

Ding

Chen

et al. 2009

Circulation

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“…The total RNA of the aorta was extracted using Trizol reagent (Life Technologies) and dissolved in 0.1% diethyl pyrocarbonate-treated water (25). RT to cDNA was accomplished by analyzing 5 μg of the total RNA sample with SuperScript II reverse transcriptase and oligo(dT)12-18 primer (Invitrogen, Carlsbad, USA).…”

Section: Reverse Transcription (Rt)-pcrmentioning

confidence: 99%

Chymase Inhibition Prevents Cardiac Fibrosis and Dysfunction after Myocardial Infarction in Rats

et al. 2006

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Human chymase activates not only angiotensin II but also transforming growth factor-S , a major stimulator of myocardial fibrosis, while rat chymase activates transforming growth factor-S , but not angiotensin II. To clarify the role of chymase-dependent transforming growth factor-S activation, we evaluated whether chymase inhibition prevents cardiac fibrosis and cardiac dysfunction after myocardial infarction in rats. Myo-

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“…ANP has been used as a diuretic and vasodilator in clinical settings. ANP has been shown to play an important function in the inhibition of RAAS [44,45]. ANP and brain natriuretic peptide (BNP) have been reported to prevent cardiac fibrosis [44,46] and renal fibrosis [47][48][49], and to reduce infarct size in acute myocardial infarction [50].…”

Section: Scraping Modelmentioning

confidence: 99%

Peritonitis-induced peritoneal injury models for research in peritoneal dialysis review of infectious and non-infectious models

et al. 2017

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Peritonitis is an important complication of peritoneal dialysis. Several animal peritonitis models have been described, including bacterial and fungal models that are useful for studying inflammation in peritonitis. However, these models have limitations for investigating peritoneal fibrosis induced by acute inflammation and present difficulties in handling the infected animals. Animal models of peritonitis which induced peritoneal fibrosis are important for establishing new therapies to improve peritoneal damage induced by peritonitis. Here, we present an overview of representative animal models of peritoneal dialysis-associated infectious and non-infectious peritonitis, including our novel animal models (scraping and zymosan models) that mimic peritoneal injury associated with fibrosis and neoangiogenesis caused by bacterial or fungal peritonitis.

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Atrial Natriuretic Peptide Helps Prevent Late Remodeling After Left Ventricular Aneurysm Repair

Cited by 35 publications

References 28 publications

Increased Expression of Integrin-Linked Kinase Attenuates Left Ventricular Remodeling and Improves Cardiac Function After Myocardial Infarction

Increased Expression of Integrin-Linked Kinase Attenuates Left Ventricular Remodeling and Improves Cardiac Function After Myocardial Infarction

Chymase Inhibition Prevents Cardiac Fibrosis and Dysfunction after Myocardial Infarction in Rats

Peritonitis-induced peritoneal injury models for research in peritoneal dialysis review of infectious and non-infectious models

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