Rescue of retinal function by BDNF in a mouse model of glaucoma.
loss of vision in glaucoma is caused by progressive dysfunction of the retinal ganglion cells (RGCs) and optic nerve atrophy. Here, we investigate the effectiveness of BDNF treatment to preserve vision in glaucoma experimental models. As an established experimental model, we use the DBA / 2J mouse, which develops chronic elevation of intraocular pressure (IOP) that mimics primary open-angle glaucoma (POAG). IOP was measured at different ages in DBA / 2J mice. visual function was monitored using a well-established pattern electroretinogram (P-ERG) and cortical visual evoked potentials (VEP). change RGC assessed using Brn3 immunolabeling and confocal microscopy analysis.
Human recombinant BDNF was dissolved in saline (0.9% NaCl); the effect of repeated intravitreal injections and topical eye BDNF application independently evaluated in DBA / 2J mice with ocular hypertension. BDNF levels were measured in retinal homogenates by ELISA and Western blot. We found a progressive decline of P-ERG and VEP responses in DBA / 2J mice between 4 and 7 months of age, in connection with the development of ocular hypertension and reduction of RGCs immunopositive Brn3. Conversely, repeated intravitreal injection ( BDNF concentration = 2 mg / ml, volume = 1 ml, for each injection, 1 injection every four days, three injections over two weeks) and the application of eye topical BDNF eye drops (12 ug / ml, 5 ml of eye-drops every 4 8 hours over two weeks) were able to rescue the visual response within 7 months of DBA / 2J mice.
In particular, BDNF topical eye treatment to recover the P-ERG and VEP Decrease increase the number of RGCs Brn3 immunopositive. We showed that BDNF independent effect of IOP reduction. Thus, topical eye treatment with BDNF is a promisingly safe and feasible strategy to preserve visual function and reduce the vulnerability of RGC ocular hypertension.
Migration and differentiation of HUC-MSCs (CXCR4 / GFP) packed in BDNF / chitosan scaffolds for tissue engineering of the brain.
We previously developed a biomaterial scaffold that can effectively provide seed cells into the lesion cavity resulting from trauma brain injury. However, we later found out that some of the transplanted Human umbilical cord mesenchymal stem cell (HUC-MSCs) can migrate from the scaffold to the lesion boundary.
Stroma derived -cell factor -1α and chemokine receptor (CXC motif) receptor (CXCR) 4 is chemotactic factor s that controls cell migration and recruitment of stem cells into the target area. Given the level of expression of the low CXCR 4 on the membrane HUC-MSCs, lentiviral vectors are used to generate the HUC-MSCs stably express CXCR 4 the fusion of green fluorescent protein (GFP) (HUC-MSCs ( CXCR 4 / GFP)).
We build scaffolding where recombinant Human brain – derived neurotrophic factor ( BDNF ) is related to the scaffold of chitosan with genipin crosslinking (CGB scaffold). Scaffold containing HUC-MSCs (CXCR 4 / GFP) were transplanted into the lesion cavity of mice brain , providing exogenous Huc-MSCs for both the lesion and cavity boundary. These results suggest a new strategy to encourage tissue regeneration after traumatic brain injury.
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Rats were divided into five groups: (1) non-carbon control monoxide-treated, (2) acute poisoning of carbon monoxide, (3) carbon monoxide poisoning acute followed by a 7-day treatment of hyperbaric oxygen (4) carbon monoxide + hyperbaric oxygen with intracerebroventricular infusion of additional Fc fragment of the receptor protein tyrosine kinase B (TrkB-Fc) chimera, and (5) acute carbon monoxide poisoning followed by intracerebroventricular infusion of neurotrophic factor derived from the brain.