In this study we demonstrate the potential for combining biocompatible polymers with genetically engineered cells to elicit axon regrowth across tissue defects in the injured CNS. Eighteen- to 21-day-old rats received implants of poly N-(2-hydroxypropyl)-methacrylamide (HPMA) hydrogels containing RGD peptide sequences that had been infiltrated with control (untransfected) fibroblasts (n = 8), fibroblasts engineered to express brain-derived neurotrophic factor (BDNF) (n = 5), ciliary neurotrophic factor (CNTF) (n = 5), or a mixture of BDNF and CNTF expressing fibroblasts (n = 11). Fibroblasts were prelabeled with Hoechst 33342. Cell/polymer constructs were inserted into cavities made in the left optic tract, between thalamus and superior colliculus. After 4-8 weeks, retinal projections were analyzed by injecting right eyes with cholera toxin (B-subunit). Rats were perfused 24 h later and sections were immunoreacted to visualize retinal axons, other axons (RT97 antibody), host astrocytes and macrophages, donor fibroblasts, and extracellular matrix molecules. The volume fraction (VF) of each gel that was occupied by RT97(+) axons was quantified. RT-PCR confirmed expression of the transgenes prior to, and 5 weeks after, transplantation. Compared to control rats (mean VF = 0.02 +/- 0.01% SEM) there was increased ingrowth of RT97(+) axons into implants in CNTF (mean VF = 0.33 +/- 0.19%) and BDNF (mean VF = 0.62 +/-0.19%) groups. Axon growth into hydrogels in the mixed BDNF/CNTF group (mean VF = 3.58 +/- 0.92%) was significantly greater (P < 0.05) than in the BDNF or CNTF fibroblast groups. Retinal axons exhibited a complex branching pattern within gels containing BDNF or BDNF/CNTF fibroblasts; however, they regrew the greatest distances within implants containing both BDNF and CNTF expressing cells.
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http://dx.doi.org/10.1006/exnr.2001.7692 | DOI Listing |
Mol Neurobiol
January 2025
Department of Ophthalmology, Ruijin Hospital, Affiliated Shanghai Jiaotong University School of Medicine, 197 Ruijin Er Road, Shanghai, 200025, China.
VEGF is not only the most potent angiogenic factor, but also an important neurotrophic factor. In this study, vitreous expression of six neurotrophic factors were examined in proliferative diabetic retinopathy (PDR) patients with prior anti-VEGF therapy (n = 48) or without anti-VEGF treatment (n = 41) via ELISA. Potential source, variation and impact of these factors were further investigated in a mouse model of oxygen-induced retinopathy (OIR), as well as primary Müller cells and 661W photoreceptor cell line under hypoxic condition.
View Article and Find Full Text PDFTraumatic optic neuropathies cause the death of retinal ganglion cells (RGCs) and axon degeneration. This is a result of the blockage of neurotrophic factor (NTF) supply from the brain and a vicious cycle of neurotoxicity, possibly mediated by increased levels of retinal Zn . Ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) are two NTFs that are known to support RGC survival and promote axon regeneration.
View Article and Find Full Text PDFJ Neurodev Disord
November 2024
Department of Biomedical and Neuromotor Science, University of Bologna, Piazza Di Porta San Donato 2, 40126, Bologna, Italy.
Background: Mutations in the X-linked CDKL5 gene underlie a severe epileptic encephalopathy, CDKL5 deficiency disorder (CDD), characterized by gross motor impairment, autistic features and intellectual disability. Absence of Cdkl5 negatively impacts neuronal proliferation, survival, and maturation in in vitro and in vivo models, resulting in behavioral deficits in the Cdkl5 KO mouse. While there is no targeted therapy for CDD, several studies showed that treatments enabling an increase in brain BDNF levels give rise to structural and behavioral improvements in Cdkl5 KO mice.
View Article and Find Full Text PDFNutrients
October 2024
Department of Food and Nutrition, Institute of Basic Science, Obesity/Diabetes Research Center, Hoseo University, Asan 31499, Republic of Korea.
Background/objectives: Fructus (SCF) is a traditional medicinal herb containing lignans that improves glucose metabolism by mitigating insulin resistance. We aimed to investigate the therapeutic potential and action mechanism of SCF for Alzheimer's disease (AD) using a network pharmacology analysis, followed by experimental validation in an AD rat model.
Methods: The biological activities of SCF's bioactive compounds were assessed through a network pharmacology analysis.
Int J Mol Sci
September 2024
Department Food and Nutrition, Hoseo University, Asan 31499, Republic of Korea.
Alzheimer's disease (AD) is characterized by impaired insulin/insulin-like growth factor-1 signaling in the hippocampus. Zeaxanthin and lutein, known for their antioxidant and anti-inflammatory properties, have been reported to protect against brain damage and cognitive decline. However, their mechanisms related to insulin signaling in AD remain unclear.
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