18 research outputs found
High-Throughput Monitoring of Single Vesicle Fusion Using Freestanding Membranes and Automated Analysis
In
vivo membrane fusion primarily occurs between highly curved
vesicles and planar membranes. A better understanding of fusion entails
an accurate in vitro reproduction of the process. To date, supported
bilayers have been commonly used to mimic the planar membranes. Soluble <i>N</i>-ethylmaleimide-sensitive factor attachment protein receptor
(SNARE) proteins that induce membrane fusion usually have limited
fluidity when embedded in supported bilayers. This alters the kinetics
and prevents correct reconstitution of the overall fusion process.
Also, observing content release across the membrane is hindered by
the lack of a second aqueous compartment. Recently, a step toward
resolving these issues was achieved by using membranes spread on holey
substrates. The mobility of proteins was preserved but vesicles were
prone to bind to the substrate when reaching the edge of the hole,
preventing the observation of many fusion events over the suspended
membrane. Building on this recent advance, we designed a method for
the formation of pore-spanning lipid bilayers containing t-SNARE proteins
on Si/SiO<sub>2</sub> holey chips, allowing the observation of many
individual vesicle fusion events by both lipid mixing and content
release. With this setup, proteins embedded in the suspended membrane
bounced back when they reached the edge of the hole which ensured
vesicles did not bind to the substrate. We observed SNARE-dependent
membrane fusion with the freestanding bilayer of about 500 vesicles.
The time between vesicle docking and fusion is âŒ1 s. We also
present a new multimodal open-source software, Fusion Analyzer Software,
which is required for fast data analysis
Nanohole-Array Induced Metallic Molybdenum Selenide Nanozyme for Photoenhanced Tumor-Specific Therapy
Deficient catalytic sensitivity to the tumor microenvironment
is
a major obstacle to nanozyme-mediated tumor therapy. Electron transfer
is the intrinsic essence for a nanozyme-catalyzed redox reaction.
Here, we developed a nanohole-array-induced metallic molybdenum selenide
(n-MoSe2) that is enriched with Se vacancies
and can serve as an electronic transfer station for cycling electrons
between H2O2 decomposition and glutathione (GSH)
depletion. In a MoSe2 nanohole array, the metallic phase
reaches up to 84.5%, which has been experimentally and theoretically
demonstrated to exhibit ultrasensitive H2O2 responses
and enhanced peroxidase (POD)-like activities for H2O2 thermodynamic heterolysis. More intriguingly, plenty of delocalized
electrons appear due to phase- and vacancy-facilitated band structure
reconstruction. Combined with the limited characteristic sizes of
nanoholes, the surface plasmon resonance effect can be excited, leading
to the broad absorption spectrum spanning of n-MoSe2 from the visible to near-infrared region (NIR) for photothermal
conversion. Under NIR laser irradiation, metallic MoSe2 is able to induce out-of-balance redox and metabolism homeostasis
in the tumor region, thus significantly improving therapeutic effects.
This study that takes advantage of phase and defect engineering offers
inspiring insights into the development of high-efficiency photothermal
nanozymes
High-Throughput Monitoring of Single Vesicle Fusion Using Freestanding Membranes and Automated Analysis
In
vivo membrane fusion primarily occurs between highly curved
vesicles and planar membranes. A better understanding of fusion entails
an accurate in vitro reproduction of the process. To date, supported
bilayers have been commonly used to mimic the planar membranes. Soluble <i>N</i>-ethylmaleimide-sensitive factor attachment protein receptor
(SNARE) proteins that induce membrane fusion usually have limited
fluidity when embedded in supported bilayers. This alters the kinetics
and prevents correct reconstitution of the overall fusion process.
Also, observing content release across the membrane is hindered by
the lack of a second aqueous compartment. Recently, a step toward
resolving these issues was achieved by using membranes spread on holey
substrates. The mobility of proteins was preserved but vesicles were
prone to bind to the substrate when reaching the edge of the hole,
preventing the observation of many fusion events over the suspended
membrane. Building on this recent advance, we designed a method for
the formation of pore-spanning lipid bilayers containing t-SNARE proteins
on Si/SiO<sub>2</sub> holey chips, allowing the observation of many
individual vesicle fusion events by both lipid mixing and content
release. With this setup, proteins embedded in the suspended membrane
bounced back when they reached the edge of the hole which ensured
vesicles did not bind to the substrate. We observed SNARE-dependent
membrane fusion with the freestanding bilayer of about 500 vesicles.
The time between vesicle docking and fusion is âŒ1 s. We also
present a new multimodal open-source software, Fusion Analyzer Software,
which is required for fast data analysis
High-Throughput Monitoring of Single Vesicle Fusion Using Freestanding Membranes and Automated Analysis
In
vivo membrane fusion primarily occurs between highly curved
vesicles and planar membranes. A better understanding of fusion entails
an accurate in vitro reproduction of the process. To date, supported
bilayers have been commonly used to mimic the planar membranes. Soluble <i>N</i>-ethylmaleimide-sensitive factor attachment protein receptor
(SNARE) proteins that induce membrane fusion usually have limited
fluidity when embedded in supported bilayers. This alters the kinetics
and prevents correct reconstitution of the overall fusion process.
Also, observing content release across the membrane is hindered by
the lack of a second aqueous compartment. Recently, a step toward
resolving these issues was achieved by using membranes spread on holey
substrates. The mobility of proteins was preserved but vesicles were
prone to bind to the substrate when reaching the edge of the hole,
preventing the observation of many fusion events over the suspended
membrane. Building on this recent advance, we designed a method for
the formation of pore-spanning lipid bilayers containing t-SNARE proteins
on Si/SiO<sub>2</sub> holey chips, allowing the observation of many
individual vesicle fusion events by both lipid mixing and content
release. With this setup, proteins embedded in the suspended membrane
bounced back when they reached the edge of the hole which ensured
vesicles did not bind to the substrate. We observed SNARE-dependent
membrane fusion with the freestanding bilayer of about 500 vesicles.
The time between vesicle docking and fusion is âŒ1 s. We also
present a new multimodal open-source software, Fusion Analyzer Software,
which is required for fast data analysis
High-Throughput Monitoring of Single Vesicle Fusion Using Freestanding Membranes and Automated Analysis
In
vivo membrane fusion primarily occurs between highly curved
vesicles and planar membranes. A better understanding of fusion entails
an accurate in vitro reproduction of the process. To date, supported
bilayers have been commonly used to mimic the planar membranes. Soluble <i>N</i>-ethylmaleimide-sensitive factor attachment protein receptor
(SNARE) proteins that induce membrane fusion usually have limited
fluidity when embedded in supported bilayers. This alters the kinetics
and prevents correct reconstitution of the overall fusion process.
Also, observing content release across the membrane is hindered by
the lack of a second aqueous compartment. Recently, a step toward
resolving these issues was achieved by using membranes spread on holey
substrates. The mobility of proteins was preserved but vesicles were
prone to bind to the substrate when reaching the edge of the hole,
preventing the observation of many fusion events over the suspended
membrane. Building on this recent advance, we designed a method for
the formation of pore-spanning lipid bilayers containing t-SNARE proteins
on Si/SiO<sub>2</sub> holey chips, allowing the observation of many
individual vesicle fusion events by both lipid mixing and content
release. With this setup, proteins embedded in the suspended membrane
bounced back when they reached the edge of the hole which ensured
vesicles did not bind to the substrate. We observed SNARE-dependent
membrane fusion with the freestanding bilayer of about 500 vesicles.
The time between vesicle docking and fusion is âŒ1 s. We also
present a new multimodal open-source software, Fusion Analyzer Software,
which is required for fast data analysis
High-Throughput Monitoring of Single Vesicle Fusion Using Freestanding Membranes and Automated Analysis
In
vivo membrane fusion primarily occurs between highly curved
vesicles and planar membranes. A better understanding of fusion entails
an accurate in vitro reproduction of the process. To date, supported
bilayers have been commonly used to mimic the planar membranes. Soluble <i>N</i>-ethylmaleimide-sensitive factor attachment protein receptor
(SNARE) proteins that induce membrane fusion usually have limited
fluidity when embedded in supported bilayers. This alters the kinetics
and prevents correct reconstitution of the overall fusion process.
Also, observing content release across the membrane is hindered by
the lack of a second aqueous compartment. Recently, a step toward
resolving these issues was achieved by using membranes spread on holey
substrates. The mobility of proteins was preserved but vesicles were
prone to bind to the substrate when reaching the edge of the hole,
preventing the observation of many fusion events over the suspended
membrane. Building on this recent advance, we designed a method for
the formation of pore-spanning lipid bilayers containing t-SNARE proteins
on Si/SiO<sub>2</sub> holey chips, allowing the observation of many
individual vesicle fusion events by both lipid mixing and content
release. With this setup, proteins embedded in the suspended membrane
bounced back when they reached the edge of the hole which ensured
vesicles did not bind to the substrate. We observed SNARE-dependent
membrane fusion with the freestanding bilayer of about 500 vesicles.
The time between vesicle docking and fusion is âŒ1 s. We also
present a new multimodal open-source software, Fusion Analyzer Software,
which is required for fast data analysis
Table1_HJ11 decoction restrains development of myocardial ischemia-reperfusion injury in rats by suppressing ACSL4-mediated ferroptosis.XLSX
HJ11 is a novel traditional Chinese medicine developed from the appropriate addition and reduction of Si-Miao-Yong-An decoction, which has been commonly used to treat ischemia-reperfusion (I/R) injury in the clinical setting. However, the mechanism of action of HJ11 components remains unclear. Ferroptosis is a critical factor that promotes myocardial I/R injury, and the pathophysiological ferroptosis-mediated lipid peroxidation causes I/R injury. Therefore, this study explored whether HJ11 decoction ameliorates myocardial I/R injury by attenuating ACSL4-mediated ferroptosis. This study also explored the effect of ACSL4 expression on iron-dependent programmed cell death by preparing a rat model of myocardial I/R injury and oxygen glucose deprivation/reperfusion (OGD/R)âinduced H9c2 cells. The results showed that HJ11 decoction improved cardiac function; attenuated I/R injury, apoptosis, oxidative stress, mitochondrial damage, and iron accumulation; and reduced infarct size in the myocardial I/R injury rat model. Additionally, HJ11 decoction suppressed the expression of ferroptosis-promoting proteins [Acyl-CoA synthetase long-chain family member 4 (ACSL4) and cyclooxygenase-2 (COX2)] but promoted the expression of ferroptosis-inhibiting proteins [ferritin heavy chain 1 (FTH1) and glutathione-dependent lipid hydroperoxidase glutathione peroxidase 4 (GPX4)] in the myocardial tissues of the I/R injury rat model. Similar results were found with the OGD/R-induced H9c2 cells. Interestingly, ACSL4 knockdown attenuated iron accumulation, oxidative stress, and ferroptosis in the OGD/R-treated H9c2 cells. However, ACSL4 overexpression counteracted the inhibitory effect of the HJ11 decoction on OGD/R-triggered oxidative stress and ferroptosis in H9c2 cells. These findings suggest that HJ11 decoction restrained the development of myocardial I/R injury by regulating ACSL4-mediated ferroptosis. Thus, HJ11 decoction may be an effective medication to treat myocardial I/R injury.</p
Table7_HJ11 decoction restrains development of myocardial ischemia-reperfusion injury in rats by suppressing ACSL4-mediated ferroptosis.XLSX
HJ11 is a novel traditional Chinese medicine developed from the appropriate addition and reduction of Si-Miao-Yong-An decoction, which has been commonly used to treat ischemia-reperfusion (I/R) injury in the clinical setting. However, the mechanism of action of HJ11 components remains unclear. Ferroptosis is a critical factor that promotes myocardial I/R injury, and the pathophysiological ferroptosis-mediated lipid peroxidation causes I/R injury. Therefore, this study explored whether HJ11 decoction ameliorates myocardial I/R injury by attenuating ACSL4-mediated ferroptosis. This study also explored the effect of ACSL4 expression on iron-dependent programmed cell death by preparing a rat model of myocardial I/R injury and oxygen glucose deprivation/reperfusion (OGD/R)âinduced H9c2 cells. The results showed that HJ11 decoction improved cardiac function; attenuated I/R injury, apoptosis, oxidative stress, mitochondrial damage, and iron accumulation; and reduced infarct size in the myocardial I/R injury rat model. Additionally, HJ11 decoction suppressed the expression of ferroptosis-promoting proteins [Acyl-CoA synthetase long-chain family member 4 (ACSL4) and cyclooxygenase-2 (COX2)] but promoted the expression of ferroptosis-inhibiting proteins [ferritin heavy chain 1 (FTH1) and glutathione-dependent lipid hydroperoxidase glutathione peroxidase 4 (GPX4)] in the myocardial tissues of the I/R injury rat model. Similar results were found with the OGD/R-induced H9c2 cells. Interestingly, ACSL4 knockdown attenuated iron accumulation, oxidative stress, and ferroptosis in the OGD/R-treated H9c2 cells. However, ACSL4 overexpression counteracted the inhibitory effect of the HJ11 decoction on OGD/R-triggered oxidative stress and ferroptosis in H9c2 cells. These findings suggest that HJ11 decoction restrained the development of myocardial I/R injury by regulating ACSL4-mediated ferroptosis. Thus, HJ11 decoction may be an effective medication to treat myocardial I/R injury.</p
Table3_HJ11 decoction restrains development of myocardial ischemia-reperfusion injury in rats by suppressing ACSL4-mediated ferroptosis.XLSX
HJ11 is a novel traditional Chinese medicine developed from the appropriate addition and reduction of Si-Miao-Yong-An decoction, which has been commonly used to treat ischemia-reperfusion (I/R) injury in the clinical setting. However, the mechanism of action of HJ11 components remains unclear. Ferroptosis is a critical factor that promotes myocardial I/R injury, and the pathophysiological ferroptosis-mediated lipid peroxidation causes I/R injury. Therefore, this study explored whether HJ11 decoction ameliorates myocardial I/R injury by attenuating ACSL4-mediated ferroptosis. This study also explored the effect of ACSL4 expression on iron-dependent programmed cell death by preparing a rat model of myocardial I/R injury and oxygen glucose deprivation/reperfusion (OGD/R)âinduced H9c2 cells. The results showed that HJ11 decoction improved cardiac function; attenuated I/R injury, apoptosis, oxidative stress, mitochondrial damage, and iron accumulation; and reduced infarct size in the myocardial I/R injury rat model. Additionally, HJ11 decoction suppressed the expression of ferroptosis-promoting proteins [Acyl-CoA synthetase long-chain family member 4 (ACSL4) and cyclooxygenase-2 (COX2)] but promoted the expression of ferroptosis-inhibiting proteins [ferritin heavy chain 1 (FTH1) and glutathione-dependent lipid hydroperoxidase glutathione peroxidase 4 (GPX4)] in the myocardial tissues of the I/R injury rat model. Similar results were found with the OGD/R-induced H9c2 cells. Interestingly, ACSL4 knockdown attenuated iron accumulation, oxidative stress, and ferroptosis in the OGD/R-treated H9c2 cells. However, ACSL4 overexpression counteracted the inhibitory effect of the HJ11 decoction on OGD/R-triggered oxidative stress and ferroptosis in H9c2 cells. These findings suggest that HJ11 decoction restrained the development of myocardial I/R injury by regulating ACSL4-mediated ferroptosis. Thus, HJ11 decoction may be an effective medication to treat myocardial I/R injury.</p
Table8_HJ11 decoction restrains development of myocardial ischemia-reperfusion injury in rats by suppressing ACSL4-mediated ferroptosis.XLSX
HJ11 is a novel traditional Chinese medicine developed from the appropriate addition and reduction of Si-Miao-Yong-An decoction, which has been commonly used to treat ischemia-reperfusion (I/R) injury in the clinical setting. However, the mechanism of action of HJ11 components remains unclear. Ferroptosis is a critical factor that promotes myocardial I/R injury, and the pathophysiological ferroptosis-mediated lipid peroxidation causes I/R injury. Therefore, this study explored whether HJ11 decoction ameliorates myocardial I/R injury by attenuating ACSL4-mediated ferroptosis. This study also explored the effect of ACSL4 expression on iron-dependent programmed cell death by preparing a rat model of myocardial I/R injury and oxygen glucose deprivation/reperfusion (OGD/R)âinduced H9c2 cells. The results showed that HJ11 decoction improved cardiac function; attenuated I/R injury, apoptosis, oxidative stress, mitochondrial damage, and iron accumulation; and reduced infarct size in the myocardial I/R injury rat model. Additionally, HJ11 decoction suppressed the expression of ferroptosis-promoting proteins [Acyl-CoA synthetase long-chain family member 4 (ACSL4) and cyclooxygenase-2 (COX2)] but promoted the expression of ferroptosis-inhibiting proteins [ferritin heavy chain 1 (FTH1) and glutathione-dependent lipid hydroperoxidase glutathione peroxidase 4 (GPX4)] in the myocardial tissues of the I/R injury rat model. Similar results were found with the OGD/R-induced H9c2 cells. Interestingly, ACSL4 knockdown attenuated iron accumulation, oxidative stress, and ferroptosis in the OGD/R-treated H9c2 cells. However, ACSL4 overexpression counteracted the inhibitory effect of the HJ11 decoction on OGD/R-triggered oxidative stress and ferroptosis in H9c2 cells. These findings suggest that HJ11 decoction restrained the development of myocardial I/R injury by regulating ACSL4-mediated ferroptosis. Thus, HJ11 decoction may be an effective medication to treat myocardial I/R injury.</p