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Collagen Density (collagen + density)
Selected AbstractsRho plays a central role in regulating local cell-matrix mechanical interactions in 3D cultureCYTOSKELETON, Issue 6 2007N. Lakshman Abstract The purpose of this study was to assess quantitatively the role of the small GTPase Rho on cell morphology, f-actin organization, and cell-induced matrix remodeling in 3D culture. Human corneal fibroblasts (HTK) were infected with adenoviruses that express green fluorescent protein (GFP) or GFP-N19Rho (dominant negative Rho). One day later cells were plated inside collagen matrices and allowed to spread for 24 h. Cells were fixed and stained for f-actin. Fluorescent (for f-actin) and reflected light (for collagen fibrils) images were acquired using confocal microscopy. Fourier transform analysis was used to assess local collagen fibril alignment, and changes in cell morphology and collagen density were measured using MetaMorph. The decrease in matrix height was used as an indicator of global matrix contraction. HTK and HTK-GFP cells induced significant global matrix contraction; this was inhibited by N19Rho. HTK and HTK-GFP fibroblasts generally had a bipolar morphology and occasional intracellular stress fibers. Collagen fibrils were compacted and aligned parallel to stress fibers and pseudopodia. In contrast, HTK-GFPN19 cells were elongated, and had a more cortical f-actin distribution. Numerous small extensions were also observed along the cell body. In addition, both local collagen fibril density and alignment were significantly reduced. Rho plays a key role in regulating both the morphology and mechanical behavior of corneal fibroblasts in 3D culture. Overall, the data suggest that Rho-kinase dependent cell contractility contributes to global and local matrix remodeling, whereas Rho dependent activation of mDia and/or other downstream effectors regulates the structure and number of cell processes. Cell Motil. Cytoskeleton 2007. © 2007 Wiley-Liss, Inc. [source] Treatment of Striae Rubra and Striae Alba With the 585-nm Pulsed-Dye LaserDERMATOLOGIC SURGERY, Issue 4 2003Gloria P. Jimeénez MD BACKGROUND The treatment of striae distensae has recently been reported with various lasers such as the 585-nm pulsed dye laser. At lower fluences (2.0 to 4.0 J/cm2), this laser has been purported to increase the amount of collagen in the extracellular matrix. OBJECTIVE To determine whether the 585-nm pulsed dye laser is effective in both striae rubra and striae alba after two treatments and, in addition, to determine whether there is a net effect on collagen density in treated samples. METHODS Twenty patients (skin types II to VI) with either striae rubra (9) or striae alba (11) were treated at baseline and at week 6. The total length of the study was 12 weeks. Untreated striae on the same patient were used as control subjects. Striae clinical parameters such as color and area were measured before the first and after the last treatment by an independent examiner using a visual analog scale. A hydroxyproline assay was used to measure collagen changes in two of the striae quantitatively. RESULTS The 585 nm had a moderate beneficial effect in reducing the degree of erythema in striae rubra. There was no apparent clinical change on striae alba. Total collagen per gram of dry weight of sampled tissue increased in striae treated with pulsed dye laser versus control subjects. CONCLUSION We recommend the use of the 585-nm pulsed dye laser for striae rubra in patients skin types II to IV. Extreme caution or avoidance should be observed in pulsed dye laser treatments for patients with phototypes V to VI even with the use of low fluences. Tissue collagen changes measured may be an early change, which precedes significant clinical improvement. [source] Comparison of various kinds of bone marrow stem cells for the repair of infarcted myocardium: Single clonally purified non-hematopoietic mesenchymal stem cells serve as a superior source,JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2006Shaoheng Zhang Abstract A variety of adult stem cells have been used to transplant into the infarcted (MI) heart, however, comparative studies are lacking to show more suitable source of cells for transplantation. We have identified a single non-hematopoietic mesenchymal stem cell subpopulation (snMSCs) isolated from human bone marrow and clonally purified, that over 99% of them expressed MSC marker proteins and cardiomyocyte marker proteins when induction in vitro. We also compared the effects of the snMSCs with unpurified MSC (uMSCs), mononuclear cells (BMMNCs), or peripheral blood mononuclear cells (PBMNCs) on myocardial repair after induction of MI in rats. Ninety days later, we observed a better cardiac function assessed by ejection fraction, fraction of shortening and lung wet/dry weight ratios, less remodeling of left ventricle (LV), lower collagen density in the LV, and more vessels in the ischemic wall in the snMSCs transplantation group than in other cell-transplanted groups. Furthermore, the transplanted cells expressing cardiomyocyte specific proteins or vascular endothelial cell marker proteins were more in the snMSCs group than in other ones. We conclude that transplantation with single clonally purified MSCs seems to be more beneficial to the cardiac repair than with other stem cells after MI. J. Cell. Biochem. 99: 1132,1147, 2006. © 2006 Wiley-Liss, Inc. [source] Close dependence of fibroblast proliferation on collagen scaffold matrix stiffnessJOURNAL OF TISSUE ENGINEERING AND REGENERATIVE MEDICINE, Issue 2 2009E. Hadjipanayi Abstract Human dermal fibroblasts (HDFs) in free-floating collagen matrices show minimal proliferation, although this may increase when the matrix is ,under tension'. We have investigated the detailed mechanics underlying one of the possible controls of this important cell behaviour, in particular the hypothesis that this is a response to substrate stiffness. Hyperhydrated collagen gels were plastic-compressed (PC) to give a predetermined collagen density and stiffness. Mechanical properties were tested using a dynamic mechanical analyser; cell number by Alamar blue assay. In the stiffest PC matrices, cell proliferation was rapid and seeding density-dependent, with a population doubling time of 2 days. In contrast, compliant attached matrices showed a 4 day lag period and a doubling time of 6 days. HDF growth was directly related to matrix stiffness, such that increasing stiffness using a range of compression levels (0,75% fluid removal) supported increasing proliferation rate, doubling times and matrix elastic modulus. HDF quiescence in compliant matrices was reversible, such that increasing stiffness in situ by compression at 1 and 5 days initiated proliferation. We conclude that collagen matrix stiffness regulates proliferation of fibroblasts (a duro-response), with important implications for understanding fibroblast,matrix feedback controls during wound healing and the design and regulation of engineered connective tissues based on collagen and other hydrogel-based scaffolds. Copyright © 2008 John Wiley & Sons, Ltd. [source] EARLY STRUCTURAL CHANGES OF AORTIC WALL IN SINOAORTIC-DENERVATED RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2006Fu-Ming Shen SUMMARY 1The present work was designed to observe the early structural changes in the aortic wall in Sprague-Dawley rats 1, 2 and 4 weeks after sinoaortic denervation (SAD). 2Rats were examined 1, 2 and 4 weeks after SAD. Blood pressure (BP) was recorded in the conscious state. The thoracic aortas were taken for investigations, including: light microscopy, electron microscopy, immunohistochemistry and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labelling (TUNEL). 3Blood pressure variability (BPV) was significantly increased in the SAD groups 1, 2 and 4 after the operation when compared with the sham-operated ones. 4Two weeks after SAD the percentage proportion of smooth muscle cell density (SMC%) was obviously increased. 5Four weeks after SAD: the SMC%, percentage proportion of collagen density (CD%) and aortic wall thickness (WT) were obviously increased with vascular smooth muscle cells blebbing concomitantly. Endothelial cells showed degenerative changes and swelling with blebbing of the cell membrane and increased condensation of peripheral nuclear chromatin and cytoplasmic vacuolization. It was also found that the number of apoptotic endothelial cells was increased and expression of eNOS was reduced. 6This is the first study that shows the time-course of aortic wall and endothelial cell changes induced by SAD. Increased BPV might be the priming factor in the development of organ damage induced by SAD. [source] COMPARISON OF ANGIOTENSIN II-INDUCED BLOOD PRESSURE AND STRUCTURAL CHANGES IN FISCHER 344 AND WISTAR KYOTO RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2004Jocelyne Blanc SUMMARY 1.,The purpose of the present study was to evaluate the blood pressure (BP) response, the BP and heart rate (HR) components of the startle reaction and the structure of the carotid artery and the aorta during chronic infusion of angiotensin (Ang) II in Fischer 344 (F344) compared with Wistar Kyoto (WKY) rats, two in-bred normotensive contrasted strains. 2.,Osmotic mini-pumps filled with saline vehicle or AngII (120 ng/kg per min) were implanted subcutaneously in 8-week-old normotensive rats and infused for 4 weeks in F344 rats (saline, n = 10; AngII, n = 10) and WKY rats (saline, n = 10; AngII, n = 9). Basal BP, HR and the responses to an acoustic startle stimulus (duration 0.7 s, 115 dB) were recorded in conscious rats. The structure of the carotid artery and aorta was determined in 4% formaldehyde-fixed arteries. 3.,Compared with WKY rats, vehicle-treated F344 rats had lower bodyweight (BW; 266 ± 7 vs 299 ± 9 g; P < 0.05) and heart weight (0.80 ± 0.02 vs 0.98 ± 0.04 g; P < 0.05) and higher aortic systolic BP (SBP; 131 ± 1 vs 123 ± 5 mmHg; P < 0.001) and diastolic BP (98 ± 3 vs 89 ± 2 mmHg; P < 0.001). In F344 rats, compared with the WKY rats, the wall thickness/BW ratio was increased in the carotid artery (156 ± 9 vs 131 ± 6 nm/g; P < 0.05) and abdominal aorta (264 ± 13 vs 217 ± 12 nm/g; P < 0.05) and decreased in the thoracic aorta (246 ± 13 vs 275 ± 8 nm/g; P < 0.05). There was no difference in elastin and collagen density. Angiotensin II differentially enhanced BP in both strains: (SBP: 163 ± 5 and 132 ± 4 mmHg in F344 and WKY rats, respectively; Pstrain × treatment < 0.05). Circumferential wall stress was increased in the aorta of F344 rats compared with WKY rats (1176 ± 39 vs 956 ± 12 kPa (P < 0.001) and 1107 ± 42 vs 813 ± 12 kPa (P < 0.001) in thoracic and abdominal aortas, respectively). The startle response was amplified in F344 rats, with enhanced increases in SBP and pulse pressure (PP) and bradycardia compared with responses of WKY rats (+44 ± 9 mmHg, +10 ± 2 mmHg and ,40 ± 17 b.p.m., respectively, in F344 rats vs+28 ± 4 mmHg, + 4 ± 2 mmHg and ,19 ± 10 b.p.m. in WKY rats, respectively; Pstrain < 0.05 for BP and PP). The startle response was not affected by AngII. 4.,These results indicate a higher BP producing an increase in wall thickness in F344 rats compared with WKY rats. We propose that an increase in sympathetic nervous activity causes these haemodynamic differences, as suggested by the excessive increase in BP during an acoustic startle stimulus. Angiotensin II increased BP in F344 rats, but did not exaggerate the increase in BP during the startle reaction. [source] | |||||||||||||