Glucosamine modulates chondrocyte proliferation, matrix synthesis, and gene expression

Varghese, Shyni; Theprungsirikul, P.; Sahani, Shrawan Kumar; Hwang, Nathaniel S.; Yarema, Kevin J.; Elisseeff, Jennifer H.

doi:10.1016/j.joca.2006.06.008

Cited by 102 publications

(82 citation statements)

References 40 publications

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“…The effect, however small, may be due to an increase in collagen production by chondrocytes in the supplemented groups. 22 Tiku et al 23 showed that treatment of chondrocytes with a similar concentration of glucosamine prevents in vitro collagen degradation over time. More likely, the higher collagen content may reflect the fact that the supplemented group was stiffened because of a rise in PG content and yielded less matrix damage.…”

Section: Discussionmentioning

confidence: 99%

High levels of glucosamine–chondroitin sulfate can alter the cyclic preload and acute overload responses of chondral explants

Wei

Haut

2009

Journal Orthopaedic Research

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A recent study by our laboratory showed that 14 days of low intensity, intermittent cyclic preloading of chondral explants elevated the concentration of proteoglycans (PGs) to cause a mechanical stiffening of the explants prior to an acute overload and limit the extent of tissue damage. Longer term loading to 21 days resulted in tissue degradation prior to the acute traumatic event and excessive damage from an acute overload. Previous studies by others showed that bathing chondral explants in a supplement of glucosaminechondroitin sulfate (glcN-CS) upregulated the synthesis of tissue PGs, particularly in stressed tissue, and the supplement served as an antiinflammatory agent. Our current hypothesis was that the supplementation of culture media with a high concentration of glcN-CS would upregulate the production of tissue PG and limit or mitigate long-term degradation of chondral explants under cyclic preloading and limit tissue damage in an acute overload. We showed that, in the presence of supplement, cyclic preloading significantly increased tissue PG content and matrix modulus by about 65 and 300%, respectively, at 21 days, resulting in a reduction of matrix damage and cell death following an acute overload. These data show a biological action of high concentrations of this supplement and its effect on the mechanical properties in this in vitro model. In vitro studies of impact loading 1,2 on cartilage show cell death and matrix damage. In contrast, in vitro and in vivo studies showed positive aspects of low intensity, intermittent compressive loading, such as increased biosynthesis of proteoglycans (PGs). [3][4][5] Changes in PG and collagen contents of cartilage significantly alter the mechanical properties of this tissue. 6 Thus, it is reasonable to assume that cyclic preloading of cartilage can alter its mechanical properties and help determine the extent of matrix damage and cell death that will occur due to the blunt force overloading of a joint, such as during an acute knee ligament rupture. 7 Recent studies in our laboratory show that low intensity, intermittent cyclic preloading of chondral explants prior to an acute overload yields an increase in the synthesis of tissue PGs, resulting in a less severe traumatic insult for an acute overload. 8 Between 14 and 21 days of cyclic preloading, the explants experience a significant PG loss that leads to a dramatic loss in mechanical properties. Acute overloading of the explanted tissue then yields matrix damage and cell death significantly greater than nonpreloaded controls. A recent study by others shows a significant loss of tissue PG and cell death with production of matrix metalloproteinase (MMP-3) adjacent to damaged collagen fibers under cyclic compression at 0.5 Hz for intensities of 1 and 5 MPa over 24 h. 9 Similarly, under 0.5 MPa of 1 Hz cyclic loading, a significant increase in the MMP-2 and -9 synthesis was found after 3 h. 10 The combination of glucosamine-chondroitin sulfate (glcN-CS) was shown in in vitro studies to function as a ''...

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Section: Discussionmentioning

confidence: 99%

High levels of glucosamine–chondroitin sulfate can alter the cyclic preload and acute overload responses of chondral explants

Wei

Haut

2009

Journal Orthopaedic Research

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“…The volume of the acellular space between the bilayer, however, needs to be optimized properly, as we have observed the distance-dependent response of co-cultured cells. In our bilayer PEODA hydrogel system with approximate 10-nm pore size, when 40 l of acellular space, instead of 20 l, was used in between co-cultured cells, no significant effect of co-culture has been observed (data not shown) [33]. This result indicates the importance of close proximity between cocultured cells.…”

Section: Discussionmentioning

confidence: 74%

Enhanced Chondrogenic Differentiation of Embryonic Stem Cells by Coculture with Hepatic Cells

Lee

Chansakul

et al. 2008

Stem Cells and Development

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“…Although GlcN is a well-tolerated monosaccharide that is naturally made from glucose and glutamine in the body [13], a few studies have reported that large doses of GlcN induce cell death in chondrocytes and several malignant cell lines [22][23][24][25]. To examine the effect of GlcN on viability of human ESCs, human ESC-Ts [26] were cultured for 3, 6, or 9 days in the presence of 0, 2.5, or 5 mM GlcN, and the MTT assay [27] was used to determine cell viability and proliferation.…”

Section: Glucosamine Is Not Toxic To Human Escsmentioning

confidence: 99%

Glucosamine Inhibits Decidualization of Human Endometrial Stromal Cells and Decreases Litter Sizes in Mice1

Tsai

Schulte

O’Neill

et al. 2013

Biology of Reproduction

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Embryo implantation in the uterus depends on decidualization of the endometrial stromal cells (ESCs), and glucose utilization via the pentose phosphate pathway is critical in this process. We hypothesized that the amino sugar glucosamine may block the pentose phosphate pathway via inhibition of the rate-limiting enzyme glucose-6-phosphate dehydrogenase in ESCs and therefore impair decidualization and embryo implantation, thus preventing pregnancy. Both human primary and immortalized ESCs were decidualized in vitro in the presence of 0, 2.5, or 5 mM glucosamine for 9 days. Viability assays demonstrated that glucosamine was well tolerated by human ESCs. Exposure of human ESCs to glucosamine resulted in significant decreases in the activity and expression of glucose-6-phosphate dehydrogenase and in the mRNA expression of the decidual markers prolactin, somatostatin, interleukin-15, and left-right determination factor 2. In mouse ESCs, expression of the decidual marker Prp decreased upon addition of glucosamine. In comparison with control mice, glucosamine-treated mice showed weak artificial deciduoma formation along the stimulated uterine horn. In a complementary in vivo experiment, a 60-day-release glucosamine (15, 150, or 1500 lg) or placebo pellet was implanted in a single uterine horn of mice. Mice with a glucosamine pellet delivered fewer live pups per litter than those with a control pellet, and pup number returned to normal after the end of the pellet-active period. In conclusion, glucosamine is a nonhormonal inhibitor of decidualization of both human and mouse ESCs and of pregnancy in mice. Our data indicate the potential for development of glucosamine as a novel, reversible, nonhormonal contraceptive. decidualization, glucosamine, human endometrial stromal cells, pentose phosphate pathway

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Glucosamine modulates chondrocyte proliferation, matrix synthesis, and gene expression

Cited by 102 publications

References 40 publications

High levels of glucosamine–chondroitin sulfate can alter the cyclic preload and acute overload responses of chondral explants

High levels of glucosamine–chondroitin sulfate can alter the cyclic preload and acute overload responses of chondral explants

Enhanced Chondrogenic Differentiation of Embryonic Stem Cells by Coculture with Hepatic Cells

Glucosamine Inhibits Decidualization of Human Endometrial Stromal Cells and Decreases Litter Sizes in Mice1

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