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Expression of immunoregulatory tumor necrosis factor-like molecule TL1A in chicken chondrocyte differentiation.

ABSTRACT: The proinflammatory cytokine tumor necrosis factor (TNF) alpha is not encoded in the chicken genome. However, 1 member of the TNF family, TNF-like molecule 1A (TL1A), which is an important immunoregulatory protein, has recently been characterized in chickens. In this study, chicken TL1A (chTL1A) and 1 of its receptors, decoy receptor 3 (DcR3) were found to be expressed in developing bone of 14.5-day-old chicken embryos. Chicken chondrocytes were shown to express TL1A by polymerase chain reaction (PCR) amplification of cDNA and by immunohistochemical studies. Tissue expression was localized to the epiphyeal region of tubular bones, particularly cells of the epiphyseal plate, the outer chondrocytes of the cartilage-interfacing synovia, most of the synovial cells, and the stromal fibroblastic cells of the vascular channels of the femoral head. A tissue-specific developmental function of TL1A was supported by the presence of DcR3 in the embryonic connective tissue.

SUBMITTER: Tubak V

PROVIDER: S-EPMC2613594 | biostudies-literature | 2009 Jan

REPOSITORIES: biostudies-literature

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Expression of immunoregulatory tumor necrosis factor-like molecule TL1A in chicken chondrocyte differentiation.

Tubak Vilmos V Határvölgyi Erika E Krenács László L Korpos Eva E Kúsz Erzsébet E Duda Ernõ E Monostori Eva E Rauch Tibor T

Canadian journal of veterinary research = Revue canadienne de recherche veterinaire 20090101 1

The proinflammatory cytokine tumor necrosis factor (TNF) alpha is not encoded in the chicken genome. However, 1 member of the TNF family, TNF-like molecule 1A (TL1A), which is an important immunoregulatory protein, has recently been characterized in chickens. In this study, chicken TL1A (chTL1A) and 1 of its receptors, decoy receptor 3 (DcR3) were found to be expressed in developing bone of 14.5-day-old chicken embryos. Chicken chondrocytes were shown to express TL1A by polymerase chain reaction ...[more]

PMID: 19337393

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Project description:Despite the numerous studies of protein kinase CK2, little progress has been made in understanding its function in chondrocyte death. Our previous study first demonstrated that CK2 is involved in apoptosis of rat articular chondrocytes. Recent studies have suggested that CK2 downregulation is associated with aging. Thus examining the involvement of CK2 downregulation in chondrocyte death is an urgently required task. We undertook this study to examine whether CK2 downregulation modulates chondrocyte death. We first measured CK2 activity in articular chondrocytes of 6-, 21- and 30-month-old rats. Noticeably, CK2 activity was downregulated in chondrocytes with advancing age. To build an in vitro experimental system for simulating tumor necrosis factor (TNF)-α-induced cell death in aged chondrocytes with decreased CK2 activity, chondrocytes were co-treated with CK2 inhibitors and TNF-α. Viability assay demonstrated that CK2 inhibitors facilitated TNF-α-mediated chondrocyte death. Pulsed-field gel electrophoresis, nuclear staining, flow cytometry, TUNEL staining, confocal microscopy, western blot and transmission electron microscopy were conducted to assess cell death modes. The results of multiple assays showed that this cell death was mediated by apoptosis. Importantly, autophagy was also involved in this process, as supported by the appearance of a punctuate LC3 pattern and autophagic vacuoles. The inhibition of autophagy by silencing of autophage-related genes 5 and 7 as well as by 3-methyladenine treatment protected chondrocytes against cell death and caspase activation, indicating that autophagy led to the induction of apoptosis. Autophagic cells were observed in cartilage obtained from osteoarthritis (OA) model rats and human OA patients. Our findings indicate that CK2 down regulation facilitates TNF-α-mediated chondrocyte death through apoptosis and autophagy. It should be clarified in the future if autophagy observed is a consequence versus a cause of the degeneration in vivo.

Project description:Interleukin-1? (IL-1?) and tumor necrosis factor ? (TNF?) stimulate chondrocyte matrix catabolic responses, thereby compromising cartilage homeostasis in osteoarthritis (OA). AMP-activated protein kinase (AMPK), which regulates energy homeostasis and cellular metabolism, also exerts antiinflammatory effects in multiple tissues. This study was undertaken to test the hypothesis that AMPK activity limits chondrocyte matrix catabolic responses to IL-1? and TNF?.Expression of AMPK subunits was examined, and AMPK? activity was ascertained by the phosphorylation status of AMPK? Thr(172) in human knee articular chondrocytes and cartilage by Western blotting and immunohistochemistry, respectively. Procatabolic responses to IL-1? and TNF?, such as release of glycosaminoglycan, nitric oxide, and matrix metalloproteinases 3 and 13 were determined by dimethylmethylene blue assay, Griess reaction, and Western blotting, respectively, in cartilage explants and chondrocytes with and without knockdown of AMPK? by small interfering RNA.Normal human knee articular chondrocytes expressed AMPK?1, ?2, ?1, ?2, and ?1 subunits. AMPK activity was constitutively present in normal articular chondrocytes and cartilage, but decreased in OA articular chondrocytes and cartilage and in normal chondrocytes treated with IL-1? and TNF?. Knockdown of AMPK? resulted in enhanced catabolic responses to IL-1? and TNF? in chondrocytes. Moreover, AMPK activators suppressed cartilage/chondrocyte procatabolic responses to IL-1? and TNF? and the capacity of TNF? and CXCL8 (IL-8) to induce type X collagen expression.Our findings indicate that AMPK activity is reduced in OA cartilage and in chondrocytes following treatment with IL-1? or TNF?. AMPK activators attenuate dephosphorylation of AMPK? and procatabolic responses in chondrocytes induced by these cytokines. These observations suggest that maintenance of AMPK activity supports cartilage homeostasis by protecting cartilage matrix from inflammation-induced degradation.

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Expression of immunoregulatory tumor necrosis factor-like molecule TL1A in chicken chondrocyte differentiation.

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Expression of immunoregulatory tumor necrosis factor-like molecule TL1A in chicken chondrocyte differentiation.

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