Experimental use of a modified fibrin glue to induce site-directed angliogenesis from the aorta to the heart

Fasol, Roland; Schumacher, B.; Schlaudraff, K.; Hauenstein, Karlheinz; Seitelberger, Rainald

doi:10.1016/s0022-5223(94)70419-8

Cited by 35 publications

(10 citation statements)

References 22 publications

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“…The results of these experiments were encouraging; chronic treatment with VEGF caused a 40% increase in collateral blood flow and an 89% increase in the numerical density of intramyocardial distribution vessels at 4 weeks. Similar results were reported for FGF administration to heart and skeletal muscles of mice, rats, and dogs (30)(31)(32)(33). Neoangiogenesis in response to FGF-1 was reported to occur in both ischemic and non-ischemic tissues.…”

Section: Animal Studiessupporting

confidence: 80%

Gene and Cell Therapy for Heart Disease

2002

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SummaryHeart disease is the most common cause of morbidity and mortality in Western society and the incidence is projected to increase significantly over the next few decades as our population ages. Heart failure occurs when the heart is unable to pump blood at a rate to commensurate with tissue metabolic requirements and represents the end stage of a variety of pathological conditions. Causes of heart failure include ischemia, hypertension, coronary artery disease, and idiopathic dilated cardiomyopathy. Hypertension and ischemia both cause infarction with loss of function and a consequent contractile deficit that promotes ventricular remodeling. Remodeling results in dramatic alterations in the size, shape, and composition of the walls and chambers of the heart and can have both positive and negative effects on function. In 30-40% of patients with heart failure, left ventricular systolic function is relatively unaffected while diastolic dysfunction predominates. Recent progress in our understanding of the molecular and cellular bases of heart disease has provided new therapeutic targets and led to novel approaches including the delivery of proteins, genes, and cells to replace defective or deficient components and restore function to the diseased heart. This review focuses on three such strategies that are currently under development: (a) gene transfer to modulate contractility, (b) therapeutic angiogenesis for the treatment of ischemia, and (c) embryonic and adult stem cell transfer to replace damaged myocardium. of all forms of heart disease. Impairment of left ventricular diastolic function often occurs before systolic dysfunction particularly in dilated cardiomyopathy and ischemic heart disease (1) and there is debate over which elements of the contractile system should be targeted. At the molecular level the cause of defective muscle contractility can be broadly attributed to abnormal sarcoplasmic reticulum (SR) calcium handling and alterations in myofilament calcium sensitivity, both of which are under β-adrenergic control. In this section of this review we focus on the evidence that implicates abnormal intracellular calcium handling and altered β-adrenergic receptor signaling in heart failure and the molecular approaches that are being pursued to correct them. Molecular Regulation of Muscle ContractionMuscle contraction and relaxation occurs through a series of coordinated steps. Electrical excitation across the sarcolemma leads to the opening of voltage-gated (L-type) Ca 2+ channels. Entry of a small amount of Ca 2+ into the cell triggers the release of larger stores of Ca 2+ from the sarcoplasmic reticulum (SR) through the Ca 2+ release channels known as ryanodine receptors (RyR). The rise in the intracellular Ca 2+ concentration ([Ca 2+ ]i) initiates contraction by binding to the myofilament protein troponin C. Conformational changes within the troponin complex disrupt the high-affinity binding sites on tropomyosin, resulting in acto-myosin cross-bridge formation and muscle contraction. Maximum force-...

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Section: Animal Studiessupporting

confidence: 80%

Gene and Cell Therapy for Heart Disease

2002

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“…Where indicated, the cells in the medium/FCS were exposed to the beads/discs with the complete mineralization activation cocktail (MAC), composed of 5 mM β‐glycerophosphate, 50 mM ascorbic acid and 10 nM dexamethasone, or the MAC, lacking β‐glycerophosphate.…”

Section: Methodsmentioning

confidence: 99%

“…This size is 2 mm larger than the critical size defect of 8 mm, proposed for rats, to ensure that the defect does not completely heal over the natural lifetime of the animal. We have selected slightly smaller discs as implants also to allow the fibrin clot to develop and to exploit the high content of growth facts in those clots for attracting cells, including osteoblasts …”

Section: Methodsmentioning

confidence: 99%

Polyphosphate as a Bioactive and Biodegradable Implant Material: Induction of Bone Regeneration in Rats

Wang

et al. 2016

Adv Eng Mater

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Inorganic polyphosphate (polyP) is a naturally occurring polymer that is bioresorbable and anabolically active on bone forming cells in vitro. In order to demonstrate if polyP also shows morphogenetic activity in vivo, animal studies are performed applying the rat calvarial defect model. Poly(D,L-lactide-co-glycolide) (PLGA) microspheres with a narrow size distribution (%820 mm) are prepared, containing either encapsulated polyP or b-tricalcium phosphate (b-TCP), used as a reference material. Discs are prepared from the microspheres and inserted into 10 mm large defects created in the calvaria of rats. Both the formation of COL-I and the expression of ALP is upregulated, as well as the extent of mineralization within and around the polyP implant. Our data demonstrate that amorphous and resorbable inorganic polyP is also morphogenetically active in vivo.

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“…FG undergoes the same polymerization, or network formation, process as fibrin in the blood coagulation cascade. In addition, FG has been capable to induce angiogenesis per se when loaded with growth factors 14…”

Section: Introductionmentioning

confidence: 99%

“…When used in combination with CaP ceramics, FG enhances early bone formation and influences angiogenesis positively 24, 25. FG can act as porogen which is relatively quickly replaced by tissue and allows cell invasion 14, 25. Hence, CPC‐FG composites are promising in creating improved bone substitutes with better biological properties such as cell attachment and bone remodeling.…”

Section: Introductionmentioning

confidence: 99%

Bulk physicochemical, interconnectivity, and mechanical properties of calcium phosphate cements–fibrin glue composites for bone substitute applications

Lopez‐Heredia

Pattipeilohy

Hsu

et al. 2012

J Biomedical Materials Res

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Calcium phosphate cements (CPCs) and fibrin glue (FG) are used for surgical applications. Their combination is promising to create bone substitutes able to promote cell attachment and bone remodeling. This study proposes a novel approach to create CPC-FG composites by simultaneous CPC setting and FG fibrinogenesis. CPC-FG composites were obtained by mixing CPC powders, i.e. α-tricalcium phosphate, dicalcium phosphate anhydrous and precipitated hydroxyapatite, with FG powder components, i.e. fibrinogen and thrombin, and a 2% Na(2) HPO(4) solution. To study the effect of FG quantity and fibrinogenesis kinetics, long and fast setting FGs were evaluated in amounts of 0.125, 0.250, and 0.500 mL on CPC-FG composites. Physicochemical, interconnectivity, and mechanical properties were measured. Scanning electron microscopy, Micro-computed tomography (μ-CT), X-ray diffraction, and Fourier transform Infrared spectroscopy (FTIR) analyzed morphology, structure, crystallographic, and chemical composition, respectively. FG fibrinogenesis was performed within the CPC. FTIR confirmed this and its interfacial bonding with CPC. μ-CT confirmed a good FG distribution. FG addition affected the CPC when compared with pristine CPC. Adding FG to CPC changed their morphology, density, porosity, setting, cohesion, injectability, interconnectivity, crystallographic and chemical composition and mechanical properties. Moreover, 0.500 mL of long setting FG modified the observed fracture behavior of the CPC-FG.

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Experimental use of a modified fibrin glue to induce site-directed angliogenesis from the aorta to the heart

Cited by 35 publications

References 22 publications

Gene and Cell Therapy for Heart Disease

Gene and Cell Therapy for Heart Disease

Polyphosphate as a Bioactive and Biodegradable Implant Material: Induction of Bone Regeneration in Rats

Bulk physicochemical, interconnectivity, and mechanical properties of calcium phosphate cements–fibrin glue composites for bone substitute applications

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