For the first time, increased Dp71 in ischemia-reperfusion injured rat heart were identified, both Dp71 mRNA and protein reached its peak expression 8 h after reperfusion. In HO stimulated H9c2 cells, Dp71 mRNA and protein gradually increased and reached a peak at 16 h. Enhanced Dp71 in H9c2 could resist HO-induced cell apoptosis, while Dp71 depletion accelerated the apoptosis induced by HO Enhanced Bcl-2 expression and Bcl-2∕Bax protein expression ratio was identified in Dp71 overexpressed H9c2 cells, while knocking down Dp71 significantly decreased the Bcl-2 and Bcl-2∕Bax protein expression ratio. Increased Dp71 can accelerate FAK and p65 phosphorylation, which finally resulted in enhanced Bcl-2 expression and explains the highly possible cardiac protection role of Dp71.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.tice.2022.101951 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Impact of distinct dystrophin gene mutations on behavioral phenotypes of Duchenne muscular dystrophy.
Dis Model Mech
December 2024
CNRS, Institut des Neurosciences Paris-Saclay, Université Paris-Saclay, 91400 Saclay, France.
The severity of brain comorbidities in Duchenne muscular dystrophy (DMD) depends on the mutation position within the DMD gene and differential loss of distinct brain dystrophin isoforms (i.e. Dp427, Dp140, Dp71).
View Article and Find Full Text PDFSocial and emotional alterations in mice lacking the short dystrophin-gene product, Dp71.
Behav Brain Funct
August 2024
Université Paris-Saclay, CNRS, Institut des Neurosciences Paris-Saclay, 91400, Saclay, France.
Article Synopsis
- Duchenne and Becker muscular dystrophies (DMD, BMD) are neuromuscular disorders linked to cognitive and behavioral issues, with studies suggesting that the severity of these issues may be connected to the loss of different dystrophin proteins.
- This study focused on Dp71-null mice, which lack the shortest dystrophin isoform, revealing abnormal social behaviors, vocalization, and changes in anxiety levels, but no impact on myopathy or learning/memory related to fear.
- The findings suggest that mutations affecting Dp71 might contribute to social and emotional problems commonly seen in DMD, supporting the idea that losing multiple dystrophin isoforms can exacerbate behavioral issues.
Dystrophin 71 deficiency causes impaired aquaporin-4 polarization contributing to glymphatic dysfunction and brain edema in cerebral ischemia.
Neurobiol Dis
September 2024
Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China; Institute of Stroke Research, Soochow University, Suzhou, Jiangsu Province, China.
Objective: The glymphatic system serves as a perivascular pathway that aids in clearing liquid and solute waste from the brain, thereby enhancing neurological function. Disorders in glymphatic drainage contribute to the development of vasogenic edema following cerebral ischemia, although the molecular mechanisms involved remain poorly understood. This study aims to determine whether a deficiency in dystrophin 71 (DP71) leads to aquaporin-4 (AQP4) depolarization, contributing to glymphatic dysfunction in cerebral ischemia and resulting in brain edema.
View Article and Find Full Text PDFAblation of the dystrophin Dp71f alternative C-terminal variant increases sarcoma tumour cell aggressiveness.
Hum Mol Genet
June 2024
School of Pharmacy and Biomedical Sciences, University of Portsmouth, White Swan Road, Portsmouth PO1 2DT, United Kingdom.
Alterations in Dp71 expression, the most ubiquitous dystrophin isoform, have been associated with patient survival across tumours. Intriguingly, in certain malignancies, Dp71 acts as a tumour suppressor, while manifesting oncogenic properties in others. This diversity could be explained by the expression of two Dp71 splice variants encoding proteins with distinct C-termini, each with specific properties.
View Article and Find Full Text PDFThe IAAM LTBP4 Haplotype is Protective Against Dystrophin-Deficient Cardiomyopathy.
J Neuromuscul Dis
March 2024
Department of Neurosciences DNS, University of Padova, Padova, Italy.
Background: Dilated cardiomyopathy (DCM) is a major complication of, and leading cause of mortality in Duchenne muscular dystrophy (DMD). Its severity, age at onset, and rate of progression display wide variability, whose molecular bases have been scarcely elucidated. Potential DCM-modifying factors include glucocorticoid (GC) and cardiological treatments, DMD mutation type and location, and variants in other genes.
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!