Proteoglycan synthesis is increased in cells with …

T1 - Proteoglycan synthesis in increased in cells with impaired clathrin-dependent endocytosis

Proteoglycan Synthesis by Bovine Keratocytes and …

In summary, polyhexanide has more toxic potential than hydrogen peroxide. Both antiseptics inhibit the proteoglycan synthesis of human chondrocytes. Based on the fact that the cell number and morphology were not altered by the substances at the examined concentrations, the lower intensity of Alcian blue staining of treated chondrocytes indicates a direct decrease of cartilage specific matrix synthesis by polyhexanide more than by hydrogen peroxide and control.

T1 - Regulation of vascular proteoglycan synthesis by metabolic factors associated with diabetes

Proteoglycan synthesis in increased in cells with …

T1 - Chondroitin sulfate proteoglycan synthesis and reutilization of β-d-xyloside-initiated chondroitin/dermatan sulfate glycosaminoglycans in fetal kidney branching morphogenesis

T1 - Regulation of Proteoglycan Synthesis by Leukotriene D4 and Epidermal Growth Factor in Bronchial Smooth Muscle Cells

The 'response to retention' hypothesis of atherogenesis proposes that proteoglycans bind and retain low-density lipoproteins (LDL) in the vessel wall. Platelet-derived growth factor (PDGF) is strongly implicated in atherosclerosis and stimulates proteoglycan synthesis. Here we investigated the action of the PDGF receptor inhibitor imatinib on PDGF-mediated proteoglycan biosynthesis in vitro, lipid deposition in the aortic wall in vivo and the carotid artery ex vivo. In human vSMCs, imatinib inhibited PDGF mediated 35S-SO 4 incorporation into proteoglycans by 31% (P -/- mice, imatinib reduced total lipid staining area by ∼31% (P

This page discusses the structure and function of the glycosaminoglycans and proteoglycans and ..


Proteoglycan Synthesis and Golgi Organization in …

At present no quantitative non-invasive method for determining the anabolic (building up) and catabolic (breaking down) activity of NSAIDs on human cartilage in vivo exists. Most information on the effects of NSAIDs on the turnover of extra-cellular matrix macromolecules comes from short-term organ culture studies. Initial evaluations into the pathophysiology of osteoarthritis concentrated on the effects of NSAIDs on glycosaminoglycan synthesis. It was established that in all but the most severe cases of osteoarthritis, the chondrocyte response to proteoglycan depletion was an increase in glycosaminoglycan synthesis.72, 73 One of the first to show that NSAIDs diminished glycosaminoglycan synthesis in aged human cartilage cells (taken during hip surgery) in vitro was a research group from the University of Sydney in 1976.74 J.T. Dingle, led several of the follow-up studies on the effects of NSAIDs on human cartilage metabolism. The initial studies revealed significant declines in glycosaminoglycan synthesis in both normal and osteoarthritic human cartilages.75 (See Figure 11.)

Proteoglycan synthesis in two murine bone marrow …

In another study on canine articular cartilage, these researchers found that the inhibitory effect of the NSAID indomethacin was greater when the articular cartilage was depleted of glycosaminoglycans.57 In other words, there is a greater inhibition of PRG synthesis in osteoarthritic cartilage than normal cartilage. Other researchers have confirmed these findings that NSAIDs consistently suppress proteoglycan and glycosaminoglycan synthesis.58-60 This depletion of matrix proteoglycans has been shown to be one cause of the increased degeneration of cartilage chondrocytes from the use of NSAIDs.61 Taken to the extreme, one researcher put it this way, “…depending on dose and at concentrations that in many cases correspond to therapeutic plasma levels, these drugs may lead to a pronounced reduction or complete blockade of synthesis of the proteoglycans and collagen of the cartilage matrix.” They went on to say that the medications can “induce progressive joint degeneration within three to four months.”62 Animal studies have also shown the effects of NSAIDs on proliferation, cell cycle kinetics, cytotoxicity, and cell death of chondrocytes. In one study the NSAIDs indomethacin, ketorolac, diclofenac, piroxicam, and celecoxib inhibited thymidine incorporation of chondrocytes at therapeutic concentrations. NSAIDs also arrested chondrocytes in their cell cycles, thus inhibiting chondrocyte cell replication. Upon 24 hour exposure to indomethacin, ketorolac, diclofenac, and piroxicam, chondrocyte cell death (both apoptosis and necrosis) was induced in cell cultures.63 One mechanism by which NSAIDs are toxic to chondrocytes is by inhibiting PGE2 synthesis by chondrocytes.64 PGE2 elicits differentiation of chondrocytes and is an important contributor to cartilage formation and promotes DNA and matrix synthesis in chondrocytes.65, 66 PGE2 has a growth stimulatory effect on chondrocytes, thereby increasing chondrocyte DNA synthesis.67, 68 NSAIDs inhibit the enzyme cyclooxygenase which is responsible for PGE2 release in chondrocytes.69