The optic nerve is a viscoelastic solid-like biomaterial. Its normal stress relaxation and creep properties enable the nerve to resist constant strain and protect it from injury. We hypothesized that stress relaxation and creep properties of the optic nerve change after injury. More-over, human brain-derived neurotrophic factor or umbilical cord blood-derived stem cells may restore these changes to normal. To validate this hypothesis, a rabbit model of optic nerve injury was established using a clamp approach. At 7 days after injury, the vitreous body re-ceived a one-time injection of 50 μg human brain-derived neurotrophic factor or 1 × 10(6) human umbilical cord blood-derived stem cells. At 30 days after injury, stress relaxation and creep properties of the optic nerve that received treatment had recovered greatly, with patho-logical changes in the injured optic nerve also noticeably improved. These results suggest that human brain-derived neurotrophic factor or umbilical cord blood-derived stem cell intervention promotes viscoelasticity recovery of injured optic nerves, and thereby contributes to nerve recovery.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4870926 | PMC |
| http://dx.doi.org/10.4103/1673-5374.180753 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Retinoid X receptor agonist 9CDHRA mitigates retinal ganglion cell apoptosis and neuroinflammation in a mouse model of glaucoma.
FASEB J
March 2025
Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.
Glaucoma, a leading cause of irreversible blindness, is characterized by the progressive loss of retinal ganglion cells (RGCs) and optic nerve damage, often associated with elevated intraocular pressure (IOP). Retinoid X receptors (RXRs) are ligand-activated transcription factors crucial for neuroprotection, as they regulate gene expression to promote neuronal survival via several biochemical networks and reduce neuroinflammation. This study investigated the therapeutic potential of 9-cis-13,14-dihydroretinoic acid (9CDHRA), an endogenous retinoid RXR agonist, in mitigating RGC degeneration in a high-IOP-induced experimental model of glaucoma.
View Article and Find Full Text PDFWnt5a regulates the expression of developmental genes in the adult retina following optic nerve crush injury.
Histol Histopathol
February 2025
Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, USA.
Canonical and non-canonical Wnt signaling pathways are well-characterized regulators of retinal development. Wnt signaling also promotes neuroprotection and regeneration in adult tissues, including retinal ganglion cell (RGC) survival and axonal regrowth after optic nerve injury. However, it is unknown whether Wnt-dependent neuroprotection after injury in the adult CNS is associated with altered expression of developmental genes.
View Article and Find Full Text PDFOrbital hydatid cyst from Echinococcus granulosus: a case report.
J Surg Case Rep
March 2025
Faculty of Medicine, University of Aleppo, Aleppo, Syria.
In endemic regions, intra-orbital hydatid cysts are a rare manifestation of Echinococcus granulosus infection, classically disturbing the liver and lungs. This report details a patient's case with an intra-orbital cyst presenting. Diagnostic imaging revealed a cystic lesion causing optic nerve displacement.
View Article and Find Full Text PDFCore genes and immune dysregulation in primary open-angle glaucoma: A molecular insight.
Technol Health Care
December 2024
Institute of Ophthalmology, Anhui University of Science and Technology, Huainan, Anhui Province, China.
BackgroundPrimary open-angle glaucoma (POAG) is a chronic, progressive and irreversible eye disease. Currently, there is no effective way to prevent optic nerve damage.ObjectiveThis study explored POAG gene markers to identify high-risk groups at an early stage and to find new effective therapeutic targets.
View Article and Find Full Text PDFLink Between Metabolic Syndrome, Inflammation, and Eye Diseases.
Int J Mol Sci
February 2025
Department of Ophthalmology and Eye Rehabilitation, Medical University of Bialystok, 15-089 Bialystok, Poland.
Metabolic syndrome (MetS)-a cluster of conditions including obesity, hypertension, dyslipidemia, and insulin resistance-is increasingly recognized as a key risk factor for the development of various eye diseases. The metabolic dysfunctions associated with this syndrome contribute to vascular and neurodegenerative damage within the eye, influencing disease onset and progression. Understanding these links highlights the importance of early diagnosis and management of metabolic syndrome to prevent vision loss and improve ocular health outcomes.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!