Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
In this work, a plant-derived polysaccharide carboxymethylcellulose (CMC) was chemically modified to incorporate sulfate groups to facilitate binding of cationic growth factors. The sulfated CMC (heparin mimic) was then used with CMC (glycosaminoglycan mimic) and gelatin (collagen mimic) to fabricate injectable pre-formed, macroporous scaffolds for cartilage tissue engineering. These scaffolds demonstrated high resilience and shape memory, thereby making them injectable through a 14G needle for up to 4-6 aspiration and injection cycles. Further, the scaffolds could sequester cationic proteins and growth factors (TGF-β1) through affinity-based interactions. When seeded with infrapatellar fat pad derived MSCs, the scaffolds demonstrated enhanced chondrogenesis after 28 days of in vitro culture when compared to controls. Taken together; these results demonstrate a polysaccharide-based minimally-invasive and translatable pre-formed injectable scaffold-based cell and growth factor delivery system for cartilage regeneration.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.carbpol.2018.03.091 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Exosome-mediated microglia-astrocyte interactions drive neuroinflammation in Parkinson's disease with Peli1 as a potential therapeutic target.
Pharmacol Res
September 2025
Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China; State key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Electronic address:
Neuroinflammation is a key feature of Parkinson's disease (PD), characterized by activated microglia and the conversion of astrocytes into the neurotoxic phenotype, exacerbating the neuroinflammation. In PD, microglia critically drive neurotoxic reactive astrocytes (A1, A1-like, or neuroinflammatory reactive astrocytes)-though the underlying mechanisms remain elusive. Given the established role of exosomes as critical intercellular messengers, we investigated whether microglia-derived exosomes contribute to neurotoxic astrocyte transformation.
View Article and Find Full Text PDFUnlabelled: α-Synuclein (α-syn) is an abundant monomeric protein that can aggregate into fibrils and form neuropathological inclusions in the brains of patients with synucleinopathies. New evidence suggests that the mouse-human transmission barrier of α-syn is lower than previously reported, emphasizing the need for improved biosafety procedures when working with α-syn aggregates. Histopathology of α-syn-infected brain represents a significant potential source of occupational exposure, and current methods for tissue fixation do not inactivate the ability of pathologic α-syn to seed the conversion of endogenous, monomeric α-syn into fibrils.
View Article and Find Full Text PDFCortical α-synuclein pathology induces cell autonomous neuronal hypoactivity and compensatory circuit changes in a model of early Lewy body dementia.
bioRxiv
August 2025
Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.
Cognitive impairment is a common non-motor symptom of Parkinson's disease (PD) and a defining feature of Dementia with Lewy Bodies (DLB). Although many cognitive domains can be affected, impairments in visuospatial/perceptual function are relatively specific for PD and DLB compared to other dementias. Across populations, cognitive impairments correlate with the presence of α-synuclein (α-syn) pathology in limbic and neocortical brain regions.
View Article and Find Full Text PDFTemplating of monomeric alpha-synuclein results in inflammation and SNpc dopamine neuron death in a genetic mouse model of induced synucleinopathy.
Sci Rep
July 2025
Department of Neuroscience, Thomas Jefferson University, 900 Walnut St, Philadelphia, PA, 19107, USA.
While the etiology of most cases of Parkinson's disease (PD) are idiopathic, it has been estimated that 5-10% of PD arise from known genetic mutations. The first mutations described that leads to the development of an autosomal dominant form of PD are in the SNCA gene that codes for the protein alpha-synuclein (α-syn). α-syn is an abundant presynaptic protein that is natively disordered and whose function is still unclear.
View Article and Find Full Text PDFThe influence of the glymphatic system on α-synuclein propagation: the role of aquaporin-4.
Brain
July 2025
Centre for Advanced Biomedical Imaging, Department of Imaging, Division of Medicine, University College London, London, WC1E 6DD, UK.
Propagation and aggregation of prion proteins, such as tau and α-synuclein (αSyn), are key pathological features of neurodegenerative diseases. Extracellular clearance pathways, such as the glymphatic system, may play a crucial role in the removal of these toxic proteins from the brain. Primarily active during sleep, this system relies on aquaporin-4 (AQP4) water channel expression and polarisation to astrocytic endfeet, facilitating interstitial solute clearance.
View Article and Find Full Text PDF