Endogenous hydrogen sulfide production is reduced in OA cartilage. Possible contribution to the pathogenesis of OA

Vela-Anero, Á.; Gato-Calvo, L.; Ruiz-Romero, C.; Meijide-Faílde, Rosa; Blanco, Francisco J.; Burguera, Elena F.

doi:10.1016/j.joca.2015.02.563

Cited by 2 publications

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“…In contrast, Whiteman et al [36] and similar studies by our group did not reveal any differences in H 2 S concentration in serum between OA patients and healthy controls. On the contrary, we have preliminary evidence that indicates that H 2 S biosynthesis in OA joints might be reduced [35].…”

Section: Endogenous H 2 S and Rheumatic Diseasescontrasting

confidence: 53%

“…A recent publication reports that chondrocyte-like cells (chondrogenically differentiated mesenchymal pro-genitor cells, CH-MPCs) and primary human (h) Aes express both CBS and CTH, and that CTH is induced in both cell types by IL-lβ, TNF-α, IL-6 or lipopolysaccharide (LPS) treatment [34]. Our group bas found these three enzymes at mRNA and protein levels in cartilage, synovial membrane and subchondral bone from OA and normal patients [35]. Other studies have shown that synovial fluid (SF) H 2 S concentrations in patients with RA [36,37] or gout [37] were significantly higher than those in paired H 2 S plasma values and those in the SF of age-matched OA patients.…”

Section: Endogenous H 2 S and Rheumatic Diseasesmentioning

confidence: 65%

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Hydrogen Sulfide and Inflammatory Joint Diseases

Burguera

Meijide-Faílde

Blanco

2017

CDT

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Several authors have found that H2S exhibited anti-inflammatory, anti-catabolic and/or anti-oxidant effects in rodent models of acute arthritis and in in vitro models using human synoviocytes and articular chondrocytes from RA and OA tissues. The earliest studies used fast-dissolving salts, such as NaSH, but GYY4137, which produces H2S more physiologically, shortly appeared. More recently still, new H2S-forming compounds that target mitochondria have been synthesized. These compounds open exciting opportunities for investigating the role of H2S in cell bioenergetics, typically altered in arthritides. Positive results have also been obtained when H2S is administered as a sulphurous water bath, an option meriting further study. These findings suggest that exogenous supplementation of H2S may provide a viable therapeutic option for these diseases, particularly in OA.

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Section: Endogenous H 2 S and Rheumatic Diseasescontrasting

confidence: 53%

Section: Endogenous H 2 S and Rheumatic Diseasesmentioning

confidence: 65%

Hydrogen Sulfide and Inflammatory Joint Diseases

Burguera

Meijide-Faílde

Blanco

2017

CDT

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“…Additionally, several reports have also provided evidence that H 2 S biosynthesis or its endogenous levels are reduced or correlate with disease severity in some chronic pathologies such as hypertension [32], type II diabetes [33] or chronic obstructive pulmonary disease [34]. With respect to OA, our group has some preliminary evidence that H 2 S biosynthesis might be reduced in the osteoarthritic joint [35]. We believe this might be another factor contributing to the onset of OA, though more research is needed in this direction.…”

Section: Discussionmentioning

confidence: 65%

Long-term effects of hydrogen sulfide on the anabolic-catabolic balance of articular cartilage in vitro

et al. 2017

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Healthy cartilage maintenance relies on an equilibrium among the anabolic and catabolic processes in chondrocytes. With the onset of osteoarthritis (OA), increased interleukin (IL)-1β levels induce an inhibition of the synthesis of extracellular matrix (ECM) proteins, as well as an increase in proteases. This eventually leads to a predominance of the catabolic phenotype and the progressive loss of articular cartilage. Hydrogen sulfide (HS) is a small gaseous molecule recognized as the third endogenous gasotransmitter. When administered exogenously, it has shown anti-inflammatory and anti-catabolic properties in several in vitro and in vivo models. Here, OA cartilage disks were co-cultured in vitro with IL-1β (5 ng/ml) and NaSH or GYY4137 (200 or 1000 μM) for 21 days. The ability of these two HS-producing compounds to avoid long term extracellular matrix (ECM) destruction was evaluated. We used a glycosaminoglycan (GAG) quantification kit histology and immunohistochemistry (IHC) to evaluate matrix proteins degradation and matrix metalloproteinases (MMP) abundance. Through the GAGs quantification assay, safranin O (S-O) and toluidine blue (TB) stains, and keratan/chondroitin sulfate (KS/ChS) IHCs it was shown that co-stimulation with HS-forming reagents effectively avoided GAGs destruction. Both Masson's trichrome (MT) stain and collagen (col) type II IHC, as well as aggrecan (agg) IHC demonstrated that not only were these proteins protected but even promoted, their abundance being higher than in the basal condition. Further, stains also demonstrated that positivity in the inter-territorial and intra-cellular for the different matrix components were rescued, suggesting that NaSH and GYY4137 might also have pro-anabolic effects. In addition, a clear protective effect against the increased MMPs levels was seen, since increased MMP3 and 13 levels were subsequently reduced with the co-stimulation with sulfide compounds. In general, GYY4137 was more effective than NaSH, and increasing the dose improved the results. This study demonstrates that HS anti-catabolic effects, which had been previously proven in short-term (24-48 h) in vitro cellular models, are maintained over time directly in OA cartilage tissue.

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Endogenous hydrogen sulfide production is reduced in OA cartilage. Possible contribution to the pathogenesis of OA

Abstract: In contralateral knees, baseline lower peak hip flexion moment Lower peak knee extension moment in the 1st half of stance phase and lower peak knee adduction moment in the 2nd half of stance phase were significantly correlated with increased cartilage T1p at 12-months.

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Hydrogen Sulfide and Inflammatory Joint Diseases

Hydrogen Sulfide and Inflammatory Joint Diseases

Long-term effects of hydrogen sulfide on the anabolic-catabolic balance of articular cartilage in vitro

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