scholarly journals Marathon Running Increases Synthesis and Decreases Catabolism of Joint Cartilage Type II Collagen Accompanied by High-Energy Demands and an Inflamatory Reaction

2021 ◽  
Vol 12 ◽  
Author(s):  
José A. Hernández-Hermoso ◽  
Lexa Nescolarde ◽  
Emma Roca ◽  
Elena Revuelta-López ◽  
Jordi Ara ◽  
...  
Keyword(s):  
Inflammatory Reaction ◽  
Matrix Protein ◽  
Chondroitin Sulphate ◽  
Type Ii Collagen ◽  
Serum Levels ◽  
High Energy ◽  
Marathon Running ◽  
Type Ii ◽  
Energy Demands ◽  
And Cartilage

Objective: To determine the effect of marathon running on serum levels of inflammatory, high energy, and cartilage matrix biomarkers and to ascertain whether these biomarkers levels correlate.Design: Blood samples from 17 Caucasian male recreational athletes at the Barcelona Marathon 2017 were collected at the baseline, immediately and 48 h post-race. Serum C reactive protein (CRP), creatin kinase (CK), and lactate dehydrogenase (LDH) were determined using an AU-5800 chemistry analyser. Serum levels of hyaluronan (HA), cartilage oligomeric matrix protein (COMP), aggrecan chondroitin sulphate 846 (CS846), glycoprotein YKL-40, human procollagen II N-terminal propeptide (PIINP), human type IIA collagen N-propeptide (PIIANP), and collagen type II cleavage (C2C) were measured by sandwich enzyme-linked immune-sorbent assay (ELISA).Results: Medians CK and sLDH levels increased (three-fold, two-fold) post-race [429 (332) U/L, 323 (69) U/L] (p < 0.0001; p < 0.0001) and (six-fold, 1.2-fold) 48 h post-race [658 (1,073) U/L, 218 (45) U/L] (p < 0.0001; p < 0.0001). Medians CRP increased (ten-fold) after 48 h post-race [6.8 (4.1) mg/L] (p < 0.0001). Mean sHA levels increased (four-fold) post-race (89.54 ± 53.14 ng/ml) (p < 0.0001). Means PIINP (9.05 ± 2.15 ng/ml) levels increased post-race (10.82 ± 3.44 ng/ml) (p = 0.053) and 48 h post-race (11.00 ± 2.96 ng/ml) (p = 0.001). Mean sC2C levels (220.83 ± 39.50 ng/ml) decreased post-race (188.67 ± 38.52 ng/ml) (p = 0.002). In contrast, means COMP, sCS846, sPIIANP, and median sYKL-40 were relatively stable. We found a positive association between sCK levels with sLDH pre-race (r = 0.758, p < 0.0001), post-race (r = 0.623, p = 0.008) and 48-h post-race (r = 0.842, p < 0.0001); sHA with sCRP post-race vs. 48 h post-race (r = 0.563, p = 0.019) and sPIINP with sCK pre-race vs. 48-h post-race (r = 0.499, p = 0.044) and with sLDH 48-h pre-race vs. post-race (r = 0.610, p = 0.009) and a negative correlation of sPIIANP with sCRP 48-h post-race (r = −0.570, p = 0.017).Conclusion: Marathon running is an exercise with high-energy demands (sCK and sLDH increase) that provokes a high and durable general inflammatory reaction (sCRP increase) and an immediately post-marathon mechanism to protect inflammation and cartilage (sHA increase). Accompanied by an increase in type II collagen cartilage fibrils synthesis (sPIINP increase) and a decrease in its catabolism (sC2C decrease), without changes in non-collagenous cartilage metabolism (sCOMP, sC846, and sYKL-40). Metabolic changes on sPIINP and sHA synthesis may be related to energy consumption (sCK, sLDH) and the inflammatory reaction (sCRP) produced.

scholarly journals PSVI-33 Undenatured type II collagen mitigates inflammation and cartilage degeneration in healthy untrained Labrador retrievers after exercise

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 313-314
Author(s):  
Jessica L Varney ◽  
Jason W Fowler ◽  
Craig N Coon
Keyword(s):  
Matrix Protein ◽  
Inflammatory Marker ◽  
Type Ii Collagen ◽  
Cartilage Degeneration ◽  
Type Ii ◽  
Cell Counts ◽  
Healthy Dogs ◽  
Labrador Retrievers ◽  
And Cartilage ◽  
Undenatured Type Ii Collagen

Abstract Exercise can cause microtrauma in the tissue and joints of dogs, resulting in a cycle of inflammation and discomfort even in healthy dogs. The aim of this trial was to evaluate the effect of undenatured type II collagen supplemented on inflammation and cartilage degeneration after exercise in untrained, healthy dogs. In this experiment, 40 healthy Labrador retrievers (20m/20f; Range-5-12yrs; Avg-8yrs) were sorted into two groups: undenatured type II collagen group receiving 40mg UC-II® (10mg Collagen Type II/Min. 3% Undenatured Type II Collagen; Lonza Consumer Health, Inc.) and placebo (P) group receiving 40mg maltodextrin daily by capsule. After 2wks supplement loading, all dogs performed a 4.66 ± 0.34km endurance run. Blood was collected at baseline, 1h pre-run, and 24h post-run for hematology/biomarkers including interleukin-6 (IL-6) as an inflammatory marker and cartilage oligomeric matrix protein (COMP) as a cartilage degeneration marker. Undenatured type II collagen supplemented dogs had significantly lower IL-6 vs P at post-run (p< 0.01), as well as significant decreases from pre to post-run (P = 0.03), vs P with no significant change (P = 0.16). COMP was significantly lower in undenatured type II collagen supplemented dogs at 24h post-run compared to pre-run (P = 0.02), with P dogs having no significant differences between timepoints (P = 0.24). At both 1h pre- and 24h post-run undenatured type II collagen supplemented dogs had no significant increases in neutrophil:lymphocyte ratio (NLR; inflammatory marker), but P dogs had significantly higher NLR compared to baseline (P = 0.01). NLR was also significantly lower in undenatured type II collagen supplemented dogs compared to P dogs at pre-run (P < 0.01). Undenatured type II collagen supplemented dogs showed significantly lower white blood cell counts after supplementation compared to P dogs (P < 0.05) (Table 1). In summary, untrained Labrador retrievers supplemented with undenatured type II collagen had decreased inflammation and cartilage degeneration compared to non-supplemented dogs after exercise.

Gene regulation during cartilage differentiation: temporal and spatial expression of link protein and cartilage matrix protein in the developing limb

Development ◽  
1989 ◽  
Vol 107 (1) ◽  
pp. 23-33
Author(s):  
N.S. Stirpe ◽  
P.F. Goetinck
Keyword(s):  
Matrix Protein ◽  
Core Protein ◽  
Type Ii Collagen ◽  
Cartilage Matrix ◽  
Type Ii ◽  
Spatial Expression ◽  
Link Protein ◽  
Genes Encoding ◽  
Temporal And Spatial ◽  
And Cartilage

The temporal and spatial expression of link protein and cartilage matrix protein genes was defined during chondrogenesis in the developing chick embryonic wing bud, using RNA in situ hybridization. For comparison, the expression of genes encoding type II collagen and cartilage proteoglycan core protein was also examined. Link protein transcripts are first detected at stage 25 of Hamburger and Hamilton, together with proteoglycan core protein transcripts. Type II collagen transcripts were first detected as early as stage 23 whereas cartilage matrix protein transcripts could not be detected before stage 26. The results of the study indicate that the temporal expression of the genes for cartilage matrix protein and type II collagen are independent of each other and also independent of that for link protein and proteoglycan core protein.

scholarly journals Undenatured type II collagen mitigates inflammation and cartilage degeneration in healthy Labrador Retrievers during an exercise regimen

2021 ◽  
Author(s):  
J L Varney ◽  
J W Fowler ◽  
C N Coon
Keyword(s):  
Matrix Protein ◽  
Type Ii Collagen ◽  
Cartilage Degeneration ◽  
Mean Corpuscular Hemoglobin ◽  
Type Ii ◽  
Exercise Regimen ◽  
Collagen Group ◽  
Labrador Retrievers ◽  
And Cartilage ◽  
Undenatured Type Ii Collagen

Abstract The aim of this experiment was to evaluate the effect of undenatured type II collagen supplementation on inflammation and cartilage degeneration after exercise in healthy dogs. Forty healthy Labrador Retrievers (20 male/20 female; Range 5-12yrs; Avg 8yrs) were sorted into two groups: undenatured type II collagen group receiving 40mg UC-II (10mg Collagen Type II/Min. 3% Undenatured Type II Collagen; Lonza Consumer Health, Inc.) and placebo group receiving 40mg maltodextrin daily by capsule. After 2-weeks loading, all dogs began an 11-week endurance exercise regimen consisting of two weekly runs, starting at 5km and increasing incrementally to 8km, with one final 16km run. Blood samples were collected at baseline, pre and post first 5km run, and pre and post 16km run. Activity per kilometer was greater in male undenatured type II collagen vs male placebo over all runs (P=0.004), and average moving speed was greater in all undenatured type II collagen dogs compared with placebo over all runs (P<0.001). Hematology analysis indicated that during the first insult, undenatured type II collagen dogs had a greater lymphocyte count (P<0.001) and lymphocyte percentage (P=0.001) vs placebo dogs. Undenatured type II collagen dogs had a lesser neutrophil percentage (P=0.042) and neutrophil to lymphocyte ratios (P=0.001) compared to placebo dogs. For the final insult, undenatured type II collagen dogs had greater lymphocyte percentage (P=0.013) and lesser mean corpuscular hemoglobin concentration (P=0.043) compared with placebo dogs. Both groups had significant changes between timepoints for several hematological parameters. Biomarker IL-6 was lesser in undenatured type II collagen dogs compared with placebo at post 5km (P=0.037). Cartilage oligomeric matrix protein (COMP) was lesser in undenatured type II collagen dogs at post 16km (P=0.023), and only the placebo dogs had a significant increase in COMP from pre to post 16km (P=0.021). In summary, Labrador Retrievers supplemented with undenatured type II collagen had decreased inflammation and cartilage degeneration compared with non-supplemented dogs during exercise.

Healing of Circular Defects in the Rabbit Medial Meniscus Can Occur Spontaneously and Is not Improved by Intra-Articular Hyaluronic Acid

1996 ◽  
Vol 09 (02) ◽  
pp. 60-5 ◽  
Author(s):  
N. Hope ◽  
P. Ghosh ◽  
S. Collier
Keyword(s):  
Hyaluronic Acid ◽  
Medial Meniscus ◽  
Chondroitin Sulphate ◽  
Rabbit Model ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Keratan Sulphate ◽  
Meniscal Healing ◽  
Meniscus Healing ◽  
Made In

SummaryThe aim of this study was to determine the effects of intra-articular hyaluronic acid on meniscal healing. Circular defects, 1.0 mm in diameter, were made in the anterior third of the medial meniscus in rabbits. In one joint, 0.4 ml hyaluronic acid (Healon®) was instilled, and in the contralateral (control) joint, 0.4 ml Ringer’s saline. Four rabbits were killed after four, eight and 12 weeks and the menisci examined histologically. By eight weeks most of the lesions had healed by filling with hyaline-like cartilage. Healing was not improved by hyaluronic acid treatment. The repair tissue stained strongly with alcian blue, and the presence of type II collagen, keratan sulphate, and chondroitin sulphate was demonstrated by immunohistochemical localisation. In contrast to the circular defects, longitudinal incisions made in the medial menisci of a further six rabbits did not show any healing after 12 weeks, indicating that the shape of the lesion largely determined the potential for healing.The effect of hyaluronic acid on meniscal healing was tested in a rabbit model. With one millimeter circular lesions in the medial meniscus, healing by filling with hyalinelike cartilage was not significantly affected by the application of hyaluronic acid intra-articularly at the time of surgery, compared to saline controls, as assessed histologically four, eight and 12 weeks after the operation.

scholarly journals 113 Effects of aquatic conditioning in young horses. I. Markers of inflammation and cartilage metabolism

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 86-87
Author(s):  
Brittany L Silvers ◽  
Jessica L Leatherwood ◽  
Brian D Nielsen ◽  
Carolyn E Arnold ◽  
Brandon Dominguez ◽  
...  
Keyword(s):  
Treadmill Exercise ◽  
Random Effect ◽  
Type Ii Collagen ◽  
Type I ◽  
Type Ii ◽  
Treatment Groups ◽  
Cartilage Metabolism ◽  
Markers Of Inflammation ◽  
Young Horses ◽  
And Cartilage

Abstract Aquatic treadmills improve range of motion and increase muscular strength in mature horses; however, effects of buoyancy on inflammation and cartilage metabolism in young horses are not well investigated. Therefore, thirty Quarter Horse yearlings of similar breeding were stratified by age, BW, and sex and randomly assigned to one of three treatment groups during a 140-d trial to evaluate the influence of aquatic vs. dry exercise on joint inflammation and cartilage metabolism in young horses transitioning to an advanced workload. Treatment groups included non-exercise control (CON; n = 10), dry treadmill exercise (DRY; n = 10), or aquatic treadmill exercise (H2O; n = 10; water at 60% wither height). Animals were housed in individual stalls and allowed turnout for a minimum of 10 h/d. During Phase I, DRY and H2O walked on treadmills 30 min/d, 5 d/wk from d 0 to d 112. Phase II represented transition to an advanced workload 5d/wk for 28 d (Table 1). Every 28 d following exercise, synovial fluid samples were collected and analyzed for prostaglandin E2 (PGE2), collagenase cleavage neopeptide (C2C), collagenase of type I and type II collagen (C1,2C), and carboxypeptide of type II collagen (CPII) using commercial ELISA kits. All data were analyzed using PROC MIXED of SAS, including random effect of horse within treatment, and repeated effect of day. Baseline treatment differences were accounted for using a covariate structure. There were no treatment ′ day interactions of synovial inflammation or markers of cartilage metabolism; however, there was an effect of day for each selected marker (P < 0.03). Changes in biomarkers of cartilage turnover in horses exercised at the walk, whether dry or aquatic, could not be distinguished from horses with access to turnout alone. This indicates that there are no negative effects of buoyancy on cartilage metabolism in yearlings transitioned from aquatic exercise to 28-d advanced workload.

scholarly journals Osthole Inhibits Proliferation and Induces Catabolism in Rat Chondrocytes and Cartilage Tissue

2015 ◽  
Vol 36 (6) ◽  
pp. 2480-2493 ◽  
Author(s):  
Guoqing Du ◽  
Yi Song ◽  
Lei Wei ◽  
Linghui Li ◽  
Xuezong Wang ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Cartilage Explants ◽  
Cartilage Tissue ◽  
Blue Staining ◽  
Marker Genes ◽  
Dependent Manner ◽  
Type Ii ◽  
Expression Levels ◽  
Safranine O ◽  
And Cartilage

Background/Aims: Cartilage destruction is thought to be the major mediator of osteoarthritis. Recent studies suggest that inhibition of subchrondral bone loss by anti-osteoporosis (OP) drug can protect cartilige erosion. Osthole, as a promising agent for treating osteoporosis, may show potential in treating osteoarthritis. The purpose of this study was to investigate whether Osthole affects the proliferation and catabolism of rat chondrocytes, and the degeneration of cartilage explants. Methods: Rat chondrocytes were treated with Osthole (0 μM, 6.25 μM, 12.5 μM, and 25 μM) with or without IL1-β (10ng/ml) for 24 hours. The expression levels of type II collagen and MMP13 were detected by western Blot. Marker genes for chondrocytes (A-can and Sox9), matrix metalloproteinases (MMPs), aggrecanases (ADAMTS5) and genes implicated in extracellular matrix catabolism were evaluated by qPCR. Cell proliferation was assessed by measuring proliferating cell nuclear antigen (PCNA) expression and fluorescence activated cell sorter. Wnt7b/β-catenin signaling was also investigated. Cartilage explants from two-week old SD rats were cultured with IL-1β, Osthole and Osthole plus IL-1β for four days and glycosaminoglycan (GAG) synthesis was assessed with toluidine blue staining and Safranine O/Fast Green FCF staining, collagen type II expression was detected by immunofuorescence. Results: Osthole reduced expression of chondrocyte markers and increased expression of MMP13, ADAMTS5 and MMP9 in a dose-dependent manner. Catabolic gene expression levels were further improved by Osthole plus IL-1β. Osthole inhibited chondrocyte proliferation. GAG synthesis and type II collagen were decreased in both the IL-1β groups and the Osthole groups, and significantly reduced by Osthole plus IL-1β. Conclusions: Our data suggested that Osthole increases the catabolism of rat chondrocytes and cartilage explants, this effect might be mediated through inhibiting Wnt7b/β-catenin pathway.

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