Analysis of genes from inner ear developmental-stage cDNA subtraction reveals molecular regionalization of the otic capsule

Ficker, Michael; Powles, Nicola; Warr, Nick; Pirvola, Ulla; Maconochie, Mark

doi:10.1016/j.ydbio.2003.11.023

Cited by 18 publications

(14 citation statements)

References 38 publications

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“…Thus, CYTL1 appears to have originated early in vertebrate evolution, suggesting a possible functions in cartilage and bone development. Indeed, CYTL1 expression has been found in cartilagi-nous tissues, such as mouse inner ear and human articular cartilage (10,11). In our previous study (8), we showed that mouse Cytl1 expression was chondrocyte-specific, and further demonstrated that Cytl1 expression was very low in mesenchymal cells, dramatically increased during chondrogenesis, and decreased during hypertrophic maturation, both in vivo and in vitro.…”

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confidence: 73%

Cytokine-like 1 Knock-out Mice (Cytl1−/−) Show Normal Cartilage and Bone Development but Exhibit Augmented Osteoarthritic Cartilage Destruction

Jeon

Lee

et al. 2011

Journal of Biological Chemistry

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We have shown that cytokine-like 1 (Cytl1) is a novel autocrine regulatory factor that regulates chondrogenesis of mouse mesenchymal cells (Kim, J. S., Ryoo, Z. Y., and Chun, J. S. (2007) J. Biol. Chem. 282, 29359 -29367). In this previous work, we found that Cytl1 expression was very low in mesenchymal cells, increased dramatically during chondrogenesis, and decreased during hypertrophic maturation, both in vivo and in vitro. Moreover, exogenous addition or ectopic expression of Cytl1 caused chondrogenic differentiation of mouse limb bud mesenchymal cells. In the current study, we generated a Cytl1 knockout (Cytl1 ؊/؊ ) mouse to investigate the in vivo role of Cytl1. Although a number of regulatory factors have been identified, the precise regulatory mechanisms underlying chondrogenesis and cartilage and bone development remain to be elucidated. In permanent cartilage tissue, cartilage homeostasis is maintained by chondrocytes, which are a cell type unique to cartilage tissue. Cartilage homeostasis is disrupted in osteoarthritis (OA), leading to eventual cartilage destruction. OA is a progressive and degenerative disorder of the joint primarily characterized by articular cartilage destruction. A variety of potential OA-causing mechanisms have been proposed (5-7). Biophysical and biochemical factors, such as mechanical stress and proinflammatory cytokines, respectively, are responsible for disruption of cartilage homeostasis and initiation of the catabolic pathway. This, in turn, activates intracellular pathways in chondrocytes that lead to the production of pro-inflammatory cytokines, inflammation, degradation of the ECM by matrixdegrading enzymes, and cessation of ECM synthesis via dedifferentiation and apoptosis of chondrocytes (5-7). Deletion of theWe have previously shown that cytokine-like 1 (Cytl1) is a novel autocrine regulatory factor involved in chondrogenesis of mouse mesenchymal cells in vitro (8). CYTL1 was originally cloned as a functionally unknown cytokine candidate from human bone marrow and cord blood mononuclear cells bearing the CD34 surface marker (9). The CYTL1 protein contains four ␣-helices and six conserved cysteine residues, which may form intra-disulfide bonds to yield a globular structure, a common structural characteristic of cytokines. CYTL1 also contains an N-terminal secretory signal peptide, and its secretion is associated with post-translational modifications, although the nature of these modifications remains to be established (8

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confidence: 73%

Cytokine-like 1 Knock-out Mice (Cytl1−/−) Show Normal Cartilage and Bone Development but Exhibit Augmented Osteoarthritic Cartilage Destruction

Jeon

Lee

et al. 2011

Journal of Biological Chemistry

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“…Chao et al (12) demonstrated that CYTL1 could significantly prevent inflammatory arthritis. High CYTL1 expression in cartilaginous tissues (13,14) and proteomics analyses on human osteoarthritic patients (15) further supported that CYTL1 was required for the maintenance of cartilage homeostasis. CYTL1 expression was reportedly also significantly positively correlated with perfluoroalkyl and polyfluoroalkyl substances (16).…”

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confidence: 85%

Cytokine-like 1 Chemoattracts Monocytes/Macrophages via CCR2

Wang

et al. 2016

The Journal of Immunology

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Cytokine-like 1 (CYTL1) is a novel potential cytokine that was first identified in CD34+ cells derived from bone marrow and cord blood, and it was also found using our immunogenomics strategy. The immunobiological functions of CYTL1 remain largely unknown, and its potential receptor(s) has not been identified. A previous proposed hypothesis suggested that CYTL1 had structural similarities with CCL2 and that CCR2 was a potential receptor of CYTL1. In this study, we verify that CYTL1 possesses chemotactic activity and demonstrate that its functional receptor is CCR2B using a series of experiments performed in HEK293 cells expressing CCR2B or CCR2B-EGFP, including chemotaxis, receptor internalization, and radioactive binding assays. CYTL1 chemoattracts human monocytes but not PBLs, and its chemotactic activity toward monocytes is dependent on the CCR2B-ERK pathway. Furthermore, both human and mouse recombinant CYTL1 protein have chemotactic effects on macrophages from wild-type mice but not from Ccr2−/− mice. Furthermore, the chemotactic activity of CYTL1 is sensitive to pertussis toxin. All of the above data confirm that CCR2B is a functional receptor of CYTL1.

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“…Cytl1 is a functionally unknown cytokine candidate originally cloned from bone marrow and cord blood mononuclear cells that bear the CD34 surface marker (9). Previous studies report Cytl1 mRNA and protein expression in cartilaginous tissues, including mouse inner ear and human articular cartilage, respectively (10,11). Alignment of the predicted primary amino acid sequences of Cytl1 proteins from multiple species (human, mouse, chicken, and puffer) reveals an N-terminal secretory signal peptide and four ␣-helices, a common characteristic of cytokines.…”

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confidence: 99%

Cytokine-like 1 (CYTL1) Regulates the Chondrogenesis of Mesenchymal Cells

Kim

Ryoo

Chun

2007

Journal of Biological Chemistry

101

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To identify novel molecules regulating chondrogenesis and cartilage development, we screened a cartilage-specific expressed sequence tag data base. Cytokine-like 1 (Cytl1), a possible cytokine candidate with unknown function that was originally identified in bone marrow-derived CD34-positive cells, was selected for functional characterization. In view of the initial observation that Cytl1 is predominantly expressed in chondrocytes and cartilage, we investigated its possible role in chondrogenesis and hypertrophic maturation of chondrocytes. Cytl1 expression was very low in mesenchymal cells, dramatically increased during chondrogenesis, and decreased during hypertrophic maturation, both in vivo and in vitro. The role of Cytl1 in chondrogenesis and hypertrophic maturation was examined by treating chondrifying mesenchymal cells with exogenous Cytl1 or ectopic expression of Cytl1. Notably, exogenous Cytl1 caused chondrogenic differentiation of mouse limb bud mesenchymal cells during micromass culture. Lentivirus-mediated overexpression of Cytl1 additionally induced chondrogenic differentiation of mesenchymal cells. However, Cytl1 did not affect the hypertrophic maturation of chondrocytes. Cytl1 exerted its chondrogenic effect via stimulation of Sox9 transcriptional activity. In addition, Cytl1 caused expression of insulin-like growth factor 1, which has a capacity to induce chondrogenesis. Thus, our results collectively suggest that chondrocyte-specific Cytl1 regulates chondrogenesis as a novel autocrine factor, but not hypertrophic maturation of chondrocytes during cartilage development.Cartilage formation during embryonic development begins with the aggregation of mesenchymal cells, which ultimately differentiate into chondrocytes. Differentiated chondrocytes proliferate rapidly and secrete a cartilage-specific extracellular matrix such as type II collagen and sulfated proteoglycan to form cartilage. The cartilage serves as a template for endochondral ossification, which requires the maturation of hypertrophic chondrocytes (1-4). These sequential events during chondrogenesis and cartilage formation are precisely regulated by various growth factors released from cartilage elements and perichondrium. Secreted growth factors exert their effects by modulating intracellular signaling (1, 2). Although several regulatory growth factors have been identified, including bone morphogenetic proteins, fibroblast growth factors, insulin-like growth factor-1 (IGF-1), 2 transforming growth factor-␤, and parathyroid hormone-related peptide, the precise mechanisms of regulation of chondrogenesis and cartilage development remain to be elucidated. In this study, we analyze a cartilagespecific expressed sequence tag (EST) data base in an attempt to identify novel molecules that modulate chondrogenesis and cartilage development.The EST data base provides important information on novel genes displaying tissue-specific expression profiles (5-7). We analyzed the human cartilage UniGene library (8), and selected Cytl1 as a possible candid...

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Analysis of genes from inner ear developmental-stage cDNA subtraction reveals molecular regionalization of the otic capsule

Cited by 18 publications

References 38 publications

Cytokine-like 1 Knock-out Mice (Cytl1−/−) Show Normal Cartilage and Bone Development but Exhibit Augmented Osteoarthritic Cartilage Destruction

Cytokine-like 1 Knock-out Mice (Cytl1−/−) Show Normal Cartilage and Bone Development but Exhibit Augmented Osteoarthritic Cartilage Destruction

Cytokine-like 1 Chemoattracts Monocytes/Macrophages via CCR2

Cytokine-like 1 (CYTL1) Regulates the Chondrogenesis of Mesenchymal Cells

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