Control Peptide to Opa1, 100 ug...
- Known as:
- Control Peptide Opa1, 100 ug...
- Catalog number:
- P25019
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- Control Peptide Opa1 100 ...
Related genes to: Control Peptide to Opa1, 100 ug...
- Gene:
- OPA1 NIH gene
- Name:
- OPA1 mitochondrial dynamin like GTPase
- Previous symbol:
- -
- Synonyms:
- NTG, KIAA0567, FLJ12460, NPG, MGM1
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 1987-09-11
- Date modifiied:
- 2019-04-23
Related products to: Control Peptide to Opa1, 100 ug...
Related articles to: Control Peptide to Opa1, 100 ug...
- Background The molecular mechanisms governing adaptive neuroprotection during the postpartum period remain unknown. We hypothesized that circulating exosomes contain bioactive cargo (such as Hsp20) that confer neuroprotection against ischemic injury during the postpartum period. Methods Exosomes were isolated from plasma of postpartum female mice (ppExos) and control female mice, and from serial blood samples obtained from healthy human volunteers during pregnancy (3rd trimester) and again on postpartum day 2. Exosomal size and protein markers were confirmed nanoparticle tracking analysis and Western blotting. Neuroprotection with exosome treatment was assessed using mouse neuronal and astrocyte cultures and human retinal pigment cell line subjected to simulated ischemia. I neuroprotection was assessed using transient middle cerebral artery occlusion (MCAO) in young adult and aged mice. Mitochondrial integrity and reactive oxygen species (ROS) production were evaluated by live cell imaging. neuroprotection was evaluated by assessing infarct volume and neurobehavioral scores. Changes in mitochondrial dynamics were measured by immunofluorescence and Western blot. Human exosomes were sent for proteomic assessment (SomaScan™) followed by differential expression analysis (R software v4). Protein quantification was validated by immunoblot. Results ppExos significantly reduced infarct volumes and improved neurological deficits post-MCAO in both young and aged female mice. , ppExos reduced ROS generation in all cell types after simulated ischemia and reduced mitochondrial fragmentation in astrocytes. Mitochondrial fusion proteins Mfn2 and Opa1 proteins were elevated in maternal postpartum brains, and preserved in both astrocyte and neuronal cell cultures after ischemia with ppExo treatment. Proteomics revealed significant upregulation of heat shock protein 20 (Hsp20) in human ppExos, while Western blot validated elevated Hsp20 in both human and mouse ppExos. Simulated ischemia significantly reduced Hsp20 in astrocyte and neuronal cultures which was reversed by treatment with ppExos. In conclusion, ppExos represent a previously unrecognized, naturally optimized neuroprotective agent that enhances mitochondrial resilience and antioxidant defenses associated with enhanced Hsp20 expression. These findings establish a novel platform for sex-informed, cell-free therapies in ischemic cerebrovascular accidents. - Source: PubMed
Publication date: 2026/05/27
Sun XiaoyunXu LijunGreer MajestyMcMillan ElijahArvola OivaSultan PervezAndo KazuoMin Jiong-JinChavda VishalWolf JulianMahajan VinitCarvalho BrendanStary Creed M - Arginine-rich poly-glycine-arginine (poly-GR), a toxic dipeptide repeat protein generated from C9orf72 hexanucleotide repeat expansion, drives mitochondrial dysfunction, oxidative stress, and neuronal loss in amyotrophic lateral sclerosis (ALS). Hyperoside, a bioactive flavonoid, exhibits antioxidant and cytoprotective properties, but its therapeutic relevance to C9orf72-associated ALS remains unclear. - Source: PubMed
Publication date: 2026/06/04
Hsieh Wen-ChiLin Chun-YuWu Hsuan-ChengWeng Eddie Feng-JuWang Shao-Ming - Prion diseases are fatal neurodegenerative diseases caused by misfolded prion protein. DL-3-n-butylphthalide (NBP), a synthetic agent derived from celery seeds, exhibits neuroprotective effects in multiple neurological disorders. However, its effects against prion peptide-induced neurotoxicity remain unclear. - Source: PubMed
Wu WeiZhang XixiJiang MingyueMa Ning - The deubiquitinating enzyme OTULIN has been implicated in the development of lung injury, and regulating its expression may either exacerbate or alleviate pulmonary inflammatory damage. In this study, we aimed to investigate the role of deubiquitinating enzyme OTULIN in hyperoxia-induced lung injury and the underlying mechanisms involved. A bronchopulmonary dysplasia (BPD) model was established by exposing neonatal mice to a hyperoxic environment, and the effects of regulating OTULIN expression on mitochondrial homeostasis in pulmonary epithelial cells were further examined under hyperoxic conditions. In addition, we investigated the mechanisms through which OTULIN regulates mitochondrial-associated proteins and the ubiquitination mechanisms of differential mitochondrial protein OPA1. The results showed that hyperoxia induced significant lung injury in neonatal mice and was accompanied by upregulation of OTULIN expression. Additionally, hyperoxia disrupted mitochondrial homeostasis in neonatal mice lung tissue, as observed by a reduction in mitochondrial number and increased mitochondrial fusion and autophagy. After hyperoxia exposure, overexpression of OTULIN significantly reduced mitochondrial reactive oxygen species (ROS) levels in alveolar epithelial cells, maintained mitochondrial membrane potential, and promoted mitochondrial homeostasis. Mechanistically, OTULIN was found to directly interact with OPA1 and regulate its ubiquitination status. The E3 ubiquitin ligase RNF31 was identified as a key regulator of OPA1 stability, with knockdown of RNF31 reducing OPA1 levels. Moreover, OTULIN regulated the expression of both OPA1 and RNF31 and affected the stability of OPA1 and mitochondrial function through RNF31-dependent mechanisms. In vivo experiments further showed that knockdown of OTULIN aggravated hyperoxia-induced lung injury in neonatal mice, characterized by alveolar simplification, increased fibrosis, and further impairment of mitochondrial function, whereas overexpression of OTULIN alleviated these pathological changes. In conclusion, deubiquitinating enzyme OTULIN protected hyperoxia-induced neonatal lung injury and modulates mitochondrial protein OPA1 in association with the E3 ubiquitin ligase RNF31. These findings provide new insights into the pathogenesis of BPD and highlight the therapeutic potential of targeting the OTULIN/RNF31-OPA1 axis. - Source: PubMed
Publication date: 2026/05/30
Huang LiLiu QingZhang AiminLiu YanhanHuang FurongWang JuanmeiTan MantingWang DuaneZhao MenghuaWu Xu - Mitochondrial morphology varies by neuronal cell type and subcellular compartment; however, the functional significance of these differences is unclear. Hippocampal CA2 neurons are enriched for genes encoding mitochondrial proteins compared to CA1, suggesting a difference in metabolic demand across hippocampal circuits. However, whether CA2 neuron mitochondria are structurally or functionally distinct to support circuit-specific energy demands is unknown. Here we compared mitochondrial morphology, protein expression, and calcium levels across CA1 and CA2 circuits. We found that CA2 dendritic mitochondria were larger than in CA1. However, both subregions harbored larger mitochondria in the entorhinal cortex (EC)-contacting distal dendrites compared to CA3-contacting proximal dendrites. Together, these data demonstrate cell type- and input-specific regulation of mitochondrial morphology that likely influences the function of these distinct circuits. To determine whether differences in mitochondrial fission or fusion account for cell and/or layer specific differences in morphology, we immunostained for MFF and OPA1, which showed a general enrichment in distal relative to proximal dendrites, and an unexpected increase in CA1 distal dendrites compared to CA2 distal dendrites. To show whether these morphological differences result in functionally distinct mitochondria, we measured mitochondrial calcium levels in live slices. We found a striking enrichment of mitochondrial calcium levels in CA2 distal dendrites relative to proximal dendrites, and this layer-specific effect was significantly different from that in CA1 at baseline and after activity. Collectively, these findings reveal discrete morphological and functional differences in mitochondria across hippocampal subregions and dendritic layers, which likely confer unique circuit properties and/or vulnerability to disease. - Source: PubMed
Publication date: 2026/05/26
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