Hearing Improvement in A/J Mice via the Mouse Nerve Growth Factor.

Clin Exp Otorhinolaryngol

Key Laboratory for Genetic Hearing Disorders in Shandong, Binzhou Medical University, Yantai, China.

Published: December 2017


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Objectives: To investigate the otoprotective effects of mouse nerve growth factor (mNGF) in A/J mice.

Methods: The mice at postnatal day 7 (P7) were randomly separated into a mNGF treated group (mNGF group) and a distilled water (for injection) treated group (control group). The mNGF dissolved in distilled water or distilled water alone was given to the mice once every other day from P7 by intramuscular injection in the hips. The otoprotective effects of mNGF in A/J mice were observed in a time course manner. The thresholds of auditory-evoked brainstem response (ABR) were tested from the age of the 3rd to the 8th week. Sections of the inner ears were stained by hematoxylin and eosin, and spiral ganglion neurons (SGNs) were observed at the age of the 3rd, the 6th,and the 8th week. Counts of whole mount outer hair cells (OHCs) in the cochleae were made at the age of 8 weeks. Expression of apoptosis related genes was determined by quantitative real-time polymerase chain reaction and Western blotting.

Results: ABR thresholds of the mNGF group were significantly lower than those of the control group at the age of the 6th and the 8th week. Moreover, the mNGF preserved OHC and SGN in the mouse cochleae in this period. Further experiments showed that the expression of caspase genes (including caspase-3) was inhibited in the mouse inner ears in the mNGF group.

Conclusion: The mNGF improves hearing in A/J mice by preserving SGN and OHC in the cochleae.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5678043PMC
http://dx.doi.org/10.21053/ceo.2016.01354DOI Listing

Publication Analysis

Top Keywords

a/j mice
12
distilled water
12
8th week
12
mngf
9
mouse nerve
8
nerve growth
8
growth factor
8
otoprotective effects
8
mngf a/j
8
treated group
8

Similar Publications

The brain avidly consumes glucose to fuel neurophysiology. Cancers of the brain, such as glioblastoma, relinquish physiological integrity and gain the ability to proliferate and invade healthy tissue. How brain cancers rewire glucose use to drive aggressive growth remains unclear.

View Article and Find Full Text PDF

Anthrax remains a formidable bioterrorism threat for which new, optimized and thermostable vaccines are needed. We previously demonstrated that five immunizations of rabbits with a multiple-antigenic-peptide (MAP) vaccine in either Freund's adjuvant or human-use adjuvants can elicit antibody (Ab) against the loop-neutralizing determinant (LND), a cryptic neutralizing epitope in the 2β2-2β3 loop of protective antigen from (), which mediates complete protection of rabbits from inhalation spore challenge with the Ames strain. To develop a more immunogenic vaccine, we molecularly constructed a virus-like particle (VLP) vaccine, comprising the Woodchuck hepatitis core antigen capsid (WHcAg) displaying 240 copies of the LND epitope on each nanoparticle.

View Article and Find Full Text PDF

Background: Accumulating evidence indicates that SARS-CoV-2 infection results in long-term multiorgan complications, with the kidney being a primary target. This study aimed to characterize the long-term transcriptomic changes in the kidney following coronavirus infection using a murine model of MHV-1-induced SARS-like illness and to evaluate the therapeutic efficacy of SPIKENET (SPK).

Methods: A/J mice were infected with MHV-1.

View Article and Find Full Text PDF

Glucagon-like peptide 1 (GLP-1), a hormone derived from the proglucagon gene, regulates various physiological processes; however, its impact on pregnancy outcomes remains poorly understood. Assessing the effects of GLP-1 on neonates is vital as GLP-1 is increasingly administered during pregnancy. This study evaluates the effect of GLP-1 exposure on maternal complications and neonatal defects in mice.

View Article and Find Full Text PDF

Heparanase 2 Modulates Vascular Permeability via Heparan Sulfate-Dependent Growth Factor Signaling.

Arterioscler Thromb Vasc Biol

August 2025

Department of Nephrology, Institute of Functional and Applied Anatomy, Hannover Medical School, Germany. (Y.B., S.T., N.S., S.R., A.A., H.S., Y.K., H.H.).

Background: Vessel-lining endothelial cells (ECs) rely on heparan sulfate (HS) proteoglycans to regulate vascular permeability and to maintain vascular homeostasis. Hpa2 (heparanase 2) is a little-known, nonenzymatic, HS-binding protein. We hypothesized major functions and thus characterized the role of endogenous Hpa2 in the vertebrate vascular system.

View Article and Find Full Text PDF