Hyaluronan (HA)-based microgels generated in a microfluidic approach, containing an artificial extracellular matrix composed of collagen and high-sulfated hyaluronan (sHA3), were incorporated into a HA/collagen-based hydrogel matrix. This significantly enhanced the retention of noncrosslinked sHA3 within the gels enabling controlled sHA3 presentation. Gels containing sHA3 bound higher amounts of transforming growth factor-β1 (TGF-β1) compared to pure HA/collagen hydrogels. Moreover, the presence of sHA3-containing microgels improved the TGF-β1 retention within the hydrogels. These findings are promising for developing innovative biomaterials with adjustable sHA3 release and growth factor interaction profiles to foster skin repair, e.g., by rebalancing dysregulated TGF-β1 levels.
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http://dx.doi.org/10.1007/s10856-019-6267-1 | DOI Listing |
Mater Today Bio
April 2024
Centre for Translational Bone, Joint- and Soft Tissue Research, Faculty of Medicine and University Hospital, TUD University of Technology, Fetscherstraße 74, 01307, Dresden, Germany.
Bone remodelling, important for homeostasis and regeneration involves the controlled action of osteoblasts, osteocytes and osteoclasts. The present study established a three-dimensional human bone model as triple culture with simultaneously differentiating osteocytes and osteoclasts, in the presence of osteoblasts. Since high sulfated hyaluronan (sHA3) was reported as a biomaterial to enhance osteogenesis as well as to dampen osteoclastogenesis, the triple culture was exposed to sHA3 to investigate cellular responses compared to the respective bone cell monocultures.
View Article and Find Full Text PDFACS Appl Mater Interfaces
July 2023
School of Materials Science and Engineering, South China University of Technology, Guangzhou 510006, China.
Corneal scarring caused by epithelial-stromal injury impairs corneal transparency and visual acuity. Excess secretion of transforming growth factor-beta 1 (TGF-β1), which promotes wound closure, penetrates the corneal stroma via defects in the epithelial basement membrane and induces the differentiation of corneal fibroblasts to myofibroblasts, leading to scar formation. Modulating TGF-β1 penetration might alleviate corneal scar formation and restore transparency.
View Article and Find Full Text PDFBiomaterials
June 2023
Division of Endocrinology, Diabetes and Bone Diseases & Center for Healthy Aging, Department of Medicine III, Technische Universität Dresden Medical Center, Fetscherstraße 74, D-01307, Dresden, Germany; Center for Regenerative Therapies Dresden, Technische Universität Dresden, Fetscherstraße 105, D-01307, Dresden, Germany. Electronic address:
The WNT signaling pathway is a central regulator of bone development and regeneration. Functional alterations of WNT ligands and inhibitors are associated with a variety of bone diseases that affect bone fragility and result in a high medical and socioeconomic burden. Hence, this cellular pathway has emerged as a novel target for bone-protective therapies, e.
View Article and Find Full Text PDFInt J Mol Sci
December 2022
University Center for Orthopaedics, Trauma and Plastic Surgery, University Hospital Carl Gustav Carus, Technische Universität Dresden, 01307 Dresden, Germany.
Bone in diabetes mellitus is characterized by an altered microarchitecture caused by abnormal metabolism of bone cells. Together with diabetic neuropathy, this is associated with serious complications including impaired bone healing culminating in complicated fractures and dislocations, especially in the lower extremities, so-called Charcot neuroarthropathy (CN). The underlying mechanisms are not yet fully understood, and treatment of CN is challenging.
View Article and Find Full Text PDFInt J Mol Sci
May 2022
Department of Biochemistry, Hoshi University School of Pharmacy, 2-4-41, Ebara, Shinagawa-ku, Tokyo 144-8501, Japan.
We examined whether sulfated hyaluronan exerts inhibitory effects on enzymatic and biological actions of heparanase, a sole endo-beta-glucuronidase implicated in cancer malignancy and inflammation. Degradation of heparan sulfate by human and mouse heparanase was inhibited by sulfated hyaluronan. In particular, high-sulfated hyaluronan modified with approximately 2.
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