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

  title={Increase of fibronectin and osteopontin in porcine hearts following ischemia and reperfusion},
  author={Peter Walter Kossmehl and Johann Sch{\"o}nberger and Mehdi Shakibaei and Shideh Faramarzi and E J Kurth and Britta Habighorst and R{\"u}diger Bauer and Markus Wehland and Reinhold Kreutz and Manfred Infanger and Gundula Gesine Schulze-Tanzil and Martin Paul and Daniela Grimm},
  journal={Journal of Molecular Medicine},
Following a severe ischemic injury or myocardial infarction, the extracellular matrix (ECM) of the heart is involved in pathophysiological conditions such as dilatation and cardiac dysfunction. Osteopontin (OPN) has been shown to interact with fibronectin suggesting its possible role in matrix organization, stability and wound healing. There is increased expression of OPN in several tissues in response to injury. Therefore, we tested the hypothesis that acute ischemia (2 h), followed by… 
Blockage of Fibronectin 1 Ameliorates Myocardial Ischemia/Reperfusion Injury in Association with Activation of AMP-LKB1-AMPK Signaling Pathway
It is identified that blocking Fn1 protects against myocardial I/RI likely through activating the LKB1-AMPK-dependent signals and highlights that inhibition of Fn1 may be a novel therapeutic option for treating ischemic heart diseases.
Mechanisms of apoptosis after ischemia and reperfusion: Role of the renin-angiotensin system
The data suggest that the RAS plays a pivotal role in cardiac apoptosis which is the early and predominant form of death in myocardial infarction.
Osteopontin deficiency aggravates hepatic injury induced by ischemia–reperfusion in mice
OPN partially protects from hepatic injury and inflammation induced in this experimental model of liver I–R, due to its ability to partially prevent death of hepatocytes and to limit the production of toxic iNOS-derived NO by macrophages.
Expression of vascular endothelial growth factor and receptor tyrosine kinases in cardiac ischemia/reperfusion injury.
  • M. Infanger, S. Faramarzi, D. Grimm
  • Biology, Medicine
    Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
  • 2007
Osteopontin is proteolytically processed by matrix metalloproteinase 9.
This study highlights the importance of osteopontin processing, and confirms that different cleavage sites generate osteoponin peptides with distinct biological functions.
Pretreatment of Endothelial Progenitor Cells with Osteopontin Enhances Cell Therapy for Peripheral Vascular Disease
It is concluded that OPN acts in an autocrine manner on EPCs to induce the secretion of angiogenic proteins, thereby playing a critical role in EPC-mediated neovascularization.
Matricellular proteins in cardiac adaptation and disease.
Understanding the role of matricellular proteins in myocardial pathophysiology and identification of the functional domains responsible for their actions may lead to design of peptides with therapeutic potential for patients with heart disease.


Plasma fibronectin during myocardial ischemia‐reperfusion: Effects of magnesium, diltiazem, and a novel Mac‐1 inhibitor
Ability of Mg, diltiazem, and leumedins to modulate plasma Fn level may have direct clinical implications for the use of these agents in patients with coronary artery disease.
Ischemia and reperfusion of the porcine myocardium: effect on collagen.
In this porcine model of acute myocardial infarction and late reperfusion no release of collagen degradation products from the myocardium or any decrease in or damage to myocardian collagen was detected.
Increased amounts of collagenase and gelatinase in porcine myocardium following ischemia and reperfusion.
Investigation of the presence of collagen degrading enzymes in porcine myocardium following ischemia and late reperfusion showed increased amounts of collagenase (MMP-1) and gelatinase ( MMP-9) in ischemic/ reperfusedMyocardium, indicating the appearance of increased amount of collagen degradation enzymes very early following ischemical and reperfusions.
Regulation of collagen degradation in the rat myocardium after infarction.
Collagen degradation in ischaemic rat hearts.
The results suggest that the increased activities of collagenase and other neutral proteinases may be responsible for the rapid degradation of extracellular matrix collagen in myocardial infarct.
Exaggerated Left Ventricular Dilation and Reduced Collagen Deposition After Myocardial Infarction in Mice Lacking Osteopontin
Increased OPN expression plays an important role in regulating post-MI LV remodeling, at least in part, by promoting collagen synthesis and accumulation.
Rapid expression of fibronectin in the rabbit heart after myocardial infarction with and without reperfusion.
Fibronectin mRNA and protein expression increased rapidly postinfarction suggesting a functional role in the repair process and increases in steady-state mRNA levels for several collagen types were found in both groups.
Early degradation of collagen after acute myocardial infarction in the rat.
Intracoronary application of C1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and reperfusion.
C1-INH significantly protects ischemic tissue from reperfusion damage, reduces myocardial necrosis, and improves local cardiac function.
Spatially and temporally different expression of osteonectin and osteopontin in the infarct zone of experimentally induced myocardial infarction in rats.