Granulocyte-macrophage colony stimulating factor is anabolic and interleukin-1β is catabolic for rat articular chondrocytes

Quintero, Maritza; Riera, Humberto; Colantuoni, Gladys; Khatib, Abdel‐Majid; Attalah, Habiba; Moldovan, Florina; Mitrović, D; Lomri, Abderrahim

doi:10.1016/j.cyto.2008.10.003

Cited by 10 publications

(10 citation statements)

References 35 publications

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“…TNF-α and IFN-γ were concentration-dependently diminished by both RHP and GLGPG (Figure 2b, Table 3). Furthermore, in PBL RHP increased the expression of GM-CSF, an anabolic factor for chondrocytes [27]. Next, expression levels of inflammatory mediators were determined in human PBL.…”

Section: Resultsmentioning

confidence: 99%

Rose hip and its constituent galactolipids confer cartilage protection by modulating cytokine, and chemokine expression

Schwager¹,

Hoeller²,

Wolfram³

et al. 2011

BMC Complement Altern Med

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BackgroundClinical studies have shown that rose hip powder (RHP) alleviates osteoarthritis (OA). This might be due to anti-inflammatory and cartilage-protective properties of the complete RHP or specific constituents of RHP. Cellular systems (macrophages, peripheral blood leukocytes and chondrocytes), which respond to inflammatory and OA-inducing stimuli, are used as in vitro surrogates to evaluate the possible pain-relief and disease-modifying effects of RHP.Methods(1) Inflammatory processes were induced in RAW264.7 cells or human peripheral blood leukocytes (PBL) with LPS. Inflammatory mediators (nitric oxide (NO), prostaglandin E2 (PGE2) and cytokines/chemokines) were determined by the Griess reaction, EIA and multiplex ELISA, respectively. Gene expression was quantified by RT-PCR. RHP or its constituent galactolipid, GLGPG (galactolipid (2S)-1, 2-di-O-[(9Z, 12Z, 15Z)-octadeca-9, 12, 15-trienoyl]-3-O-β-D-galactopyranosyl glycerol), were added at various concentrations and the effects on biochemical and molecular parameters were evaluated. (2) SW1353 chondrosarcoma cells and primary human knee articular chondrocytes (NHAC-kn) were treated with interleukin (IL)-1β to induce in vitro processes similar to those occurring during in vivo degradation of cartilage. Biomarkers related to OA (NO, PGE2, cytokines, chemokines, metalloproteinases) were measured by multiplex ELISA and gene expression analysis in chondrocytes. We investigated the modulation of these events by RHP and GLGPG.ResultsIn macrophages and PBL, RHP and GLGPG inhibited NO and PGE2 production and reduced the secretion of cytokines (TNF-α, IFN-γ, IL-1β, IL-6, IL-12) and chemokines (CCL5/RANTES, CXCL10/IP-10). In SW1353 cells and primary chondrocytes, RHP and GLGPG diminished catabolic gene expression and inflammatory protein secretion as shown by lower mRNA levels of matrix metalloproteinases (MMP-1, MMP-3, MMP-13), aggrecanase (ADAMTS-4), macrophage inflammatory protein (MIP-2, MIP-3α), CCL5/RANTES, CXCL10/IP-10, IL-8, IL-1α and IL-6. The effects of GLGPG were weaker than those of RHP, which presumably contains other chondro-protective substances besides GLGPG.ConclusionsRHP and GLGPG attenuate inflammatory responses in different cellular systems (macrophages, PBLs and chondrocytes). The effects on cytokine production and MMP expression indicate that RHP and its constituent GLGPG down-regulate catabolic processes associated with osteoarthritis (OA) or rheumatoid arthritis (RA). These data provide a molecular and biochemical basis for cartilage protection provided by RHP.

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Section: Resultsmentioning

confidence: 99%

Rose hip and its constituent galactolipids confer cartilage protection by modulating cytokine, and chemokine expression

Schwager¹,

Hoeller²,

Wolfram³

et al. 2011

BMC Complement Altern Med

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“…Alternatively or in combination, chondro‐induction may rely on direct cell–cell contacts through heterotopic gap junctions or transmembrane proteins such as cadherins (Donahue et al, 1995; Djouad et al, 2007b), or indirectly on the secretion of bioactive molecules following heterotopic cell–cell contacts (Yamamoto et al, 2004). Indeed, using the coculture model in pellets, we observed that the release of several factors regulating matrix remodeling (i.e., TIMP‐1 and TIMP‐2), cell proliferation and synthesis of cartilage‐specific protein (i.e., FGF‐4, FGF‐6, TGFβ3, GM‐CSF, and GCSF) (Gelse et al, 2003; Brittberg et al, 2005; Quintero et al, 2008), and MSC commitment/differentiation (i.e., TGFβ3, IL‐12, RANTES, IL‐2, and LIF) (Falconi et al, 2007; Cristino et al, 2008; Chung and Burdick, 2009) was strongly enhanced by BM‐MSC/AC.…”

Section: Discussionmentioning

confidence: 99%

Enhanced chondrocyte proliferation and mesenchymal stromal cells chondrogenesis in coculture pellets mediate improved cartilage formation

Acharya

Adesida

Zajac

et al. 2011

Journal Cellular Physiology

232

273

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In this study, we aimed at investigating the interactions between primary chondrocytes and mesenchymal stem/stromal cells (MSC) accounting for improved chondrogenesis in coculture systems. Expanded MSC from human bone marrow (BM-MSC) or adipose tissue (AT-MSC) were cultured in pellets alone (monoculture) or with primary human chondrocytes from articular (AC) or nasal (NC) cartilage (coculture). In order to determine the reached cell number and phenotype, selected pellets were generated by combining: (i) human BM-MSC with bovine AC, (ii) BM-MSC from HLA-A2+ with AC from HLA-A2- donors, or (iii) human green fluorescent protein transduced BM-MSC with AC. Human BM-MSC and AC were also cultured separately in transwells. Resulting tissues and/or isolated cells were assessed immunohistologically, biochemically, cytofluorimetrically, and by RT-PCR. Coculture of NC or AC (25%) with BM-MSC or AT-MSC (75%) in pellets resulted in up to 1.6-fold higher glycosaminoglycan content than what would be expected based on the relative percentages of the different cell types. This effect was not observed in the transwell model. BM-MSC decreased in number (about fivefold) over time and, if cocultured with chondrocytes, increased type II collagen and decreased type X collagen expression. Instead, AC increased in number (4.2-fold) if cocultured with BM-MSC and maintained a differentiated phenotype. Chondro-induction in MSC-chondrocyte coculture is a robust process mediated by two concomitant effects: MSC-induced chondrocyte proliferation and chondrocyte-enhanced MSC chondrogenesis. The identified interactions between progenitor and mature cell populations may lead to the efficient use of freshly harvested chondrocytes for ex vivo cartilage engineering or in situ cartilage repair.

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“…The role of bacterial products as contributing elements in the onset of cartilage degradation in septic arthritis is well established . Within inflammed joints, catabolic products accelerate cartilage matrix degradation and are associated with increases in HO‐1 expression . Increased HO‐1 may serve a protective stress‐response since HO‐1 decreases chondrocyte apoptosis induced by the nitric oxide donor, sodium nitroprusside .…”

Section: Discussionmentioning

confidence: 99%

Effects of heme oxygenase‐1 on bacterial antigen‐induced articular chondrocyte catabolism in vitro

Mawatari

Nakamichi

Suenaga

et al. 2013

Journal Orthopaedic Research

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This study tested the hypothesis that heme oxygenase-1 (HO-1) expression counteracts bacterial antigen-induced catabolic metabolism in human articular chondrocytes. HO-1 expression was induced in chondrocytes by the iron-containing porphoryin, hemin. Anti-catabolic and anti-apoptotic effects of HO-1 expression were evaluated following bacterial antigen (lipopolysaccharides, LPS) activation of chondrocytes by quantification of cytokine and cartilage matrix protein expression. Effects of HO-1 over-expression on chondrocyte matrix metabolism were evaluated using plasmid-driven protein synthesis. Hemin increased HO-1 expression and LPS increased interleukin-1beta and interleukin-6 gene and protein expression in chondrocytes. Hemin-induced HO-1 decreased LPSinduced interleukin-1beta and interleukin-6 gene and protein expression. Increased HO-1 expression partially reversed LPSsuppression of aggrecan and type II collagen gene expression and suppressed LPS-induced gene expression of IL-6, inducible nitric oxide synthase (iNOS), matrix metalloproteinases (MMPs), and IL-1beta. HO-1 induction was inversely correlated with LPS-induced chondrocyte apoptosis. HO-1 over-expression in chondrocytes decreased matrix protein gene expression. With LPS activation, increased HO-1 expression decreased chondrocyte catabolism, partially reversed LPS-dependent inhibition of cartilage matrix protein expression and protected against apoptosis. Without LPS, hemin-induced HO-1 and plasmid-based over-expression of HO-1 inhibited cartilage matrix gene expression. The results suggest that elevated HO-1 expression in chondrocytes is protective of cartilage in inflamed joints but may otherwise suppress matrix turn over. ß 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31:1943Res 31: -1949Res 31: , 2013 Keywords: heme oxygenase-1; articular chondrocytes; catabolism; bacterial antigen; cartilage matrix proteins Heme oxygenase-1 (HO-1) and heme oxygenase-2 (HO-2) are heme degrading enzymes expressed in mammalian species. 1,2 Although breakdown of heme occurs by similar mechanisms, in many tissues HO-1 is highly inducible isoform whereas HO-2 is constitutively expressed. 3,4 Two of the three heme oxygenase products, biliverdin, and carbon monoxide, modulate immune function and influence tissue metabolism and the third, free iron, is captured by ferritin for reuse. 5,6 Increases in HO-1 occur as in response to tissue stressors, including heme, reactive oxygen species (ROS), unbalanced redox conditions and various inflammatory agents, such as bacterial antigens and pro-inflammatory cytokines. 7,8 In acute or chronic pathogenic states, induction of HO-1 provides protective effects on cells and tissues. 9,10 Chondrocytes express the inducible isoform of HO-1 in osteoarthritic (OA) cartilage explants and in isolated OA chondrocytes. 11,12 In animal models, increased levels of HO-1 are protective of joint tissues for both adjuvant and antigen-induced arthritis. [13][14][15] In OA cartilage explants, HO-1 ind...

show abstract

Granulocyte-macrophage colony stimulating factor is anabolic and interleukin-1β is catabolic for rat articular chondrocytes

Cited by 10 publications

References 35 publications

Rose hip and its constituent galactolipids confer cartilage protection by modulating cytokine, and chemokine expression

Rose hip and its constituent galactolipids confer cartilage protection by modulating cytokine, and chemokine expression

Enhanced chondrocyte proliferation and mesenchymal stromal cells chondrogenesis in coculture pellets mediate improved cartilage formation

Effects of heme oxygenase‐1 on bacterial antigen‐induced articular chondrocyte catabolism in vitro

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