Differential expression of WNTs and FRPs in the synovium of rheumatoid arthritis and osteoarthritis

Imai, Kazushi; Morikawa, Masako; DʼArmiento, Jeanine; Matsumoto, Hideo; Komiya, Koichiro; Okada, Yasunori

doi:10.1016/j.bbrc.2006.05.075

Cited by 55 publications

(45 citation statements)

References 27 publications

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“…If this were the case, SFRPs could be considered as potentially valuable therapeutic tools, as already suggested by Mirotsou and colleagues, who found that treatment of myocardiocytes with SFRP2 promoted cell survival and repair (Mirotsou et al, 2007). Nevertheless, the elevated levels of SFRPs reported in the pathological conditions described above as well as in other less characterised examples (Imai et al, 2006;Koza et al, 2006;Mirotsou et al, 2007;Surendran et al, 2005) suggest that these molecules could also be valuable therapeutic targets. …”

mentioning

confidence: 78%

Beyond Wnt inhibition: new functions of secreted Frizzled-related proteins in development and disease

Bovolenta

Esteve

Ruiz

et al. 2008

Journal of Cell Science

541

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types of cancers, bone pathologies, retinal degeneration and hypophosphatemic diseases, indicating that their activity is fundamental for tissue homeostasis. Here we review some of the debated aspects of SFRP-Wnt interactions and discuss the new and emerging roles of SFRPs. Journal of Cell Science 738 were isolated either through sequence homology with Fz receptors (Rattner et al., 1997) or, independently of Wnt activity, through their involvement in apoptosis (Melkonyan et al., 1997), or their co-purification with the heparin-binding factor hepatocyte growth factor/scattered factor (Finch et al., 1997).Since their discovery, interest in this family of molecules has grown progressively, particularly because recent observations have offered a new perspective on their functions and mechanisms of action in both development and disease. These studies indicate that SFRPs are not merely Wnt-binding proteins but can also antagonise one another's activity (Yoshino et al., 2001), bind to Fz receptors (Bafico et al., 1999;Rodriguez et al., 2005) and provide axon-guidance information (Rodriguez et al., 2005). Moreover, they can interact with other receptors or matrix molecules (Chuman et al., 2004;Hausler et al., 2004; and interfere with BMP signalling (Lee, H. et al., 2006;Muraoka et al., 2006;Yabe et al., 2003) by acting as proteinase inhibitors (Lee, H. et al., 2006). Furthermore, their expression is altered in different types of cancers (Rubin et al., 2006), in bone pathologies , retinal degeneration (Jones et al., 2000) and hypophosphatemic diseases (Berndt and Kumar, 2007), which indicates that their activity is fundamental for tissue homeostasis. Reviews that centre on Wnt antagonism by SFRPs have recently been published elsewhere (Cadigan and Liu, 2006;Jones and Jomary, 2002;Kawano and Kypta, 2003); here, we discuss new aspects of SFRP activity, and review SFRP structure, expression and interactions with Wnt proteins. The family of SFRPsThe SFRP family comprises five members in humans, SFRP1 to SFRP5, in which SFRP3 is the orthologue of the founding member Frzb. Sequence comparison and phylogenetic analysis show that SFRP1, SFRP2 and SFRP5 are closely related, and cluster together in a subgroup that diverges from the one formed by the related SFRP3 and SFRP4 (Fig. 1). This clustering also reflects a different genomic organisation. SFRP1, SFRP2 and SFRP5 are encoded by three exons on chromosome 8p12-p11.1, 4q31.3 and 10q24.1, respectively (Garcia-Hoyos et al., 2004), whereas SFRP3 and SFRP4 are both encoded by six exons -on chromosome 2q31-q33 and 7p14-p13, respectively. Orthologues of the five human genes have been found in all vertebrate species analysed so far ( Fig. 1). Notably, a third subgroup, apparently not present in mammals, has been identified in Xenopus, zebrafish and chick. The components of this subgroup, named Sizzled, Crescent and Tlc, share sequence similarities with the SFRP1-SFRP2-SFRP5 subgroup (Fig. 1), and are characterised by a very restricted and anterior expression in gastrulating embryos (B...

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mentioning

confidence: 78%

Beyond Wnt inhibition: new functions of secreted Frizzled-related proteins in development and disease

Bovolenta

Esteve

Ruiz

et al. 2008

Journal of Cell Science

541

523

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“…A number of studies suggest that the Wnt pathway is involved in the degradation of the osteoarthritic cartilage (reviewed in [7,26]). Nakamura found an upregulation of WNT7B in OA cartilage, with conflicting results about SFRPs [6,9]. Others reported an upregulation of WNT5B in bone samples of patients undergoing hip arthroplasty [27].…”

Section: Discussionmentioning

confidence: 99%

“…Wnt ligands increase the expression of matrix metalloproteases by human synovium and stimulate the chondrocyte matrix catabolic action in a rabbit model of OA [8,9]. It has been recently reported that targeted deletion of the FRZB gene (which codes for the Wntbinding protein SFRP3) increases the injury-associated loss of articular cartilage in mice, in association with increased cortical bone thickness and density [10].…”

Section: Introductionmentioning

confidence: 99%

Wnt pathway genes in osteoporosis and osteoarthritis: differential expression and genetic association study

et al. 2009

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“…Total RNA was isolated from synovial tissue of OA and RA patients as described previously [37]. Briefly, arthritic synovial tissue was obtained from patients undergoing total knee joint or hip replacement.…”

Section: Isolation Of Rna and Rt-pcrmentioning

confidence: 99%

SAF‐3, a novel splice variant of the SAF‐1/MAZ/Pur‐1 family, is expressed during inflammation

et al. 2009

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The Cys2His2‐type zinc finger transcription factor serum amyloid A activating factor 1 [SAF‐1, also known as MAZ (myc‐associated zinc finger protein) or Pur‐1 (purine binding factor‐1)] plays an important role in regulation of a variety of inflammation‐responsive genes. An SAF‐2 splice variant acting as a negative regulator of SAF‐1 was identified previously, and the present study reports the identification of a novel SAF‐3 splice variant that is expressed during inflammation. SAF‐3 mRNA, isolated from a cDNA library produced from IL‐1β‐induced cells, originates from a previously unknown first coding exon, and thereby contains a unique N‐terminal domain but shares the same six zinc finger DNA‐binding domains as present in SAF‐1. In addition, a negatively functioning domain present at the N‐terminus of SAF‐1 and SAF‐2 is spliced out in SAF‐3. The expression of SAF‐3 is very low in normal tissues and in cells grown under normal conditions. However, RT‐PCR analysis of mRNAs from cytokine and growth factor‐induced cells as well of mRNAs isolated from several diseased tissues revealed abundant expression of SAF‐3. The transactivation potential of SAF‐3 is much greater than that of the predominantly expressed splice variant SAF‐1. These findings show that transcriptional regulation of downstream inflammation‐responsive genes by SAF/MAZ/Pur‐1 is likely to be more complex than previously assumed. In addition, we show that SAF‐3 expression initiates from an upstream novel promoter. This is the first report of the existence of multiple promoters regulating expression of the SAF/MAZ/Pur‐1 family of proteins.

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Differential expression of WNTs and FRPs in the synovium of rheumatoid arthritis and osteoarthritis

Cited by 55 publications

References 27 publications

Beyond Wnt inhibition: new functions of secreted Frizzled-related proteins in development and disease

Beyond Wnt inhibition: new functions of secreted Frizzled-related proteins in development and disease

Wnt pathway genes in osteoporosis and osteoarthritis: differential expression and genetic association study

SAF‐3, a novel splice variant of the SAF‐1/MAZ/Pur‐1 family, is expressed during inflammation

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