Dermatan 4-O-sulfotransferase1 ablation accelerates peripheral nerve regeneration

Akyüz, Nuray; Rost, Sandra; Mehanna, Ali; Bian, Shan; Loers, Gabriele; Oezen, Iris; Mishra, Bibhudatta; Hoffmann, Kathrin; Guseva, Daria; Laczynska, Ewa; Irintchev, Andrey; Jakovčevski, Igor; Schachner, Melitta

doi:10.1016/j.expneurol.2013.01.025

Cited by 38 publications

(46 citation statements)

References 73 publications

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“…Three different chondroitin/dermatan sulfotransferases have been deleted in the mouse, all with comparatively mild consequences. Mice lacking CHST5, a GlcNAc-6-O-sulfotransferase, exhibit disrupted organization of the cornea, reduced KS and increased amounts of CS and DS [109]; mice lacking CHST14, a predominantly DS GalNAc-4-O-sulfotransferase, exhibit reduced weight and fertility, a kinked tail and increased skin fragility [110], and reduced proliferation and neurogenesis of neural stem cells [111]; deletion of CHST11, a predominantly CS GalNAc-4-O-sulfotransferase, has no apparent effect on neural stem cell properties but Chst11 null progeny die at birth [111]; deletion of CHST2 and CHST4 GlcNAc-6-O-sulfotransferases causes a marked reduction in homing of leukocytes to peripheral lymph nodes due to the loss of 6-O-sulfation on L-selectin ligands, and Lewis X on O-glycans [112, 113]. …”

Section: Pathway-specific Glycans That Affect Postnatal Developmentmentioning

confidence: 99%

What Have We Learned from Glycosyltransferase Knockouts in Mice?

Stanley

2016

Journal of Molecular Biology

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There are five major classes of glycan including N- and O-glycans, glycosaminoglycans, glycosphingolipids and glycophosphatidylinositol anchors, all expressed at the molecular frontier of each mammalian cell. Numerous biological consequences of altering the expression of mammalian glycans are understood at a mechanistic level, but many more remain to be characterized. Mouse mutants with deleted, defective, or misexpressed genes that encode activities necessary for glycosylation have led the way to identifying key functions of glycans in biology. However, with the advent of exome sequencing, humans with mutations in genes involved in glycosylation are also revealing specific requirements for glycans in mammalian development. The aim of this review is to summarize glycosylation genes that are necessary for mouse embryonic development; pathway-specific glycosylation genes whose deletion leads to postnatal morbidity; and glycosylation genes for which effects are mild, but perturbation of the organism may reveal functional consequences. General strategies for generating and interpreting the phenotype of mice with glycosylation defects are discussed in relation to human congenital disorders of glycosylation (CDG).

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Section: Pathway-specific Glycans That Affect Postnatal Developmentmentioning

confidence: 99%

What Have We Learned from Glycosyltransferase Knockouts in Mice?

Stanley

2016

Journal of Molecular Biology

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“…[107]. In addition, axonal regrowth is initially facilitated in D4st1 −/− mice following nerve transection.…”

Section: Knockout and Transgenic Mice Of Gag Biosynthetic Enzymesmentioning

confidence: 99%

Human Genetic Disorders and Knockout Mice Deficient in Glycosaminoglycan

Mizumoto

Yamada

Sugahara

2014

BioMed Research International

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Glycosaminoglycans (GAGs) are constructed through the stepwise addition of respective monosaccharides by various glycosyltransferases and maturated by epimerases and sulfotransferases. The structural diversity of GAG polysaccharides, including their sulfation patterns and sequential arrangements, is essential for a wide range of biological activities such as cell signaling, cell proliferation, tissue morphogenesis, and interactions with various growth factors. Studies using knockout mice of enzymes responsible for the biosynthesis of the GAG side chains of proteoglycans have revealed their physiological functions. Furthermore, mutations in the human genes encoding glycosyltransferases, sulfotransferases, and related enzymes responsible for the biosynthesis of GAGs cause a number of genetic disorders including chondrodysplasia, spondyloepiphyseal dysplasia, and Ehlers-Danlos syndromes. This review focused on the increasing number of glycobiological studies on knockout mice and genetic diseases caused by disturbances in the biosynthetic enzymes for GAGs.

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“…Among inhibitory factors of neurite growth, glycosaminoglycans (GAGs) have been widely documented. Chondroitin sulfate and dermatan sulfate proteoglycans are known to have an inhibitory effect on neuronal regrowth and the degradation of GAGs by chondroitinase permits axonal regeneration . However, the role of GAGs in skin repair still needs to be further studied as they possess important functions that favour wound healing through actions on keratinocytes and fibroblasts.…”

Section: Therapeutic Strategies To Improve Wound Healing and Reinnervmentioning

confidence: 99%

New insights into the roles of myofibroblasts and innervation during skin healing and innovative therapies to improve scar innervation

Lebonvallet

Laverdet

Miséry

et al. 2018

Experimental Dermatology

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During the resolution phase of normal skin wound healing, there is a considerable loss of various cell types, including myofibroblasts by apoptosis. Inappropriate delay of apoptosis, and thus increased survival of myofibroblasts, may be a factor leading to pathologies and excessive scarring. Considerable data now clearly suggest that innervation plays a major role in wound healing, including the modulation of fibroblast cellular activity. An abnormal level of neuromediators is implicated not only in the development of chronic wounds but also in excessive scar formation.Understanding interactions between neuromediators and myofibroblasts, allowing normal reinnervation and having adequate levels of neuromediators during the healing process are clearly important to avoid the appearance of pathological healing or fibrosis/scarring. The aim of this review was first to discuss the mechanisms leading to normal or excessive scarring and then to present the roles of innervation during wound healing. Finally, the latest therapeutic strategies to help wound repair and reinnervation after skin damage will be introduced. Advantages and limitations in the use of neuropeptides, growth factors and biomaterials will be discussed as well as the most recent studies on electrostimulation and the potential of targeting resident skin mesenchymal stem cells. K E Y W O R D Sinnervation, myofibroblast, pathological scarring, skin repair, skin-derived precursor | 951LEBONVALLET ET AL.

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Dermatan 4-O-sulfotransferase1 ablation accelerates peripheral nerve regeneration

Cited by 38 publications

References 73 publications

What Have We Learned from Glycosyltransferase Knockouts in Mice?

What Have We Learned from Glycosyltransferase Knockouts in Mice?

Human Genetic Disorders and Knockout Mice Deficient in Glycosaminoglycan

New insights into the roles of myofibroblasts and innervation during skin healing and innovative therapies to improve scar innervation

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