Transcriptional and post‐translational regulation of hyaluronan synthesis

Tammi, Raija; Passi, Alberto; Rilla, Kirsi; Karousou, Evgenia; Vigetti, Davide; Makkonen, Katri M.; Tammi, Markku

doi:10.1111/j.1742-4658.2011.08070.x

Cited by 191 publications

(180 citation statements)

References 55 publications

(78 reference statements)

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“…Hyaluronan is synthesized by plasma membrane hyaluronan synthases (HAS) (10), and increased HAS activity may markedly increase serum hyaluronan in patients with collagenofibrotic glomerulopathy. However, we did not measure HAS activity in the present study, and this remains to be examined in patients with collagenofibrotic glomerulopathy.…”

Section: Discussionmentioning

confidence: 99%

Marked Elevation of Serum Hyaluronan Levels in Collagenofibrotic Glomerulopathy

et al. 2014

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Collagenofibrotic glomerulopathy is a rare glomerular disease characterized by the massive deposition of type III collagen in mesangial and subendothelial spaces. We observed markedly increased serum hyaluronan levels in patients with collagenofibrotic glomerulopathy; levels in three patients were more than 1,000-times greater than the normal upper limit. However, one kidney transplant patient had normal serum hyaluronan levels. We found that serum levels and activities of the enzyme hyaluronidase were normal, and hyaluronan was not markedly deposited in the mesangial or subendothelial spaces. Our findings suggest that serum hyaluronan levels may be a specific diagnostic marker of collagenofibrotic glomerulopathy, and kidney transplantation may alleviate marked increases in serum hyaluronan.

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Section: Discussionmentioning

confidence: 99%

Marked Elevation of Serum Hyaluronan Levels in Collagenofibrotic Glomerulopathy

et al. 2014

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“…In particular, the glycosaminoglycan hyaluronan, one of the key components of the vertebrate extracellular matrix, is essential in dynamic cellular systems such as the developing embryo (Camenish et al, 2000;Toole, 2001;Ori et al, 2006;Li et al, 2007;Matsumoto et al 2009;Tammi et al, 2011), tissue wound repair and regeneration (Jiang et al, 2007;Contreras et al, 2009), inflammation processes (Hascall et al, 2004;Jiang et al, 2011), and tumorigenesis (Toole and Slomiany, 2008;Misra et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Hyaluronan is required for cranial neural crest cells migration and craniofacial development

Casini

Nardi

Ori

2011

Developmental Dynamics

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Background: Hyaluronan is a crucial glycosaminoglycan of the vertebrate embryonic extracellular matrix able to influence cell behaviour, both by assembling the pericellular matrices and by activating signal transducing receptors such as CD44. Results: We showed that the hyaluronan synthases, Has1 and Has2, and CD44 display a dynamic expression pattern during cranial neural crest cells (NCC) development. By knocking down Has1 and Has2 gene functions, we revealed that hyaluronan synthesized by Has1 and Has2 is necessary for the proper development of the visceral skeleton. Conclusions: The data suggest that hyaluronan helps to maintain the active migratory behaviour of cranial NCC, and that its presence around pre-chondrogenic NCC is crucial for their survival. CD44 knock down also suggests that the role of hyaluronan in cranial NCC migration could be mediated, at least in part, by the activation of CD44. These findings contribute to the unveiling of the functional relation between NCC and their extracellular environment during craniofacial development. Developmental Dynamics 241:294-302, 2012. V C 2011 Wiley Periodicals, Inc.Key words: hyaluronan; neural crest cell; craniofacial development; Has1; Has2; CD44; extracellular matrix; Xenopus Key findings:Cranial NCC migrate throughout a hyaluronan rich extracellular matrix Hyaluronan synthases 1 and 2 activity is necessary to maintain the migratory behaviour of cranial NCC After NCC migration, the presence of Hyaluronan in the extracellular matrix is necessary for the survival of pre-chondrogenic cranial NCC. CD44, a Hyaluronan receptor, is required for cranial NCC migration but not for their survival. In Xenopus, the craniofacial skeleton formation is deeply influenced by the composition of the extracellular matrix during cranial NCC migration and differentiation.

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“…Such results implicate Has1 in this monocyte-adhesive ECM phenotype. Hyaluronan synthesis is regulated by a number of pathways, including the EGFR and NFB signaling pathways (71). Hyaluronan triggers the CD44-EGFR signaling pathway, which up-regulates hyaluronan synthesis in a positive feedback mechanism (33)(34)(35)(36)(37).…”

Section: V3 Resists Monocyte Adhesion By Altering Signaling Pathwaysmentioning

confidence: 99%

Expression of Versican V3 by Arterial Smooth Muscle Cells Alters Tumor Growth Factor β (TGFβ)-, Epidermal Growth Factor (EGF)-, and Nuclear Factor κB (NFκB)-dependent Signaling Pathways, Creating a Microenvironment That Resists Monocyte Adhesion

Kang

Yoon

Braun

et al. 2014

Journal of Biological Chemistry

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Background: Monocyte accumulation contributes to inflammatory disease progression. Results: ASMCs overexpressing V3 resist monocyte adhesion by promoting elastogenesis, depleting hyaluronan, and reducing VCAM1, via differentially regulating TGF␤-, EGF-, and NFB-signaling pathways. Conclusion: V3 expression by ASMCs generates a microenvironment resistant to monocyte adhesion. Significance: Modifying ECM components via V3 expression alters monocyte adhesion, which suggests therapeutic possibilities to treat inflammation.

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Transcriptional and post‐translational regulation of hyaluronan synthesis

Cited by 191 publications

References 55 publications

Marked Elevation of Serum Hyaluronan Levels in Collagenofibrotic Glomerulopathy

Marked Elevation of Serum Hyaluronan Levels in Collagenofibrotic Glomerulopathy

Hyaluronan is required for cranial neural crest cells migration and craniofacial development

Expression of Versican V3 by Arterial Smooth Muscle Cells Alters Tumor Growth Factor β (TGFβ)-, Epidermal Growth Factor (EGF)-, and Nuclear Factor κB (NFκB)-dependent Signaling Pathways, Creating a Microenvironment That Resists Monocyte Adhesion

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