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Collagen Stimulation (collagen + stimulation)
Selected AbstractsDifferential Long-Term Stimulation of Type I versus Type III Collagen After Infrared IrradiationDERMATOLOGIC SURGERY, Issue 7 2009YOHEI TANAKA MD BACKGROUND The dermis is composed primarily of type I (soft) and type III (rigid scar-like) collagen. Collagen degradation is considered the primary cause of skin aging. Studies have proved the efficacy of infrared irradiation on collagen stimulation but have not investigated the differential long-term effects of infrared irradiation on type I and type III collagen. OBJECTIVE To determine differential long-term stimulation of type I and type III collagen after infrared (1,100,1,800 nm) irradiation. METHODS AND MATERIALS In vivo rat tissue was irradiated using the infrared device. Histology samples were analyzed for type I and III collagen stimulation, visual changes from baseline, and treatment safety up to 90 days post-treatment. RESULTS Infrared irradiation provided long-term stimulation of type I collagen and temporary stimulation of type III collagen. Treatment also created long-term smoothing of the epidermis, with no observed complications. CONCLUSIONS Infrared irradiation provides safe, consistent, long-term stimulation of type I collagen but only short-term stimulation in the more rigid type III collagen. This is preferential for cosmetic patients looking for improvement in laxity and wrinkles while seeking smoother, more youthful skin. [source] Heritability of platelet function in families with premature coronary artery diseaseJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2007P. F. BRAY Summary.,Background:,Variations in platelet function among individuals may be related to differences in platelet-related genes. The major goal of our study was to estimate the contribution of inheritance to the variability in platelet function in unaffected individuals from white and African American families with premature coronary artery disease.Methods:,Platelet reactivity, in the absence of antiplatelet agents, was assessed by in vitro aggregation and the platelet function analyzer closure time. Heritability was estimated using a variance components model.Results:,Both white (n = 687) and African American (n = 321) subjects exhibited moderate to strong heritability (h2) for epinephrine- and adenosine diphosphate-induced aggregation (0.36,0.42 for white and >0.71 for African American subjects), but heritability for collagen-induced platelet aggregation in platelet-rich plasma was prominent only in African American subjects. Platelet lag phase after collagen stimulation was heritable in both groups (0.47,0.50). A limited genotype analysis demonstrated that the C825T polymorphism of GNB3 was associated with the platelet aggregation response to 2 ,M epinephrine, but the effect differed by race.Conclusions:,Considering the few and modest genetic effects reported to affect platelet function, our findings suggest the likely existence of undiscovered important genes that modify platelet reactivity, some of which affect multiple aspects of platelet biology. [source] The regulation of integrin-linked kinase in human platelets: evidence for involvement in the regulation of integrin ,2,1JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2004J. M. Stevens Summary.,Background: Activation of the platelet integrin ,2,1 is closely regulated due to the high thrombogenicity of its ligand. As a ,1 interacting kinase, ILK represents a candidate intracellular regulator of ,2,1 in human platelets. Objectives We investigated the regulation of ILK in human platelets and the role of ILK in regulating ,2,1 activation in HEL cells, a megakaryocytic cell line. Methods: An in-vitro kinase assay was used to determine the effect of platelet agonists on ILK kinase activity together with the contribution of PI3K and PKC on ILK activation. Interaction of ILK with ,1 -integrin subunits was investigated by coimmunoprecipitation and the role of ILK in regulating ,2,1 function assessed by overexpression studies in HEL cells. Results: We report that collagen and thrombin modulate ILK kinase activity in human platelets in an aggregation-independent manner. Furthermore, ILK activity is dually regulated by PI3K and PKC in thrombin-stimulated platelets and regulated by PI3K in collagen-stimulated cells. ILK associates with the ,1 -integrin subunits immunoprecipitated from platelet cell lysates, an association which increased upon collagen stimulation. Overexpression of ILK in HEL cells enhanced ,2,1 -mediated adhesion whereas overexpression of kinase-dead ILK reduced adhesion, indicating a role for this kinase in the positive regulation of ,2,1. Conclusions: Our findings that ILK regulates ,2,1 in HEL cells, is activated in platelets and associates with ,1 -integrins, raise the possibility that it may play a key role in adhesion events upon agonist stimulation of platelets. [source] Use of Green Fluorescent Protein-Conjugated ,-Actin as a Novel Molecular Marker for in Vitro Tumor Cell Chemotaxis AssayBIOTECHNOLOGY PROGRESS, Issue 6 2000Louis Hodgson To study the dynamics of actin cytoskeleton rearrangement in living cells, an eukaryotic expression vector expressing a ,-actin-GFP fusion protein was generated. The expression construct when transfected into NIH3T3 fibroblast, A2058 human melanoma and 293T human embryonic kidney carcinoma cell lines expressed ,-actin-GFP fusion protein, which colocalized with endogenous cellular actin as determined by histoimmunofluorescence staining. The ,-actin-GFP was also observed to be reorganized in response to treatments with the chemoattractant type IV collagen. Cells extended pseudopodial protrusions and altered the morphology of their cortical structure in response to type IV collagen stimulation. More importantly, ,-actin-GFP accumulated in areas undergoing these dynamic cytoskeleton changes, indicating that ,-actin-GFP could participate in actin polymerization. Although ectopic expression of ,-actin-GFP lead to minor side effects on cell proliferation, these studies suggest that this strategy provides an alternative to the invasive techniques currently used to study actin dynamics and permits real-time visualization of actin rearrangements in response to environmental cues. [source] | ||||||||||