scholarly journals Collagen Type I α1 Gene Sp1 Polymorphism in Premenopausal Women with Primary Osteoporosis: Improved Detection of Sp1 Binding Site Polymorphism in the Collagen Type 1 Gene

1999 ◽  
Vol 45 (6) ◽  
pp. 904-906 ◽  
Author(s):  
Luisa Alvarez ◽  
Josep Oriola ◽  
Judith Jo ◽  
Teresa Ferró ◽  
Francesca Pons ◽  
...  
Keyword(s):  
Binding Site ◽  
Collagen Type ◽  
Premenopausal Women ◽  
Collagen Type I ◽  
Type I ◽  
Primary Osteoporosis ◽  
Collagen Type 1

Membranes of Chitosan and Collagen-Type 1 for Biomineralization/Ostheogenesis

2013 ◽  
Vol 587 ◽  
pp. 222-226
Author(s):  
Ricardo B. Pacheco ◽  
Marina Salvarani Tonoli ◽  
Marisa Masumi Beppu
Keyword(s):  
Collagen Type ◽  
Collagen Type I ◽  
Calcium Deposition ◽  
Collagen Membrane ◽  
Type I ◽  
Chitosan Membranes ◽  
Collagen Membranes ◽  
Collagen Type 1

The main objective of this work was to produce membranes of chitosan and collagen type I and check their ability to undergo “in vitro” calcification. The membranes of chitosan-collagen blends were characterized by TGA, infra-red spectroscopy and DSC. Samples of dense and porous membranes were immersed in solution SBF (Simulated Body Fluid) in order to verify their “in vitro” calcification. The membranes were observed by SEM. The production of chitosan-collagen membranes is possible, in dense and porous versions. We can conclude that the blend is less resistant to high temperatures, in comparison to pristine chitosan membranes shown in literature. Through the initial assays of calcification, we observe that it is possible to induce the calcium deposition on a chitosan-collagen membrane, as seen by SEM. Microscopy of fracture surfaces showed fibril structures, probably formed by collagen.

scholarly journals Nephroprotective Effect of Pentoxyphylline Through Improvement in the Expression of TGF-beta1, Collagen Type-1, and Renal Interstitial Fibrosis in Swiss Strain Mice After Being Induced by Doxorubicin

2010 ◽  
Vol 2 (2) ◽  
pp. 46
Author(s):  
Bambang Purwanto ◽  
A Guntur Hermawan
Keyword(s):  
Collagen Type ◽  
Interstitial Fibrosis ◽  
Collagen Type I ◽  
Type I ◽  
Renal Interstitial Fibrosis ◽  
Collagen Type 1 ◽  
Nephroprotective Effect ◽  
Tgf Β1 ◽  
Swiss Strain

BACKGROUND: Use of doxorubicin (DXR) in the treatment of cancer has been increasing along with the increase in cancer morbidity. Nephrotoxic effects of DXR are still a problem. Pentoxyphylline (PTX) as an electron-donor material can be nephroprotective, so the combination of DXR and PTX might reduce the nephrotoxic effects of DXR. The aim of this study was to prove the nephroprotective effect of PTX and DXR nephrotoxicity through the improvement of TGF-β1, collage type-1, and renal interstitial fibrosis.METHODS: Twenty-four males Swiss strain mice, divided into three groups namely Control (C) injected with NaCl 0.9%; DXR induced nephrotoxicity (D); and effect of PTX on D (P/D) by intraperitoneally, respectively, each group consisted of 8 mice. Injections were given once a week for three consecutive weeks. At 8th week post-treatment, all eight mice of each group were sacrificed. Examination of TGF-β1 and collagen type-I expression was done by immunohistochemistry with monoclonal antibody. Renal interstitial fibrosis examination was done by a histopathologist, using Verheoff van Giesen staining. The statistic analysis was carried out using one-way ANOVA.RESULTS: TGF-β1 expression increased from C to D and subsequently decreased in P/D (4.50±3.89 vs. 177.88±68.78 vs. 36.88±9.51). Collagen type-I expression increased from C to D and subsequently decreased in P/D (12.00±14.32 vs. 186.25±125.62 vs. 36.00±29.14). Renal interstitial fibrosis expression increased from C to D and subsequently decreased in P/D (16.75±6.14 vs. 85.00±7.33 vs. 60.50±11.40). The expression of TGF-β1, collagen type-1, and renal interstitial fibrosis were higher significantly in D group as compared to C group (p<0,001). The expression of TGF-β1, collagen type-1, and renal interstitial fibrosis were lower significantly in P/D group as compared to D group (p<0.005).CONCLUSIONS: PTX was proved to be nephroprotector inducing by DXR.KEYWORDS: PTX, nephroprotector, TGF-β1, collagen type-I, renal interstitial fibrosis

scholarly journals The NF-kB and Collagen Type 1 Expression in Dental Pulp after Treated Calcium Hydroxide Combined with Propolis

2021 ◽  
Author(s):  
Nirawati Pribadi ◽  
Dwita Budiarti ◽  
Hendy Jaya Kurniawan ◽  
Ira Widjiastuti
Keyword(s):  
Calcium Hydroxide ◽  
Dental Pulp ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Treatment Groups ◽  
Pulp Inflammation ◽  
Time Frames ◽  
Collagen Type 1

Abstract Objective To analyze the expression of nuclear factor kappa B (NF-kB) and collagen type 1 on dental pulp after a treated combination of calcium hydroxide and propolis. Materials and Methods The first maxillary molars of 30 rats were mechanically perforated. Teeth were divided into three groups of 10 for two separate extraction time frames, giving a total of 60 rats. The control groups were treated with Cention, the second treatment groups were treated with calcium hydroxide, and the third treatment groups were treated with a combination of calcium hydroxide and propolis. Final restoration was done with Cention. The teeth were extracted on days 7 and 14, and the expression of NF-kB and collagen type I was analyzed using immunohistochemistry. Results There is lowest NF-kB expression and highest collagen type 1 expression on dental pulp after treated with a combination of calcium hydroxide and propolis on days 7 and 14 (p < 0.05). Conclusion The combination of calcium hydroxide and propolis inhibits pulp inflammation and stimulates regeneration through decreasing the NF-kB expression and increasing collagen type 1.

scholarly journals Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, αvβ3-integrin, and TGF-β1 in response to ANG II and high glucose

2008 ◽  
Vol 295 (1) ◽  
pp. H69-H76 ◽  
Author(s):  
Souad Belmadani ◽  
Mourad Zerfaoui ◽  
Hamid A. Boulares ◽  
Desiree I. Palen ◽  
Khalid Matrougui
Keyword(s):  
Map Kinase ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Ang Ii ◽  
Diabetic Mice ◽  
Smad2 Phosphorylation ◽  
Collagen Type 1 ◽  
Tgf Β1

This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, αvβ3-integrin, and transforming growth factor (TGF)-β1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from Type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. Isolated MRA were subjected to a pressure-passive-diameter relationship. To delineate cell types and mechanisms, cultured VSMC were prepared from MRA and stimulated with ANG II (100 nM) and high glucose (HG, 22 mM). Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. Treatment of HT and diabetic mice with neutralizing TGF-β1 antibody reduced MRA stiffness and collagen type I deposition. Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-β1, αvβ3-integrin, and collagen type 1 release in the conditioned media. TGF-β1 bioactivity and Smad2 phosphorylation were αvβ3-integrin-dependent, since β3-integrin antibody and αvβ3-integrin inhibitor (SB-223245, 10 μM) significantly prevented TGF-β1 bioactivity and Smad2 phosphorylation. Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 μM) reduced αvβ3-integrin, TGF-β1, and collagen type 1 content. Additionally, αvβ3-integrin antibody, SB-223245, TGF-β1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. Together, these data provide evidence that resistance artery fibrosis in Type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, αvβ3-integrin, and TGF-β1 signaling. This pathway could be a potential target for overcoming small artery complications in diabetes and hypertension.

scholarly journals Influence of fibrillin-1 genotype on aortic stiffness in men: a note of caution

2006 ◽  
Vol 100 (4) ◽  
pp. 1431-1432
Author(s):  
Yasmin ◽  
Ian B. Wilkinson ◽  
Kevin M. O’Shaughnessy
Keyword(s):  
Mechanical Properties ◽  
Pulse Pressure ◽  
Aortic Stiffness ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Increased Risk ◽  
Fibrillin 1 ◽  
Echo Tracking

Aortic stiffness is a predictor of cardiovascular mortality. The mechanical properties of the arterial wall depend on the connective tissue framework, with variation in fibrillin-1 and collagen I genes being associated with aortic stiffness and/or pulse pressure elevation. The aim of this study was to investigate whether variation in fibrillin-1 genotype was associated with aortic stiffness in men. The mechanical properties of the abdominal aorta of 79 healthy men (range 28–81 yr) were investigated by ultrasonographic phase-locked echo tracking. Fibrillin-1 genotype, characterized by the variable tandem repeat in intron 28, and collagen type I alpha 1 genotype characterized by the 2,064 G\?\T polymorphism, were determined by using DNA from peripheral blood cells. Three common fibrillin-1 genotypes, 2-2, 2-3, and 2-4, were observed in 50 (64%), 10 (13%), and 11 (14%) of the men, respectively. Those of 2-3 genotype had higher pressure strain elastic modulus and aortic stiffness compared with men of 2-2 or 2-4 genotype ( P = 0.005). Pulse pressure also was increased in the 2-3 genotype ( P = 0.04). There was no significant association between type 1 collagen genotype and aortic stiffness in this cohort. In conclusion, the fibrillin-1 2-3 genotype in men was associated with increased aortic stiffness and pulse pressure, indicative of an increased risk for cardiovascular disease.

scholarly journals Bone mineral density, collagen type 1 α 1 genotypes and bone turnover in premenopausal women with diabetes mellitus

Diabetologia ◽  
1998 ◽  
Vol 41 (11) ◽  
pp. 1314-1320 ◽  
Author(s):  
G. Hampson ◽  
C. Evans ◽  
R. J. Petitt ◽  
W. D. Evans ◽  
S. J. Woodhead ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Bone Mineral Density ◽  
Bone Turnover ◽  
Bone Mineral ◽  
Collagen Type ◽  
Premenopausal Women ◽  
Mineral Density ◽  
Collagen Type 1

scholarly journals Identification in Collagen Type I of an Integrin α2β1-binding Site Containing an Essential GER Sequence

1998 ◽  
Vol 273 (50) ◽  
pp. 33287-33294 ◽  
Author(s):  
C. Graham Knight ◽  
Laurence F. Morton ◽  
David J. Onley ◽  
Anthony R. Peachey ◽  
Anthea J. Messent ◽  
...  
Keyword(s):  
Binding Site ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I

Sequence Alignment between vWF and Peptides Inhibiting the vWF-collagen Interaction Does not Result in the Identification of a Collagen-binding Site in vWF

2000 ◽  
Vol 84 (10) ◽  
pp. 621-625 ◽  
Author(s):  
R. M. van der Plas ◽  
G. Vandecasteele ◽  
S. Vauterin ◽  
E. G. Huizinga ◽  
J. J. Sixma ◽  
...  
Keyword(s):  
Binding Site ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Binding Studies ◽  
Collagen Types ◽  
Collagen Binding ◽  
Human Collagen ◽  
Rat Tail ◽  
Calf Skin

SummaryWe previously found that two peptides (N- and Q-peptide) selected by phage display for binding to an anti-vWF antibody, were able to inhibit vWF-binding to collagen (1). The sequence of those peptides could be aligned with the sequence in vWF at position 1129-1136 just outside the A3-domain. As the peptides represent an epitope or mimotope of vWF for binding to collagen we next wanted to study whether the alignment resulted in the identification of a new collagen binding site in vWF. We mutated the 1129-1136 VWTLPDQC sequence in vWF to VATAPAAC. Expressing this mutant vWF (7.8-vWF) in a fur-BHK cell line resulted in well processed 7.8-vWF containing a normal distribution of molecular weight multimers. However, binding studies of this mutant vWF to rat tail, human and calf skin collagens type I, to human collagen types III and VI, revealed no decrease in vWF-binding to any of these collagens. Thus, although the N-and Q-peptides did inhibit the vWF-collagen interaction, the resulting alignment with the vWF sequence did not identify a collagen binding site, pointing out that alignments (although with a high percentage of identity) do not always result in identification of binding epitopes. However, suprisingly removal of the A3-domain or changing the vWF sequence at position 1129-1136 resulted in an increase of vWF-binding to human collagen type VI and to rat tail collagen type I, implying that these changes result in a different conformation of vWF with an increased binding to these collagens as a consequence.

Influence of fibrillin-1 genotype on the aortic stiffness in men

2005 ◽  
Vol 99 (3) ◽  
pp. 1036-1040 ◽  
Author(s):  
J. T. Powell ◽  
R. J. Turner ◽  
M. Sian ◽  
R. Debasso ◽  
T. Länne
Keyword(s):  
Mechanical Properties ◽  
Pulse Pressure ◽  
Aortic Stiffness ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Increased Risk ◽  
Fibrillin 1 ◽  
Echo Tracking

Aortic stiffness is a predictor of cardiovascular mortality. The mechanical properties of the arterial wall depend on the connective tissue framework, with variation in fibrillin-1 and collagen I genes being associated with aortic stiffness and/or pulse pressure elevation. The aim of this study was to investigate whether variation in fibrillin-1 genotype was associated with aortic stiffness in men. The mechanical properties of the abdominal aorta of 79 healthy men (range 28–81 yr) were investigated by ultrasonographic phase-locked echo tracking. Fibrillin-1 genotype, characterized by the variable tandem repeat in intron 28, and collagen type I alpha 1 genotype characterized by the 2,064 G>T polymorphism, were determined by using DNA from peripheral blood cells. Three common fibrillin-1 genotypes, 2-2, 2-3, and 2-4, were observed in 50 (64%), 10 (13%), and 11 (14%) of the men, respectively. Those of 2-3 genotype had higher pressure strain elastic modulus and aortic stiffness compared with men of 2-2 or 2-4 genotype ( P = 0.005). Pulse pressure also was increased in the 2-3 genotype ( P = 0.04). There was no significant association between type 1 collagen genotype and aortic stiffness in this cohort. In conclusion, the fibrillin-1 2-3 genotype in men was associated with increased aortic stiffness and pulse pressure, indicative of an increased risk for cardiovascular disease.

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