Increase of fibronectin and osteopontin in porcine hearts following ischemia and reperfusion

Koßmehl, Peter; Schönberger, Johann; Shakibaei, Mehdi; Faramarzi, Shideh; Kurth, Elke; Habighorst, Britta; Bauer, Rüdiger von; Wehland, Markus; Kreutz, Reinhold; Infanger, Manfred; Schulze‐Tanzil, Gundula; Paul, Martin; Grimm, Daniela

doi:10.1007/s00109-005-0642-8

Cited by 47 publications

(42 citation statements)

References 44 publications

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“…Fibronectin has long been known to play an important role in mediating cell adhesion and migration (Larsen et al, 2006). Rapid up-regulation of fibronectin in the infarcted myocardium has been reported previously after MI (Knowlton et al, 1992;Kossmehl et al, 2005). The up-regulation of fibronectin is ahead of collagens, suggesting its involvement in the acute phase of MI (Knowlton et al, 1992).…”

Section: Discussionmentioning

confidence: 92%

“…The up-regulation of fibronectin is ahead of collagens, suggesting its involvement in the acute phase of MI (Knowlton et al, 1992). In 5 h after acute MI in pigs, increased expression of fibronectin was found in fibroblast-like cells in the infarct (Kossmehl et al, 2005). Based on these findings, we decided to study whether this particular class of integrins may be responsible for stem cell homing and engraftment.…”

Section: Discussionmentioning

confidence: 99%

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Mesenchymal Stem Cells Use Integrin β1 Not CXC Chemokine Receptor 4 for Myocardial Migration and Engraftment

Huang

et al. 2007

MBoC

217

145

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Recent evidence has demonstrated the importance of bone marrow-derived mesenchymal stem cells (BM-MSCs) in the repair of damaged myocardium. The molecular mechanisms of engraftment and migration of BM-MSCs in the ischemic myocardium are unknown. In this study, we developed a functional genomics approach toward the identification of mediators of engraftment and migration of BM-MSCs within the ischemic myocardium. Our strategy involves microarray profiling (>22,000 probes) of ischemic hearts, complemented by reverse transcription-polymerase chain reaction and fluorescence-activated cell sorting of corresponding adhesion molecule and cytokine receptors in BM-MSCs to focus on the coexpressed pairs only. Our data revealed nine complementary adhesion molecules and cytokine receptors, including integrin ␤1, integrin ␣4, and CXC chemokine receptor 4 (CXCR4). To examine their functional contributions, we first blocked selectively these receptors by preincubation of BM-MSCs with specific neutralizing antibodies, and then we administered these cells intramyocardially. A significant reduction in the total number of BM-MSC in the infarcted myocardium was observed after integrin ␤1 blockade but not integrin ␣4 or CXCR4 blockade. The latter observation is distinctively different from that reported for hematopoietic stem cells (HSCs). Thus, our data show that BM-MSCs use a different pathway from HSCs for intramyocardial trafficking and engraftment. INTRODUCTIONCardiac repair and remodeling after ischemic injury involves myocyte hypertrophy, collagen deposition, and possibly ventricular dilatation (Sutton and Sharpe, 2000). Recent provocative data suggest that stem cells, either resident in the heart or originating from the bone marrow, may play an important role in the repair and regeneration of the injured myocardium (Anversa and Nadal-Ginard, 2002). We and others have shown that intramyocardial transplantation of bone marrow-derived stem cells (BMSCs) can promote cardiac repair with resulting functional improvement and reduced infarct size (Kocher et al., 2001;Mangi et al., 2003;Amado et al., 2005). In addition to direct transplantation, mobilization of BMSCs with cytokines such as granulocytecolony stimulating factor (G-CSF) and stem cell factor has been reported to enhance myocardial repair and improve cardiac function (Anversa and Nadal-Ginard, 2002;Askari et al., 2003). However, in a recent trial, the subcutaneous administration of G-CSF after acute myocardial infarction (MI) did not lead to further improvement in ventricular function compared with conventional treatment (Ripa et al., 2006). These controversial findings suggest the need to understand the molecular mechanisms involved with stem cell migration and engraftment into the infarcted myocardium.It has been reported that hematopoietic stem cells (HSCs) migrate in response to stromal-derived factor (SDF)-1␣, the ligand for the CXC chemokine receptor 4 (CXCR4) (Wright et al., 2002), and the up-regulation of SDF-1 in the ischemic myocardium mediates homing of HSCs vi...

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cells Use Integrin β1 Not CXC Chemokine Receptor 4 for Myocardial Migration and Engraftment

Huang

et al. 2007

MBoC

217

145

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“…Osteopontin has been shown to interact with fibronectin and plays an important role in matrix organization and stability. 12 Previous studies also showed that Ang II increases osteopontin expression, and the osteopontin null mice given Ang II infusion have much less cardiac fibrosis and hypertrophy. 22,23 Xie et al 24 showed that the signals for Ang II-induced osteopontin expression also involve oxidative stress and resultant p42/44 MAPK activation.…”

Section: Discussionmentioning

confidence: 98%

“…11 Osteopontin has been shown to interact with fibronectin and plays an important role in left ventricular remodeling. 12 Therefore, we determined the expression of procollagen I, osteopontin, and fibronectin in mice hearts. As shown in Figure 3A, the expression of procollagen I, osteopontin, and fibronectin increased significantly after infusion of Ang II or norepinephrine in the wild-type mice (PϽ0.01 versus salineinfused wild-type mice).…”

Section: Cardiac Remodeling After Sustained Hypertension and Effect Omentioning

confidence: 99%

Modulation of Angiotensin II–Mediated Hypertension and Cardiac Remodeling by Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 Deletion

Dandapat

Sun

et al. 2008

Hypertension

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Abstract-Angiotensin II via type 1 receptor activation upregulates the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), and LOX-1 activation, in turn, upregulates angiotensin II type 1 receptor expression. We postulated that interruption of this positive feedback loop might attenuate the genesis of angiotensin II-induced hypertension and subsequent cardiac remodeling. To examine this postulate, LOX-1 knockout and wild-type mice were infused with angiotensin II or norepinephrine (control for angiotensin II) for 4 weeks. Angiotensin II-, but not norepinephrine-, induced hypertension was attenuated in LOX-1 knockout mice. Angiotensin II-induced cardiac remodeling was also attenuated in LOX-1 knockout mice. Importantly, angiotensin II type 1 receptor expression was reduced, and the expression and activity of endothelial NO synthase were preserved in the tissues of LOX-1 knockout mice given angiotensin II. Reactive oxygen species generation, nicotinamide-adenine dinucleotide phosphate oxidase expression, and phosphorylation of p38 and p44/42 mitogen-activated protein kinases were also much less pronounced in the LOX-1 knockout mice given angiotensin II. These alterations in biochemical and structural abnormalities were associated with preservation of cardiac hemodynamics in the LOX-1 knockout mice. To confirm that fibroblast function is modulated in the absence of LOX-1, cardiac fibroblasts from wild-type and LOX-1 knockout mice were treated with angiotensin II. Indeed, LOX-1 knockout mice cardiac fibroblasts revealed an attenuated profibrotic response on treatment with angiotensin II. These observations provide strong evidence that LOX-1 is a key modulator of the development of angiotensin II-induced hypertension and subsequent cardiac remodeling. (Hypertension. 2008;52:556-562.)Key Words: angiotensin Ⅲ hypertension Ⅲ cardiac remodeling Ⅲ LOX-1 Ⅲ oxidative stress C ardiac remodeling is initially an adaptive response to several forms of cardiac stress states, such as hypertension. Sustained remodeling results in heart failure and is a powerful independent risk factor for cardiac morbidity and mortality. 1 Therefore, identification of the molecular mechanisms involved in cardiac remodeling is an important challenge for the cardiovascular biologists.The renin-angiotensin system and its effector hormone, angiotensin II (Ang II), have well-known endocrine properties that contribute to cardiac remodeling and heart failure. Previous studies have shown that Ang II via type 1 receptor (AT1R) activation stimulates the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1). 2 In turn, activation of LOX-1 upregulates AT1R expression. 3 Activation of both AT1R and LOX-1 induces a state of oxidative stress. 4 In addition, activation of both AT1R and LOX-1 enhances the growth of cardiac fibroblasts and promotes collagen synthesis. 5,6 Although LOX-1 mRNA expression is minimal in normal arterial tissues, it is markedly upregulated in vascular tissues of spontaneously hypertensive...

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“…Há relatos sobre o estímulo de OPN durante injúria cardiovascular W|ávâááûÉ | 91 (Kossmehl et al, 2005) e aumento de sua expressão em macrófagos alveolares de pacientes com doença pulmonar obstrutiva (Heguy et al, 2006). Em pacientes com DM2 foi observado expressões gênicas elevadas de Opn (Haug et al, 2014).…”

Section: W|ávâááûé | 86unclassified

Diabetes mellitus altera a sinalização osteogênica e atrasa o processo de reparo ósseo após expansão rápida da maxila

Arnez¹

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Vocês são meus verdadeiros heróis, exemplos de postura, profissionalismo, humanidade e amor. Pessoas em quem me espelho todos os dias. Obrigada pelos incentivos, apoio incondicional em todos os momentos da minha vida, pela dedicação, carinho e pelos esforços para que minha educação fosse a melhor possível. Por compreenderem os motivos da minha constante ausência e por estarem sempre presentes. Serei eternamente grata.Aos meus irmãos Marck Fernando Manfrin Arnez e Mayara Manfrin Arnez, por toda força, ajuda, amizade e compreensão. Por transformarem momentos simples em grandes lembranças inesquecíveis e por tornarem esta caminhada mais fácil, divertida e prazerosa. Sem vocês a vida seria muito mais sem graça. Muito obrigada por fazerem parte de tudo! Ao meu marido Francisco Wanderley Garcia de Paula e Silva, pelo carinho, paciência, companheirismo e apoio constante. Por compartilhar sua experiência comigo e sempre me ensinar. Por acreditar em mim, por me apoiar, me confortar nos momentos difíceis e não me deixar desistir nunca. Obrigada por tornar simples o que muitas vezes parecia complicado, por dividir todos os momentos de alegria, me incentivar na busca de vitórias e na realização dos meus sonhos. Admiro sua postura, dedicação e inteligência. Você é a parte que me falta e me completa. Pessoas especiais como você são colocadas na nossa vida para nos mostrar uma direção e fazer a diferença. Meu muito obrigada de coração!!! Introdução: O diabetes mellitus (DM) é uma doença crônica caracterizada pela hiperglicemia associada a diversas alterações sistêmicas e uma das suas complicações é o processo de reparo ósseo comprometido. Entretanto, ainda não há estudos utilizando análises celulares e biomoleculares que avaliem o processo de reparo ósseo desta desordem metabólica quando associada à expansão rápida da maxila (ERM). Objetivo: O objetivo deste estudo foi avaliar a remodelação óssea e sinalização osteogênica durante a aplicação de mecânica ortodôntica para ERM em ratos diabéticos tipo1-induzidos. Material e Métodos: Cento e cinquenta ratos Wistar, machos, foram divididos aleatoriamente em seis grupos de estudo. Grupos: controle (C, n=30), veículo (V, n=15), diabetes mellitus tipo 1 induzido com estreptozotocina (D, n=30), controle submetido à ERM (Cd, n=30), veículo submetido à ERM (Vd, n=15) e diabetes mellitus tipo 1 induzido com estreptozotocina submetido à ERM (Dd, n=30). Os animais foram eutanasiados aos 3, 7 e 10 dias após ERM . Análises histológicas, mudanças no padrão de expressão gênica e proteica de osteoprotegerina, (OPG), RANK, RANKL, osteonectina (ONC), osteocalcina (OCC), sialoproteína óssea (BSP), osteopontina (OPN) e proteína morfogenética óssea 2 (BMP2), assim como as mudanças no peso corporal, na ingestão de água na glicemia foram avaliadas. A análise da expressão gênica e proteica foram realizadas por qRT-PCR e Western Blotting, respectivamente. Os dados foram submetidos ao teste estatístico ANOVA de duas vias e pós-teste de Tukey (α= 0,05). Resultados: Histologicamente no grupo Dd foi notado m...

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Increase of fibronectin and osteopontin in porcine hearts following ischemia and reperfusion

Cited by 47 publications

References 44 publications

Mesenchymal Stem Cells Use Integrin β1 Not CXC Chemokine Receptor 4 for Myocardial Migration and Engraftment

Mesenchymal Stem Cells Use Integrin β1 Not CXC Chemokine Receptor 4 for Myocardial Migration and Engraftment

Modulation of Angiotensin II–Mediated Hypertension and Cardiac Remodeling by Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 Deletion

Diabetes mellitus altera a sinalização osteogênica e atrasa o processo de reparo ósseo após expansão rápida da maxila

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