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PubMed1992

Retinal pigment epithelium-stromal interactions modulate hyaluronic acid deposition.

Hyaluronic acid (HA) is a major component of the extracellular matrix (ECM) and is particularly prominent in various structures of the eye. Choroidal mesenchymal fibroblasts (CHM) and fetal retinal pigment epithelial (fRPE) cells were cultured individually and in cocultivation, as a paradigm for ocular stromal-epithelial interactions. Such interactions are thought to be a key mechanism for the modulation of the ECM and of HA deposition in the region of Bruch's membrane and related structures. In cocultivation, increased levels of HA production were observed, more than the sum of the two cell types grown individually. Conditioned medium from fRPE cultures placed over CHM cells was able to enhance production in such cells several-fold, demonstrating that cell-cell contact was not needed for this enhanced production. On the other hand, when conditioned medium from CHM fibroblasts was added to the fetal RPE cells, no increase in HA production was observed. A soluble HA-stimulating factor apparently released by fRPE cells in a paracrine manner enhanced HA production in CHM cells. The fRPE cell-conditioned media was unable to exert this effect on the fRPE cells themselves. The fRPE cells may lack the appropriate receptor. Alternatively, they may not have the biosynthetic machinery for augmented HA production.

Cell Communication↗
PubMed2006

Synthesis and degradation test of hyaluronic acid hydrogels.

Hyaluronic acid (HA) hydrogels prepared with three different crosslinking reagents were assessed by in vitro and in vivo degradation tests for various tissue engineering applications. Adipic acid dihydrazide grafted HA (HA-ADH) was synthesized and used for the preparation of methacrylated HA (HA-MA) with methacrylic anhydride and thiolated HA (HA-SH) with Traut's reagent (imminothiolane). (1)H NMR analysis showed that the degrees of HA-ADH, HA-MA, and HA-SH modification were 69, 29, and 56 mol%, respectively. HA-ADH hydrogel was prepared by the crosslinking with bis(sulfosuccinimidyl) suberate (BS(3)), HA-MA hydrogel with dithiothreitol (DTT) by Michael addition, and HA-SH hydrogel with sodium tetrathionate by disulfide bond formation. According to in vitro degradation tests, HA-SH hydrogel was degraded very fast, compared to HA-ADH and HA-MA hydrogels. HA-ADH hydrogel was degraded slightly faster than HA-MA hydrogel. Based on these results, HA-MA hydrogels and HA-SH hydrogels were implanted in the back of SD rats and their degradation was assessed according to the pre-determined time schedule. As expected from the in vitro degradation test results, HA-SH hydrogel was in vivo degraded completely only in 2 weeks, whereas HA-MA hydrogels were degraded only partially even in 29 days. The degradation rate of HA hydrogels were thought to be controlled by changing the crosslinking reagents and the functional group of HA derivatives. In addition, the state of HA hydrogel was another factor in controlling the degradation rate. Dried HA hydrogel at 37 degrees C for a day resulted in relatively slow degradation compared to the bulk HA hydrogel. There was no adverse effect during the in vivo tests.

Adipates↗
PubMed2001

Pro-inflammatory activity of contaminating DNA in hyaluronic acid preparations.

Hyaluronic acid (HA), an abundant non-sulfated glycosaminoglycan component of the extracellular matrix, has applications in drug delivery, tissue engineering and as an ingredient in cosmetics. HA preparations containing high-molecular-weight polymers are also used in the treatment of inflammatory disorders such as arthritis and interstitial cystitis. Low-molecular-weight fragments derived from HA have been reported to induce pro-inflammatory cytokines such as IL-12 and TNF-alpha, and could therefore potentially exacerbate existing inflammation. We therefore examined the pro-inflammatory activity of HA preparations, since inflammatory reactions are known to occur following administration of HA. We tested low-molecular-weight fragments obtained from seven different HA preparations, either by sonication (approximately equals 3 x 10(5) Da) or by hyaluronidase digestion (approximately equals 1 x 10(4) Da), for the ability to induce the synthesis of IL-12 and TNF-alpha by human monocytic cells. We found that two of the seven HA preparations tested stimulated the synthesis of IL-12 and TNF-alpha by human monocytic cells. We unexpectedly found that the induction of IL-12 and TNF-alpha by these HA preparations was not due to their degradation to low-molecular-weight fragments, since their native high-molecular-weight forms possessed the same ability to stimulate IL-12 and TNF-alpha synthesis, but was due to the presence of contaminating DNA. Treatment of these two HA preparations with deoxyribonuclease I abrogated or reduced the induction of IL-12 and TNF-alpha. It is clear from this study that HA preparations can induce the synthesis of pro-inflammatory cytokines by monocytes. The ability of HA to act as a pro-inflammatory mediator may not, however, be related to the presence of low-molecular-weight HA fragments, but to the presence of DNA. The presence of pro-inflammatory DNA in HA preparations should be evaluated before its use, not only for the treatment of patients with inflammatory disorders, but also before many other applications.

Adjuvants, Immunologic↗
PubMed2006

[Reduction of arthrosis associated knee pain through a single intra-articular injection of synthetic hyaluronic acid].

AIM: Conventional hyaluronic acids need three to five injections for therapeutic success, whereas Durolane), a synthetic hyaluronic acid, needs only a single injection. Clinical outcome using Durolane should be compared with the results of studies using hyaluronic acids or glucocorticoids. METHOD: Fifty patients with primary gonarthrosis stages I-III (Kellgren Score) were investigated for knee function, pain intensity, and quality of life. The knee and osteoarthritis outcome score (KOOS), visual analogue scale (VAS), and European quality of live score (EQ-5D), as well as motion of the knee were measured. Patients were investigated before, and 2, and 24 weeks after injection. RESULTS: Two weeks after injection, the subjective function of knee and quality of life had increased significantly. In the following 22 weeks, all parameters increased significantly (quality of life and activity +19%; range of motion active 109 vs. 115 degrees ; pain, 55 vs. 41 mm (VAS); all p<0.01). CONCLUSION: We conclude that a single injection of Durolane can reduce arthrosis associated knee pain sufficiently. Our data are comparable with those published in clinical studies using other hyaluronic acids. The effects of Durolane are delayed but more sustained compared than those found for glucocorticoids. Because of the single injection, we see an advantage in using Durolane compared to other conventional hyaluronic acids and glucocorticoids.

Activities of Daily Living↗
PubMed1982

Effect of metal chelators and antiinflammatory drugs on the degradation of hyaluronic acid.

Degradation of hyaluronic acid (measured viscometrically) by oxygen-derived free radicals (ODFR) generated 1) by autoxidation of ferrous EDTA chelates and 2) enzymatically by xanthine oxidase and hypoxanthine (XO/HX) was studied. Degradation of hyaluronic acid by XO/HX was strongly inhibited by superoxide dismutase and catalase, whereas degradation of hyaluronic acid by autoxidation of ferrous ions was weakly inhibited by catalase and unaffected by superoxide dismutase. Both ODFR-producing systems were inhibited by hydroxyl radical scavengers, suggesting that hydroxyl radical was the proximate damaging species in both systems. Penicillamine at concentrations of 1-5 mM stimulated hyaluronic acid degradation by ferrous EDTA chelates but inhibited degradation by the XO/HX system. Higher concentrations of penicillamine and all concentrations studied (1-100 mM) of other antiinflammatory drugs (chloroquine, gold sodium thiomalate, and salicylate) inhibited hyaluronic acid degradation by both the autoxidation and enzymatic ODFR-producing systems, with inhibitory potency similar to that seen with known hydroxyl radical scavengers. Both systems serve as in vitro models of ODFR-mediated tissue damage which may occur in vivo at sites of inflammation.

Animals↗
PubMed1991

Hyaluronic acid synthesis is absent in normal human endothelial cells irrespective of hyaluronic acid synthetase inhibitor activity, but is significantly high in transformed cells.

The characteristics of glycosaminoglycan (GAG) synthesis in normal and transformed human endothelial cells were analyzed by the incorporation of [3H]glucosamine and by the activities of GAG synthetases. The GAG synthesized by normal endothelial cells consisted of mainly heparan sulfate (HS) and chondroitin sulfate/dermatan sulfate but little hyaluronic acid (HA) (less than 1%). The characteristics of GAG synthesis by normal cells reflected the synthetic enzyme activities for each individual GAG: the activity of HA synthetase was very low. In spite of this, the activity of HA synthetase inhibitor, induced in growth-retarded fibroblasts with low HA synthetase activity (Matuoka et al. (1987 J. Cell Biol., 104, 1105-1115), was very low in endothelial cells. In contrast to normal cells, transformed endothelial (ECV304) cells synthesized mainly HA (62% of total GAGs). These findings suggest that the regulatory system of GAG metabolism is cell type specific, and that transformation is accompanied by high levels of HA synthesis in endothelial cells.

Acetylglucosamine↗
PubMedDate not supplied

Hyaluronic acid fillers.

Although hyaluronic acids are a relatively new treatment for facial lines and wrinkles, they have provided numerous advances in the area of cosmetic surgery. This article discusses the inherent properties of hyaluronic acid fillers that make them ideal for treatment of facial lines. It encompasses a review of the current literature on U.S. Food and Drug Administration-approved hyaluronic acid fillers and the role that each of these fillers currently has in facial cosmetics. This article also discusses the potential pitfalls and adverse effects that can be associated with using hyaluronic acids for filling facial lines. Finally, it serves as an overview of current techniques for clinical assessment of patients as well as administration and treatment of facial lines and wrinkles.

Biocompatible Materials↗
PubMed1995

Effects of hyaluronic acid on the release of cartilage matrix proteoglycan and fibronectin from the cell matrix layer of chondrocyte cultures: interactions between hyaluronic acid and chondroitin sulfate glycosaminoglycan.

Hyaluronic acid (HA) of large sizes suppressed the release of cartilage matrix proteoglycan, fibronectin, and other macromolecules from the cell matrix layer of chondrocyte cultures, perhaps because HA of large sizes formed a viscous barrier in the matrix by its interactions with other extracellular matrix macromolecules. To test this possibility, we determined the viscosity of solutions containing HA of various sizes in the presence of proteoglycan monomer or chondroitin sulfate glycosaminoglycan (GAG). Not only the monomer but also chondroitin sulfate increased the viscosity of HA solutions, depending on the size of HA. These findings suggest that HA of large sizes increases the viscosity near the surface of articular cartilage by sugar-sugar and by sugar-protein interactions and that the increase of viscosity is involved in the protective action of HA on arthritic cartilage.

Animals↗
PubMedDate not supplied

Hyaluronic acid produced by human synovial fibroblasts. Effect of polyinosinic-polycytidylic acid (poly I:C) and interferon.

Poly I:C (polyinosinic-polycytidylic acid) stimulated hyaluronic acid production by rheumatoid and non-rheumatoid human synovial fibroblasts. Stimulation was dose dependent and was inhibited by acetylsalicyclic acid and indomethacin. Poly I and Poly C, when separately added, had no stimulatory effect on hyaluronic acid production, and Poly A:U had only a slight effect on this parameter. Cells grown with Poly I:C were virus resistant and interferon was detected in their medium. Human interferon had also a dose-dependent stimulatory effect on hyaluronic acid production by synovial cells. A possible interferon-mediated relationship between virus infection and pathologic accumulation of joint fluid is suggested.

Arthritis, Rheumatoid↗
PubMed1981

The role of superoxide and hydroxyl radicals in the degradation of hyaluronic acid induced by metal ions and by ascorbic acid.

Purified commercial hyaluronic acid contains significant amounts of iron. Addition of Fe2+ to solutions of it causes depolymerization, which is inhibited by catalase and scavengers of the hydroxyl radical (. OH) but not by superoxide dismutase. Fe3+ is ineffective. Ascorbic acid also depolymerizes hyaluronic acid, apparently because it can reduce Fe3+ in the reaction mixtures to Fe2+. Ascorbate-induced depolymerization is inhibited by the specific iron chelator desferrioxamine, by catalase, and by scavengers of the hydroxyl radical. The relevance of these observations to rheumatoid arthritis and inflammatory joint diseases is discussed.

Arthritis, Rheumatoid↗
PubMed1988

Localization of epidermal hyaluronic acid using the hyaluronate binding region of cartilage proteoglycan as a specific probe.

Hyaluronate is actively synthesized by cultured epidermis and dermis, but no direct histological data have been available about its localization in normal human skin. A hyaluronate-specific biotinylated probe, prepared from the hyaluronate binding region of cartilage proteoglycan, was applied to human skin sections and visualized using the biotin-avidin-peroxidase system. The specificity of this staining was confirmed by hyaluronidase predigestion and by hyaluronate-derived oligosaccharides added to the staining solution. All dermis showed diffuse binding of the probe, but the highest staining intensity was observed in the epidermal intercellular spaces. The stainability extended from basal cells to the middle layers of the epidermis, whereas the granular layer and stratum corneum were completely negative. Also, the basal side of basal cells (basement membrane) did not bind the hyaluronate probe. The abundance of hyaluronate on surfaces and intercellular spaces of the spinous cells is suggested to have an important role in the physiology of human epidermis.

Cartilage↗