Dataset Information

Improved gliotransmission by increasing intracellular Ca²⁺ via TRPV1 on multi-walled carbon nanotube platforms.

ABSTRACT:

Background

Astrocyte is a key regulator of neuronal activity and excitatory/inhibitory balance via gliotransmission. Recently, gliotransmission has been identified as a novel target for neurological diseases. However, using the properties of nanomaterials to modulate gliotransmission has not been uncovered.

Results

We prepared non-invasive CNT platforms for cells with different nanotopography and properties such as hydrophilicity and conductivity. Using CNT platforms, we investigated the effect of CNT on astrocyte functions participating in synaptic transmission by releasing gliotransmitters. Astrocytes on CNT platforms showed improved cell adhesion and proliferation with upregulated integrin and GFAP expression. In addition, intracellular GABA and glutamate in astrocytes were augmented on CNT platforms. We also demonstrated that gliotransmitters in brain slices were increased by ex vivo incubation with CNT. Additionally, intracellular resting Ca²⁺ level, which is important for gliotransmission, was also increased via TRPV1 on CNT platforms.

Conclusion

CNT can improve astrocyte function including adhesion, proliferation and gliotransmission by increasing resting Ca²⁺ level. Therefore, our study suggests that CNT would be utilized as a new therapeutic platform for central nervous system diseases by modulating gliotransmission.

SUBMITTER: Lee WS

PROVIDER: S-EPMC9367080 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Improved gliotransmission by increasing intracellular Ca<sup>2+</sup> via TRPV1 on multi-walled carbon nanotube platforms.

Lee Won-Seok WS Kang Ji-Hye JH Lee Jung-Hwan JH Kim Yoo Sung YS Kim Jongmin Joseph JJ Kim Han-Sem HS Kim Hae-Won HW Shin Ueon Sang US Yoon Bo-Eun BE

Journal of nanobiotechnology 20220811 1

<h4>Background</h4>Astrocyte is a key regulator of neuronal activity and excitatory/inhibitory balance via gliotransmission. Recently, gliotransmission has been identified as a novel target for neurological diseases. However, using the properties of nanomaterials to modulate gliotransmission has not been uncovered.<h4>Results</h4>We prepared non-invasive CNT platforms for cells with different nanotopography and properties such as hydrophilicity and conductivity. Using CNT platforms, we investiga ...[more]

PMID: 35953847

Similar Datasets

Project description:Mutations in thin filament regulatory proteins that cause hypertrophic cardiomyopathy (HCM) increase myofilament Ca2+ sensitivity. Mouse models exhibit increased Ca2+ buffering and arrhythmias, and we hypothesized that these changes are primary effects of the mutations (independent of compensatory changes) and that increased Ca2+ buffering and altered Ca2+ handling contribute to HCM pathogenesis via activation of Ca2+-dependent signaling. Here, we determined the primary effects of HCM mutations on intracellular Ca2+ handling and Ca2+-dependent signaling in a model system possessing Ca2+-handling mechanisms and contractile protein isoforms closely mirroring the human environment in the absence of potentially confounding remodeling. Using adenovirus, we expressed HCM-causing variants of human troponin-T, troponin-I, and α-tropomyosin (R92Q, R145G, and D175N, respectively) in isolated guinea pig left ventricular cardiomyocytes. After 48 h, each variant had localized to the I-band and comprised ∼50% of the total protein. HCM mutations significantly lowered the Kd of Ca2+ binding, resulting in higher Ca2+ buffering of mutant cardiomyocytes. We observed increased diastolic [Ca2+] and slowed Ca2+ reuptake, coupled with a significant decrease in basal sarcomere length and slowed relaxation. HCM mutant cells had higher sodium/calcium exchanger activity, sarcoplasmic reticulum Ca2+ load, and sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) activity driven by Ca2+/calmodulin-dependent protein kinase II (CaMKII) phosphorylation of phospholamban. The ryanodine receptor (RyR) leak/load relationship was also increased, driven by CaMKII-mediated RyR phosphorylation. Altered Ca2+ homeostasis also increased signaling via both calcineurin/NFAT and extracellular signal-regulated kinase pathways. Altered myofilament Ca2+ buffering is the primary initiator of signaling cascades, indicating that directly targeting myofilament Ca2+ sensitivity provides an attractive therapeutic approach in HCM.

Dataset Information

Improved gliotransmission by increasing intracellular Ca²⁺ via TRPV1 on multi-walled carbon nanotube platforms.

Background

Results

Conclusion

Publications

Improved gliotransmission by increasing intracellular Ca<sup>2+</sup> via TRPV1 on multi-walled carbon nanotube platforms.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

Improved gliotransmission by increasing intracellular Ca2+ via TRPV1 on multi-walled carbon nanotube platforms.

Background

Results

Conclusion

Publications

Improved gliotransmission by increasing intracellular Ca<sup>2+</sup> via TRPV1 on multi-walled carbon nanotube platforms.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Improved gliotransmission by increasing intracellular Ca²⁺ via TRPV1 on multi-walled carbon nanotube platforms.