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Markers of collagen synthesis and degradation are increased in serum in severe sepsis: a longitudinal study of 44 patients
Fiia G?ddn?s, Marjo Koskela, Vesa Koivukangas, Juha Risteli, Aarne Oikarinen, Jouko Laurila, Juha Saarnio, Tero Ala-Kokko
Critical Care , 2009, DOI: 10.1186/cc7780
Abstract: Forty-four patients with severe sepsis participated in the study and 15 volunteers acted as controls. Blood samples were collected for 10 days after the first sepsis-induced organ dysfunction and after three and six months. Procollagen type I and III aminoterminal propeptides (PINP and PIIINP) and cross-linked telopeptides of type I collagen (ICTP) were measured.The PIIINP concentration was elevated in the septic patients (8.8 ug/L, 25th to 75th percentile = 6.8 to 26.0) when compared with controls (3.0 ug/L, 25th to 75th percentile = 2.7 to 3.3; P < 0.001) on day one. Maximum serum PIIINP concentrations during sepsis were higher in non-survivors compared with survivors (26.1 ug/L, 25th to 75th percentile = 18.7 to 84.3; vs. 15.1 ug/L, 25th to 75th percentile = 9.6 to 25.5; P = 0.033) and in multiple organ failure (MOF) compared with multiple organ dysfunction syndrome (MODS) (24.2 ug/L, 25th to 75th percentile = 13.4 to 48.2; vs. 8.9 ug/L, 25th to 75th percentile = 7.4 to 19.4; P = 0.002). Although the PINP values of the septic patients remained within the laboratory reference values, patients with MOF had higher values than patients with MODS (79.8, 25th to 75th percentile = 44.1 to 150.0; vs.40.4, 25th to 75th percentile = 23.6 to 99.3; P = 0.007). Day one ICTP levels were elevated in septic patients compared with the controls (19.4 ug/L, 25th to 75th percentile = 12.0 to 29.8; vs. 4.1 ug/L, 25th to 75th percentile = 3.4 to 5.0; P < 0.001).Markers of collagen metabolism are increased in patients with severe sepsis and can be investigated further as markers of disease severity and outcome.The host response in sepsis is a dynamic process activating the pathways of coagulation, inflammation and tissue repair. When the response becomes overwhelming, it leads to multiple organ failure (MOF) and death [1-3]. Disturbed connective tissue metabolism is the key element in complications of inflammatory disease, so it was of interest to determine whether high systemic inflam
A contribution to the study of stand degradation process on the territory of Fru ka Gora National Park  [PDF]
Bobinac Martin T.
Zbornik Matice Srpske za Prirodne Nauke , 2003, DOI: 10.2298/zmspn0305061b
Abstract: We analyzed the process of stand degradation of individual forest ecosystems in the region of the zonal community Tilio-Carpino-Qurcetum robori-cerris Jov. 79 located in the western part of Fru ka Gora National Park. Degradation occurred is consequence to regeneration felling and it progressed towards the extinction of oaks, first of all the valuable pedunculate oak and Vergilius's oak, and then also Turkey oak. The analyzed mature stands were degraded coppice and mainly predominated by the Turkey oak in the tree stratum. In juvenile stands, often initially well regenerated with Turkey oak, the dominant species in the tree stratum are lime, hornbeam, flowering ash, field maple and other secondary species, predominantly of coppice origin. Restitution of the degraded stands is possible by applying an adequate regeneration system. Taking into account the primarily protective function of the analyzed forest ecosystems and the fact that these are degraded and coppice stands, the system of regeneration should be based on combined restoration.
Effect of budesonide on fibroblast-mediated collagen gel contraction and degradation  [cached]
Fang Q,Schulte NA,Kim H,Kobayashi T
Journal of Inflammation Research , 2013,
Abstract: Qiuhong Fang,1,2 Nancy A Schulte,3 Huijung Kim,4 Tetsu Kobayashi,5 Xingqi Wang,2 Anna Miller-Larsson,6 Elisabet Wieslander,6 Myron L Toews,3 Xiangde Liu,2 Stephen I Rennard21Pulmonary and Critical Care Department, Beijing Shijitan Hospital, Capital Medical University, Beijing, People's Republic of China; 2Pulmonary, Critical Care, Sleep and Allergy Division, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, USA; 3Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, USA; 4Pulmonary and Critical Care Division, WonKwang University, Kunpo Medical Center, Seoul, Republic of Korea; 5Mie University Graduate School of Medicine, Tsu City, Japan; 6AstraZeneca R&D Molndal, Molndal, SwedenBackground: The balance between production and degradation of extracellular matrix is crucial in maintaining normal tissue structure. This study was designed to investigate the effect of budesonide on fibroblast-mediated tissue repair and remodeling.Methods: Using human fetal lung fibroblasts in a three-dimensional collagen gel culture system, we investigated the effect of budesonide (1–1000 nM) on collagen gel contraction and degradation in the presence or absence of inflammatory cytokines (interleukin-1β and tumor necrosis factor α; 5 ng/mL each) and, in order to activate latent proteases, serine protease trypsin 0.25 μg/mL. The effects of budesonide on metalloproteinase production and activation were also investigated.Results: Inflammatory cytokines significantly inhibited collagen gel contraction mediated by lung fibroblasts. Budesonide counteracted the effect of cytokines in a concentration-dependent manner (to 50%, P < 0.01). Budesonide 100 nM almost completely inhibited the release and mRNA expression of metalloproteinase-1, metalloproteinase-3, and metalloproteinase-9 induced by the cytokines (P < 0.05). Exposure to the cytokines plus trypsin increased collagen degradation and conversion of the metalloproteinases to lower molecular weight forms corresponding to their active forms. Budesonide blocked both enhanced collagen degradation (P < 0.01) and suppressed trypsin-mediated conversion of cytokine-induced metalloproteinase-9 and metalloproteinase-3 to lower molecular weight forms. Similar effects were observed with dexamethasone 1 μM, suggesting a class effect.Conclusion: These findings demonstrate that budesonide directly modulates contraction of collagen gels and can decrease collagen degradation under inflammatory conditions. The mechanism of this effect is through suppressing gene
Effect of budesonide on fibroblast-mediated collagen gel contraction and degradation
Fang Q, Schulte NA, Kim H, Kobayashi T, Wang X, Miller-Larsson A, Wieslander E, Toews ML, Liu X, Rennard SI
Journal of Inflammation Research , 2013, DOI: http://dx.doi.org/10.2147/JIR.S35136
Abstract: t of budesonide on fibroblast-mediated collagen gel contraction and degradation Original Research (480) Total Article Views Authors: Fang Q, Schulte NA, Kim H, Kobayashi T, Wang X, Miller-Larsson A, Wieslander E, Toews ML, Liu X, Rennard SI Published Date February 2013 Volume 2013:6 Pages 25 - 33 DOI: http://dx.doi.org/10.2147/JIR.S35136 Received: 19 June 2012 Accepted: 09 August 2012 Published: 27 February 2013 Qiuhong Fang,1,2 Nancy A Schulte,3 Huijung Kim,4 Tetsu Kobayashi,5 Xingqi Wang,2 Anna Miller-Larsson,6 Elisabet Wieslander,6 Myron L Toews,3 Xiangde Liu,2 Stephen I Rennard2 1Pulmonary and Critical Care Department, Beijing Shijitan Hospital, Capital Medical University, Beijing, People's Republic of China; 2Pulmonary, Critical Care, Sleep and Allergy Division, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, USA; 3Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, USA; 4Pulmonary and Critical Care Division, WonKwang University, Kunpo Medical Center, Seoul, Republic of Korea; 5Mie University Graduate School of Medicine, Tsu City, Japan; 6AstraZeneca R&D Molndal, Molndal, Sweden Background: The balance between production and degradation of extracellular matrix is crucial in maintaining normal tissue structure. This study was designed to investigate the effect of budesonide on fibroblast-mediated tissue repair and remodeling. Methods: Using human fetal lung fibroblasts in a three-dimensional collagen gel culture system, we investigated the effect of budesonide (1–1000 nM) on collagen gel contraction and degradation in the presence or absence of inflammatory cytokines (interleukin-1β and tumor necrosis factor α; 5 ng/mL each) and, in order to activate latent proteases, serine protease trypsin 0.25 μg/mL. The effects of budesonide on metalloproteinase production and activation were also investigated. Results: Inflammatory cytokines significantly inhibited collagen gel contraction mediated by lung fibroblasts. Budesonide counteracted the effect of cytokines in a concentration-dependent manner (to 50%, P < 0.01). Budesonide 100 nM almost completely inhibited the release and mRNA expression of metalloproteinase-1, metalloproteinase-3, and metalloproteinase-9 induced by the cytokines (P < 0.05). Exposure to the cytokines plus trypsin increased collagen degradation and conversion of the metalloproteinases to lower molecular weight forms corresponding to their active forms. Budesonide blocked both enhanced collagen degradation (P < 0.01) and suppressed trypsin-mediated conversion of cytokine-induced metalloproteinase-9 and metalloproteinase-3 to lower molecular weight forms. Similar effects were observed with dexamethasone 1 μM, suggesting a class effect. Conclusion: These findings demonstrate that budesonide directly modulates contraction of collagen gels and can decrease collagen degradation under inflammatory conditions. The mechanism of this effect is throu
Comparative Effects of Biodynes, Tocotrienol-Rich Fraction, and Tocopherol in Enhancing Collagen Synthesis and Inhibiting Collagen Degradation in Stress-Induced Premature Senescence Model of Human Diploid Fibroblasts  [PDF]
Suzana Makpol,Faidruz Azura Jam,Shy Cian Khor,Zahariah Ismail,Yasmin Anum Mohd Yusof,Wan Zurinah Wan Ngah
Oxidative Medicine and Cellular Longevity , 2013, DOI: 10.1155/2013/298574
Abstract: Biodynes, tocotrienol-rich fraction (TRF), and tocopherol have shown antiaging properties. However, the combined effects of these compounds on skin aging are yet to be investigated. This study aimed to elucidate the skin aging effects of biodynes, TRF, and tocopherol on stress-induced premature senescence (SIPS) model of human diploid fibroblasts (HDFs) by determining the expression of collagen and MMPs at gene and protein levels. Primary HDFs were treated with biodynes, TRF, and tocopherol prior to hydrogen peroxide (H2O2) exposure. The expression of COL1A1, COL3A1, MMP1, MMP2, MMP3, and MMP9 genes was determined by qRT-PCR. Type I and type III procollagen proteins were measured by Western blotting while the activities of MMPs were quantified by fluorometric Sensolyte MMP Kit. Our results showed that biodynes, TRF, and tocopherol upregulated collagen genes and downregulated MMP genes ( ). Type I procollagen and type III procollagen protein levels were significantly increased in response to biodynes, TRF, and tocopherol treatment ( ) with reduction in MMP-1, MMP-2, MMP-3, and MMP-9 activities ( ). These findings indicated that biodynes, TRF, and tocopherol effectively enhanced collagen synthesis and inhibited collagen degradation and therefore may protect the skin from aging. 1. Introduction Human skin which consists of epidermis, dermis, and subcutaneous tissues provides a shielding layer for internal organs. During chronological aging, increased wrinkling, sagging, pigmentation, fragility, and lack of moisture plus elasticity are the universal manifestations observed on the skin. Skin aging can be intrinsic, which is genetically determined and extrinsic, which is caused by environmental exposure such as UV light. Oxidative stress is one of the factors that contribute to skin aging [1, 2]. Fibroblasts which are the crucial collagen-producing cells provide flatten appearance and elasticity to the skin in cooperation with collagen. However, fibroblasts have collapsed appearance with little cytoplasm when they aged [3, 4]. Therefore evaluating the loss of collagen, either decreased synthesis or increased degradation, is important in analyzing the factors that may contribute to skin aging [5]. Matrix metalloproteinases (MMPs) play an important role in regulating the turnover of collagen. In aged skin, the elevated level of MMPs caused increased collagen degradation and deterioration of skin structure [6]. Previous study which used stress induced premature senescence (SIPS) model of human diploid fibroblasts has shown the role of MMPs in regulating collagen
CHANGES IN THE IMMUNOLOGIC MARKERS OF COLLAGEN TYPE IV DEGRADATION IN SUBJECTS WITH METABOLIC SYNDROME  [PDF]
Edward Mekenyan,Nadya Stancheva,Snejana Tisheva
Journal of IMAB : Annual Proceeding (Scientific Papers) , 2012,
Abstract: Background: Collagen is the major protein component of the vessels. Collagen type IV is found exclusively in the basal membrane and doesn’t form individual fibers, but instead is presented as a polygonal amorphous matrix that is associated with laminin and other matrix macromolecules to form the unique matrix basal membrane. Under the influence of the risk factors characterizing the metabolic syndrome, a variety of basal memrane degrading enzymes are activated. This leads to an early changes in vascular wall and accelerates the vascular aging The early manifestation of the metabolic syndrome in younger people in the modern society, leads to earlier manifestation of the complications of early vessels aging. Loss of elasticity is a key component in the pathogenesis of cardiovascular complications. Materials and methods: A study is conducted on 62 subjects with metabolic syndrome without vascular complications and 42 controls. The main objective of the study was to compare the imunological markers of Collagen typr IV degradation in both groups and to assess their relationship with the risk factors characterizing the metabolic syndrome. Results: When comparing the levels of Anti Coll IV Ab IgG in the control group and subjects with metabolic syndrome (respectively 0.28 + / - 0.08 and 0.40 + / - 0.11) a statistically significantly higher levels of Anti Coll IV Ab IgG were determined in the group with metabolic syndrome, F = 30.299, p = 0.000, In the whole sample Anti Col IV Ab IgG showed negative correlation with HDL with a correlation Spearman coefficient r = 0,26, and p = 0,02. The antibodies showed positive correlation with the diastolic pressure (DP), blood sugar (Gluc), total cholesterol (Tchol), triglycerides (Tg) and LDL. The positive corelations were with Pearson correlation coefficient as follows: DP - r = 0,22, p = 0,04; Gluc – r=0,27, p=0,01; TChol – r=0,30, p=0.005; Tg – r=0,34, p=0,002; LDL – r=0,32, p=0,002. Conclusion: It is proved that the ACol IVAb IgG and are significantly elevated in the subjects with metabolic syndrome without manifested cardiovascular complications compared with the control group and there is a strong correlation between the Ab and the risc factors.
Inhibition of elastin and collagen networks degradation in human skin by gingival fibroblast. In vitro, ex vivo and in vivo studies.  [PDF]
Bruno Gogly, Francois Come Ferré, Hafida Cherifi, Adrien Naveau, Benjamin Philippe Fournier
Journal of Cosmetics, Dermatological Sciences and Applications (JCDSA) , 2011, DOI: 10.4236/jcdsa.2011.11002
Abstract: Skin aging shows an imbalance between synthesis and degradation of the extracellular matrix. The overproduction of degradative enzymes (MMPs) during the chronology- and photo-induced aging leads to a degradation of the elastic and collagen networks. In a model of collagen and elastin destruction, we showed that the gingival fibroblast was able to preserve these macromolecules by inhibiting the overproduction of metalloproteinases by overproduction of TIMP-1 and modulation of the inflammatory cytokines activity. The objective of this study is to evaluate the effect of the gingival fibroblasts on human skin. The results in vitro and ex vivo show that the gingival fibroblast protects the skin collagen and elastic network by the inhibition of MMPs which leads to an overproduction of the TIMP-1. Moreover, the gingival fibroblast modulates the activity of some enzymes responsible for the inflammation; they inhibit the IL-1β and stimulate the production of TGF-β1. In vivo studies with a duration of six months and 50 women with pronounced wrinkles show that the culture supernatant of gingival fibroblasts diluted to 5% leads to a statistically significant decrease in the number and length of wrinkles.
Collaborative interactions between neutrophil elastase and metalloproteinases in extracellular matrix degradation in three-dimensional collagen gels
Yunkui Zhu, Xiangde Liu, C Sk?ld, Hangjun Wang, Tadashi Kohyama, Fu-Qiang Wen, Ronald F Ertl, Stephen I Rennard
Respiratory Research , 2001, DOI: 10.1186/rr73
Abstract: Blood monocytes from healthy donors and human fetal lung fibroblasts were cast into type I collagen gels and maintained in floating cultures for three weeks. Matrix metalloproteinases (MMPs) were assessed by gelatin zymography (MMPs 2 and 9) and immunoblotting (MMPs 1 and 3). The role of PGE2 was explored by direct quantification, and by the addition of exogenous indomethacin and/or PGE2.Gelatin zymography and immunoblots revealed that MMPs 1, 2, 3 and 9 were induced by co-cultures of fibroblasts and monocytes. Neutrophil elastase added to the medium resulted in marked conversion of latent MMPs to lower molecular weight forms consistent with active MMPs, and was associated with augmentation of both contraction and degradation (P < 0.01). PGE2 appeared to decrease both MMP production and activation.The current study demonstrates that interactions between monocytes and fibroblasts can mediate tissue remodeling.Three-dimensional (3D) collagen gel culture has been used as an in vitro model of in vivo tissue contraction, a common feature of fibrosis, as well as the resolution of granulation tissue that characterizes repair [1,2]. Short-term co-cultures of monocytes with fibroblasts result in the inhibition of collagen gel contraction [3], while co-cultures of fibroblasts with neutrophils, or with neutrophil elastase (NE), augment contraction [4].Results in the linked study [5] demonstrated that 3D collagen gel contraction was augmented in extended co-cultures of fibroblasts and monocytes. Since MMPs play a prominent role in connective tissue degradation [6,7,8], the current study, an extension of this linked study, was designed to explore the potential role of MMPs in this process.See supplementary material for further information.See Supplementary material.Collagen gels were prepared as described previously [9]. For long-term co-culture, the medium was changed every 5 days. The areas of floating gels were measured using an image analyzer.To investigate the effect of PGE
Sciatic nerve regeneration in rats by a promising electrospun collagen/poly(ε-caprolactone) nerve conduit with tailored degradation rate
Wenwen Yu, Wen Zhao, Chao Zhu, Xiuli Zhang, Dongxia Ye, Wenjie Zhang, Yong Zhou, Xinquan Jiang, Zhiyuan Zhang
BMC Neuroscience , 2011, DOI: 10.1186/1471-2202-12-68
Abstract: In this study we fabricated a collagen/poly(ε-caprolactone) (collagen/PCL) fibrous scaffold by electrospinning and explored its application as nerve guide substrate or conduit in vitro and in vivo. Material characterizations showed this electrospun composite material which was made of submicron fibers possessed good hydrophilicity and flexibility. In vitro study indicated electrospun collagen/PCL fibrous meshes promoted Schwann cell adhesion, elongation and proliferation. In vivo test showed electrospun collagen/PCL porous nerve conduits successfully supported nerve regeneration through an 8 mm sciatic nerve gap in adult rats, achieving similar electrophysiological and muscle reinnervation results as autografts. Although regenerated nerve fibers were still in a pre-mature stage 4 months postoperatively, the implanted collagen/PCL nerve conduits facilitated more axons regenerating through the conduit lumen and gradually degraded which well matched the nerve regeneration rate.All the results demonstrated this collagen/PCL nerve conduit with tailored degradation rate fabricated by electrospinning could be an efficient alternative to autograft for peripheral nerve regeneration research. Due to its advantage of high surface area for cell attachment, it is believed that this electrospun nerve conduit could find more application in cell therapy for nerve regeneration in future, to further improve functional regeneration outcome especially for longer nerve defect restoration.For peripheral nerve repair, nerve autografts have always been considered as the "gold standard" for the restoration of structural and functional nerve regeneration. Yet autograft acquisitions are also faced with several limitations, such as the sensation loss of donor area, dimension discrepancies between donor and recipient nerves and most importantly, the lack of enough nerve sources for multiple nerve injuries. To seek alternatives for autografts, artificial nerve guides or nerve conduits have been
Collagen-Binding Peptidoglycans Inhibit MMP Mediated Collagen Degradation and Reduce Dermal Scarring  [PDF]
Kate Stuart, John Paderi, Paul W. Snyder, Lynetta Freeman, Alyssa Panitch
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0022139
Abstract: Scarring of the skin is a large unmet clinical problem that is of high patient concern and impact. Wound healing is complex and involves numerous pathways that are highly orchestrated, leaving the skin sealed, but with abnormal organization and composition of tissue components, namely collagen and proteoglycans, that are then remodeled over time. To improve healing and reduce or eliminate scarring, more rapid restoration of healthy tissue composition and organization offers a unique approach for development of new therapeutics. A synthetic collagen-binding peptidoglycan has been developed that inhibits matrix metalloproteinase-1 and 13 (MMP-1 and MMP-13) mediated collagen degradation. We investigated the synthetic peptidoglycan in a rat incisional model in which a single dose was delivered in a hyaluronic acid (HA) vehicle at the time of surgery prior to wound closure. The peptidoglycan treatment resulted in a significant reduction in scar tissue at 21 days as measured by histology and visual analysis. Improved collagen architecture of the treated wounds was demonstrated by increased tensile strength and transmission electron microscopy (TEM) analysis of collagen fibril diameters compared to untreated and HA controls. The peptidoglycan's mechanism of action includes masking existing collagen and inhibiting MMP-mediated collagen degradation while modulating collagen organization. The peptidoglycan can be synthesized at low cost with unique design control, and together with demonstrated preclinical efficacy in reducing scarring, warrants further investigation for dermal wound healing.
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