Hydrogen sulfide degradation characteristics of Bordetella sp. Sulf-8 in a biotrickling filter

The applicability of Bordetella sp. Sulf-8 to degrade Hydrogen Sulfide (H₂S) gas in a biotrickling system was investigated. The isolate is a heterotrophic gram-negative, catalase- and oxidase-positive, rod-shaped bacterium which can metabolize thiosulfate or sulfide into sulfate. The mesophilic Bordetella sp. Sulf-8 can grow within a wide pH range using yeast as carbon source, with or without the presence of sulfur. In batch experiments, kinetic constants such as maximum specific growth rate (μ _max = 0.12 1/h), saturation constant (K _S = 0.017 g/L), and specific sulfur removal rate (88 mg S/g cells h) were obtained. In biotrickling experiments removal efficiencies were satisfactory, but the system performance was observed to be more influenced by empty bed residence time than by H₂S feed gas concentration. Critical and maximum elimination capacities were 78.0 and 94.5 g H₂S/m³ day, respectively. Macrokinetic analysis of the biotrickling system revealed maximum H₂S removal rate V _max = 15.97 g S/kg media-day and half saturation constant K _S′ = 12.45 ppm_v.     

Substrate specificity of 6-O-endosulfatase (Sulf-2) and its implications in synthesizing anticoagulant heparan sulfate

Heparan sulfate (HS) 6-O-endosulfatase (Sulf) catalyzes the hydrolysis of 6-O-sulfo groups from HS polysaccharides. The resultant HS has reduced sulfation levels and displays altered biological activities. The Sulfs have been associated with several cancers and developmental problems and could function as a tool for editing specific HS structures. Here, we characterize the substrate specificity of human Sulf-2 using site-specifically radiolabeled synthetic polysaccharides. The enzyme was expressed and harvested from the conditioned medium of Chinese hamster ovary cells transfected with Sulf-2 expression plasmids. The uniquely [(35)S]sulfated polysaccharides were prepared using purified recombinant HS biosynthetic enzymes. We found that Sulf-2 is particularly effective in removing the 6-O-sulfo group residing in the trisulfated disaccharide repeating unit comprising 2-O-sulfated uronic acid and N-sulfated 6-O-sulfo glucosamine, but can also hydrolyze sulfo groups from N- and 6-O-sulfated disaccharides. In addition, we found that Sulf-2 treatment significantly decreases HS's ability to bind to platelet factor 4 (PF4), a chemokine, while binding to antithrombin is maintained. Because HS-PF4 complexes are the initiating cause of heparin-induced thrombocytopenia, this finding provides a promising strategy for developing heparin therapies with reduced side effects. Further understanding of Sulf-2 activity will help elucidate HS structure-function relationships and provide a valuable tool in tailoring HS-based anticoagulant drugs.     

Tumour-necrosis factor-α induces heparan sulfate 6-O-endosulfatase 1 (Sulf-1) expression in fibroblasts

Heparan sulfate (HS) 6-O-endosulfatases (Sulfs) have emerged recently as critical regulators of many physiological and pathological processes. By removing 6-O-sulfates from specific HS sequences, they modulate the activities of a variety of growth factors and morphogens, including fibroblast growth factor (FGF)-1. However, little is known about the functions of Sulfs in inflammation. Tumour-necrosis factor (TNF)-α plays an important role in regulating the behaviour of fibroblasts. In this study, we examined the effect of this inflammatory cytokine on the expression of Sulfs in human MRC-5 fibroblasts. Compositional analysis of HS from TNF-α-treated cells showed a strong reduction in the amount of the trisulfated UA2S-GlcNS6S disaccharide, which suggested a selective reaction of 6-O-desulfation. Real-time PCR analysis revealed that TNF-α increased Sulf-1 expression in a dose- and time-dependent manner, via a mechanism involving NF-ĸB, ERK1/2 and p38 MAPK. In addition, we confirmed that cell stimulation with TNF-α was accompanied by the secretion of an active form of Sulf-1. To study the function of Sulf- 1, we examined the responses induced by FGF-1. We showed that ERK1/2 activation and cell proliferation were markedly reduced in TNF-α-treated MRC-5 cells compared with untreated cells. Silencing the expression of Sulf-1 by RNA interference restored the responses induced by FGF-1, which indicated that TNF-α-mediated induction of the sulfatase indeed resulted in alterations of HS biological properties. Taken together, our results indicate that Sulf-1 is responsive to TNF-α stimulation and may function as an autocrine regulator of fibroblast expansion in the course of an inflammatory response.     

Chondroprotective effects and mechanisms of resveratrol in advanced glycation end products-stimulated chondrocytes

Introduction  

Accumulation of advanced glycation end products (AGEs) in joints contributes to the pathogenesis of cartilage damage in osteoarthritis (OA). We aim to explore the potential chondroprotective effects of resveratrol on AGEs-stimulated porcine chondrocytes and cartilage explants.     

Cartilage oligomeric matrix protein deficiency promotes early onset and the chronic development of collagen-induced arthritis

Introduction  

Cartilage oligomeric matrix protein (COMP) is a homopentameric protein in cartilage. The development of arthritis, like collagen-induced arthritis (CIA), involves cartilage as a target tissue. We have investigated the development of CIA in COMP-deficient mice.     

Ultrasound properties of articular cartilage in the tibio-femoral joint in knee osteoarthritis: relation to clinical assessment (International Cartilage Repair Society grade)

Introduction  

There is a lack of data relating the macroscopic appearance of cartilage to its ultrasound properties. The purpose of the present study was to evaluate degenerated cartilage and healthy-looking cartilage using an ultrasound system.     

Mesenchymal progenitor cell markers in human articular cartilage: normal distribution and changes in osteoarthritis

Introduction  

Recent findings suggest that articular cartilage contains mesenchymal progenitor cells. The aim of this study was to examine the distribution of stem cell markers (Notch-1, Stro-1 and VCAM-1) and of molecules that modulate progenitor differentiation (Notch-1 and Sox9) in normal adult human articular cartilage and in osteoarthritis (OA) cartilage.     

Simulating the swelling and deformation behaviour in soft tissues using a convective thermal analogy

Background  

It is generally accepted that cartilage adaptation and degeneration are mechanically mediated. Investigating the swelling behaviour of cartilage is important because the stress and strain state of cartilage is associated with the swelling and deformation behaviour. It is well accepted that the swelling of soft tissues is associated with mechanical, chemical, and electrical events.     

Relationship of compartment-specific structural knee status at baseline with change in cartilage morphology: a prospective observational study using data from the osteoarthritis initiative

Introduction  

The aim was to investigate the relationship of cartilage loss (change in medial femorotibial cartilage thickness measured with magnetic resonance imaging (MRI)) with compartment-specific baseline radiographic findings and MRI cartilage morphometry features, and to identify which baseline features can be used for stratification of fast progressors.     

Post-translational aging of proteins in osteoarthritic cartilage and synovial fluid as measured by isomerized aspartate

Introduction  

Aging proteins undergo non-enzymatic post-translational modification, including isomerization and racemization. We hypothesized that cartilage with many long-lived components could accumulate non-enzymatically modified amino acids in the form of isomerized aspartate and that its liberation due to osteoarthritis (OA)-related cartilage degradation could reflect OA severity.     

Subchondral bone microstructural damage by increased remodelling aggravates experimental osteoarthritis preceded by osteoporosis

Introduction  

Osteoporosis (OP) increases cartilage damage in a combined rabbit model of OP and osteoarthritis (OA). Accordingly, we assessed whether microstructure impairment at subchondral bone aggravates cartilage damage in this experimental model.     

Inflammatory mediators and cartilage biomarkers in synovial fluid after a single inflammatory insult: a longitudinal experimental study

Introduction  

Inflammation is an important feature of many joint diseases, and levels of cartilage biomarkers measured in synovial fluid may be influenced by local inflammatory status. Little is known about the magnitude and time course of inflammation-induced changes in cartilage tissue turnover as measured in vivo by synovial fluid markers. We aimed to study temporal changes in concentrations of inflammatory mediators, matrix metalloproteinase activity and cartilage biomarkers over 1 week in joints with experimentally induced inflammation.     

Local adherent technique for transplanting mesenchymal stem cells as a potential treatment of cartilage defect

Introduction  

Current cell therapy for cartilage regeneration requires invasive procedures, periosteal coverage and scaffold use. We have developed a novel transplantation method with synovial mesenchymal stem cells (MSCs) to adhere to the cartilage defect.     

In vitro model for the analysis of synovial fibroblast-mediated degradation of intact cartilage

Introduction  

Activated synovial fibroblasts are thought to play a major role in the destruction of cartilage in chronic, inflammatory rheumatoid arthritis (RA). However, profound insight into the pathogenic mechanisms and the impact of synovial fibroblasts in the initial early stages of cartilage destruction is limited. Hence, the present study sought to establish a standardised in vitro model for early cartilage destruction with native, intact cartilage in order to analyse the matrix-degrading capacity of synovial fibroblasts and their influence on cartilage metabolism.     

Cartilage degradation is fully reversible in the presence of aggrecanase but not matrix metalloproteinase activity

Introduction  

Physiological and pathophysiological cartilage turnover may coexist in articular cartilage. The distinct enzymatic processes leading to irreversible cartilage damage, compared with those needed for continuous self-repair and regeneration, remain to be identified. We investigated the capacity of repair of chondrocytes by analyzing their ability to initiate an anabolic response subsequent to three different levels of catabolic stimulation.     

Antirheumatic drug response signatures in human chondrocytes: potential molecular targets to stimulate cartilage regeneration

Introduction  

Rheumatoid arthritis (RA) leads to progressive destruction of articular cartilage. This study aimed to disclose major mechanisms of antirheumatic drug action on human chondrocytes and to reveal marker and pharmacological target genes that are involved in cartilage dysfunction and regeneration.     

Joint and tendon subclinical involvement suggestive of gouty arthritis in asymptomatic hyperuricemia: an ultrasound controlled study

Introduction  

In this study, we aimed to investigate ultrasonographic (US) changes suggestive of gouty arthritis in the hyaline cartilage, joints and tendons from asymptomatic individuals with hyperuricemia.     

Relative percentage and zonal distribution of mesenchymal progenitor cells in human osteoarthritic and normal cartilage

Introduction  

Mesenchymal stem cells (MSC) are highly attractive for use in cartilage regeneration. To date, MSC are usually recruited from subchondral bone marrow using microfracture. Recent data suggest that isolated cells from adult human articular cartilage, which express the combination of the cell-surface markers CD105 and CD166, are multi-potent mesenchymal progenitor cells (MPC) with characteristics similar to MSC. MPC within the cartilage matrix, the target of tissue regeneration, may provide the basis for in situ regeneration of focal cartilage defects. However, there is only limited information concerning the presence/abundance of CD105⁺/CD166⁺ MPC in human articular cartilage. The present study therefore assessed the relative percentage and particularly the zonal distribution of cartilage MPC using the markers CD105/CD166.     

Intradiscal transplantation of synovial mesenchymal stem cells prevents intervertebral disc degeneration through suppression of matrix metalloproteinase-related genes in nucleus pulposus cells in rabbits

Introduction  

Synovial mesenchymal stem cells (MSCs) have high proliferative and chondrogenic potentials, and MSCs transplanted into the articular cartilage defect produce abundant extracellular matrix. Because of similarities between the articular cartilage and the intervertebral disc cartilage, synovial MSCs are a potential cell source for disc regeneration. Here, we examined the effect of intradiscal transplantation of synovial MSCs after aspiration of nucleus pulposus in rabbits.     

Key regulatory molecules of cartilage destruction in rheumatoid arthritis: an <Emphasis Type="Italic">in vitro</Emphasis>study

Background  

Rheumatoid arthritis (RA) is a chronic, inflammatory and systemic autoimmune disease that leads to progressive cartilage destruction. Advances in the treatment of RA-related destruction of cartilage require profound insights into the molecular mechanisms involved in cartilage degradation. Until now, comprehensive data about the molecular RA-related dysfunction of chondrocytes have been limited. Hence, the objective of this study was to establish a standardized in vitro model to profile the key regulatory molecules of RA-related destruction of cartilage that are expressed by human chondrocytes.