Biology subjects

Kameyama, T.

Publications and source records attributed to Kameyama, T..

4 recordsLinked to original sources

bioRxiv2026

In vivo brain temperature measurement using quantum dot imaging temperature sensors

Temperature regulation in the brain is essential for maintaining neuronal function and preventing thermally induced damage. Here, we report the development and in vivo application of quantum dots (QDs) to high-resolution thermometry in the mouse brain using two-photon excitation microscopy. These QDs, via the red-to-green photoluminescence (PL) intensity ratios, enabled stable temperature measurements in both normal and chronically hypo-perfused cerebral tissue. Our findings show that localized neuronal activity leads to transient heat generation, which is rapidly dissipated by cerebrovascular responses. In a chronic hypoperfusion model, impaired vascular function resulted in exaggerated and prolonged brain temperature elevations. This thermometry system provides unprecedented insight into the mechanisms of cerebral thermoregulation and highlights the importance of vascular cooling in protecting the brain from heat-induced stress, particularly in pathological conditions such as stroke.

bioengineering↗

bioRxiv2025

Astrocytic Cathepsin D truncates α-synuclein and promotes Lewy neurite-like aggregation in neurons

Parkinsons disease (PD) and related synucleinopathies are marked by the accumulation and propagation of -synuclein (-syn) aggregates, a process primarily studied in neurons. However, the contribution of astrocytes to this process remains unclear. Here, using a physiologically relevant neuron-astrocyte co-culture system that recapitulates tripartite synapse architecture, we show that astrocytes actively process and propagate -syn aggregates. Astrocytes internalize -syn pre-formed fibrils (PFFs) and cleave them into C-terminally truncated, seeding-competent species via the lysosomal protease Cathepsin D (CtsD). These truncated species are subsequently transferred to neurons, where they promote the growth of Lewy neurite (LN)-like aggregates. Notably, -syn PFF exposure disrupts lysosomal membrane integrity in astrocytes, leading to CtsD upregulation. These findings reveal a feed-forward mechanism in which astrocytic lysosomal dysfunction amplifies -syn pathogenicity. Our findings identify astrocytes as active contributors to -syn propagation and highlight the astrocytic lysosomal pathway as a potential therapeutic target in PD.

pathology↗

bioRxiv2025

NT5DC2 downregulation suppresses monoamine oxidase activity and increases catecholamine levels in PC12D cells

Back groundGenome-wide association studies have revealed the involvement of 5-nucleotidase domain-containing protein 2 (NT5DC2) in neuropsychiatric disorders such as schizophrenia and bipolar disorder; however, its function remains unclear. Recently, we found that NT5DC2 downregulation in PC12D cells increases catecholamine synthesis by promoting the activity of tyrosine hydroxylase and that monoamine oxidase A (MAO A) might bind to NT5DC2 using Affinity Purification-Mass Spectroscopy. Methods and ResultsWe investigated the role of NT5DC2 for MAO A activity in PC12D cells. Western blot analysis revealed that NT5DC2 primarily binds to the non-phosphorylated form of MAO A. siRNA-mediated NT5DC2 downregulation reduced MAO A activity, leading to decreased dopamine metabolism and increased noradrenaline synthesis. ConclusionOur findings suggest that NT5DC2 could affect both tyrosine hydroxylase and MAO A activity to control catecholamine synthesis. Therefore, our study provides valuable insights into disorders associated with catecholamine dysregulation, such as Parkinsons disease and neuropsychiatric disorders.

neuroscience↗

bioRxiv2021

The Exon Junction Complex Core Represses Caner-specific Mature mRNA Re-splicing: A Potential Key Role in Terminating Splicing

Using the TSG101 pre-mRNA, we previously discovered cancer-specific resplicing of mature mRNA that generates aberrant transcripts/proteins. The fact that mRNA is aberrantly re-spliced in various cancer cells implies there must be an important mechanism to prevent deleterious re-splicing on the spliced mRNA in normal cells. We thus postulated that the mRNA re-splicing is controlled by specific repressors, and we searched for repressor candidates by siRNA-based screening for mRNA re-splicing activity. We found that knockdown of EIF4A3, which is a core component of the exon junction complex (EJC), significantly promoted mRNA re-splicing. Remarkably, we could recapitulate cancer-specific mRNA resplicing in normal cells by knock-down of any of the core EJC proteins, EIF4A3, MAGOH or RBM8A (Y14), implicating the EJC core as the repressor of mRNA re-splicing often observed in cancer cells. We propose that the EJC core is a critical mRNA quality control factor to prevent over-splicing of mature mRNA.

molecular biology↗