Functions of heparan sulfate proteoglycans in cell signaling during development

Lin, Xinhua

doi:10.1242/dev.01522

Cited by 615 publications

(616 citation statements)

References 99 publications

(213 reference statements)

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“…Numerous heparan sulfate proteoglycans are expressed in skeletal muscle tissue, including SDCs, glycophosphatidyl‐linked glypicans, extracellular matrix perlecan, agrin or biglycan 35, 36. Here we showed that silencing of SDC4 resulted in the upregulation of heparan sulfate proteoglycans in C2C12 myoblast (SDC1, SDC2, SDC3, glypican‐1, perlecan).…”

Section: Discussionmentioning

confidence: 73%

Syndecan‐4 influences mammalian myoblast proliferation by modulating myostatin signalling and G1/S transition

et al. 2018

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Myostatin, a TGF‐β superfamily member, is a negative regulator of muscle growth. Here we describe how myostatin activity is regulated by syndecan‐4, a ubiquitous transmembrane heparan sulfate proteoglycan. During muscle regeneration the levels of both syndecan‐4 and promyostatin decline gradually after a sharp increase, concurrently with the release of mature myostatin. Promyostatin and syndecan‐4 co‐immunoprecipitate, and the interaction is heparinase‐sensitive. ShRNA‐mediated silencing of syndecan‐4 reduces C2C12 myoblast proliferation via blocking the progression from G1‐ to S‐phase of the cell cycle, which is accompanied by elevated levels of myostatin and p21(Waf1/Cip1), and decreases in cyclin E and cyclin D1 expression. Our results suggest that syndecan‐4 functions as a reservoir for promyostatin regulating the local bioavailability of mature myostatin.

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Section: Discussionmentioning

confidence: 73%

Syndecan‐4 influences mammalian myoblast proliferation by modulating myostatin signalling and G1/S transition

et al. 2018

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“…Testing for the association of this SNP with progression, together with Gleason score and stage, would allow us to assess their independent and joint contributions in predicting for disease outcome. However, an association of a SNP with Gleason score/stage alone, as demonstrated in this study, is important by itself, as Gleason score and stage are informative surrogates of disease outcome, albeit insufficient (39,40). More importantly, when high-grade/stage tumors are diagnosed, it is often too late for effective treatment.…”

Section: Discussionmentioning

confidence: 80%

Inherited genetic variant predisposes to aggressive but not indolent prostate cancer

Zheng

Isaacs

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Autopsy studies suggest that most aging men will develop lesions that, if detected clinically, would be diagnosed as prostate cancer (PCa). Most of these cancers are indolent and remain localized; however, a subset of PCa is aggressive and accounts for more than 27,000 deaths in the United States annually. Identification of factors specifically associated with risk for more aggressive PCa is urgently needed to reduce overdiagnosis and overtreatment of this common disease. To search for such factors, we compared the frequencies of SNPs among PCa patients who were defined as having either more aggressive or less aggressive disease in four populations examined in the Genetic Markers of Susceptibility (CGEMS) study performed by the National Cancer Institute. SNPs showing possible associations with disease severity were further evaluated in an additional three independent study populations from the United States and Sweden. In total, we studied 4,829 and 12,205 patients with more and less aggressive disease, respectively. We found that the frequency of the TT genotype of SNP rs4054823 at 17p12 was consistently higher among patients with more aggressive compared with less aggressive disease in each of the seven populations studied, with an overall P value of 2.1 × 10−8 under a recessive model, exceeding the conservative genome-wide significance level. The difference in frequency was largest between patients with high-grade, non–organ-confined disease compared with those with low-grade, organ-confined disease. This study demonstrates that inherited variants predisposing to aggressive but not indolent PCa exist in the genome, and suggests that the clinical potential of such variants as potential early markers for risk of aggressive PCa should be evaluated.

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“…Based on the core protein structures, they are divided into different families including glypicans, syndecans, and the secreted perlecans. They can facilitate long-range diffusion of signaling proteins, present them to target cells, or restrict the activity range of these molecules [Lin, 2004].…”

Section: Regulation Of Ihh Signaling In the Growth Platementioning

confidence: 99%

Indian hedgehog: Its roles and regulation in endochondral bone development

Lai

Mitchell

2005

J of Cellular Biochemistry

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Normal endochondral bone development requires the coordination of chondrocyte proliferation and differentiation. Indian hedgehog (Ihh) is a morphogen produced by chondrocytes in the early stage of terminal differentiation and plays several key roles in this process. Ihh regulates growth of adjacent proliferative chondrocytes and can also regulate the rate of differentiation of chondrocytes indirectly through its stimulation of parathyroid hormonerelated protein (PTHrP). In this review, we focus on recent studies that have identified new functions of Ihh and how Ihh itself is being regulated.

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Functions of heparan sulfate proteoglycans in cell signaling during development

Cited by 615 publications

References 99 publications

Syndecan‐4 influences mammalian myoblast proliferation by modulating myostatin signalling and G1/S transition

Syndecan‐4 influences mammalian myoblast proliferation by modulating myostatin signalling and G1/S transition

Inherited genetic variant predisposes to aggressive but not indolent prostate cancer

Indian hedgehog: Its roles and regulation in endochondral bone development

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