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HIV-1 Nef CAWLEAQ motif: a regulator of monocytes invasion through ENO1 modulation.

HIV-1 transmission and spread involves significant host-virus interaction. Possible targets for obstacle of HIV-1 lie at the site of mucosal barriers. Thus a better understanding of how HIV-1 infects target cells at such sites and leads their invasion is required, with prime focus on the host determinants regulating HIV-1 spread. For the viral infectivity and pathogenicity, HIV-1 Nef facilitates immune evasion through protein-protein interactions within host cell. HIV-1 Nef is significant for viral infectivity and pathogenicity. It enhances HIV-1 replication, facilitating immune evasion by interacting with various host factors and altering cellular pathways via multiple protein-protein interactions. In this study, HIV-1 Nef forms with specific mutations, revealing sequence variability, were studied for their effects in human SupT1 T cell line and (THP-1) monocyte-macrophage cell line. Proteins being downregulated by Nef in SupT1 were further observed in THP-1, and interestingly two host proteins' (ENO-1 and VDAC1) expression was found to be cell lineage specific, being stimulatory in macrophages/monocytes and inhibitory in T cells. Cell migration, invasion and ADP release studies were employed to determine the biological function affected by Nef-mediated regulation of these two host proteins. ENO1-regulated function: cell invasion was enhanced in THP-1 cells, but was inhibited in SupT1 cells by Nef RP01. In addition, the modulation of proteins and cell invasion remained unaffected by a Nef RP14. These results indicated that regulation of host protein expression and invasive property of host cells by Nef was sequence specific, suggesting involvement of a particular motif of Nef. To precisely determine this site, we designed a heptapeptide including the CAWLEAQ-regulating sequence of Nef. Macrophages/monocytes being the major cells affected by HIV-1 at mucosal barriers were particularly investigated by the peptide. The peptide led to reversal of differential expressions of ENO1 in both SupT1 and THP-1 and inhibition of enhanced invasiveness in THP-1 cells. Further AP-1 was identified as a factor involved in this Nef-mediated regulation of host proteins. Together these findings suggest a possible mechanism of host invasion by HIV-1 through the CAWLEAQ motif of Nef-mediated regulation of ENO1 and identify a potential therapeutic target for HIV-1 entry at mucosal barriers.

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[Effect of picroside Ⅱ on the expression of mitochondrial VDAC1 after cerebral ischemia/reperfusion in rats].

To explore the effect of picroside Ⅱ on the expression of mitochondrial voltage-dependent anion channel 1 (VDAC1) in rats after cerebral ischemiareperfusion.A total of 70 Wistar rats models with middle cerebral artery occlusionreperfusion (MCAO/R) were randomly divided into the sham group, model group, picroside (Picr) group, ruthenium red (RuR) group, RuR+ Picr group, Spermine (Sper) group, Sper+ Picr group (=10 per group). Modified neurological severity scale (mNSS) was used to evaluated the neurobehavioral function, the expression of reactive oxygen species (ROS) in brain tissues were measured by enzyme-linked immunosorbent assay (ELISA), the morphology of brain tissues was observed by hematoxylin-eosin (HE) staining, the apoptotic cells were counted by terminal deoxynucleotidyl transferase dUTP nick end labeling assay (TUNEL), and the expressions of VDAC1 and endonuclease G (EndoG) were determined by immunohistochemical assay and Western blot.Compared with the shame group, the mNSS scores (9.6±1.9), the expression of ROS[(47.6±2.7)U/ml], the apoptosis of neuron(23.8±2.8), and the expressions of VDAC1(0.94±0.06) and EndoG in cytoplasm (0.76±0.06) and nuclei(0.75±0.06)were enhanced in the model group (all<0.05). The Picr group had obviously decreased mNSS scores (5.7±0.9), ROS expression[(35.6±2.2)U/ml], number of apoptotic cells (14.5±2.1), VDAC1 (0.63±0.06) and EndoG in cytoplasm (0.34±0.05) and nuclei (0.31±0.06)expressions compared to the model group (<0.05).Picroside Ⅱ could attenuate cerebral I/R injury by down-regulating the expression of VDAC1 and inhibiting the EndoG release from mitochondria into cytoplasm.

1726 related Products with: [Effect of picroside Ⅱ on the expression of mitochondrial VDAC1 after cerebral ischemia/reperfusion in rats].

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Novel function of ceramide for regulation of mitochondrial ATP release in astrocytes.

We reported that amyloid beta peptide (Abeta42) activated neutral sphingomyelinase 2 (nSMase2) thereby increasing the concentration of the sphingolipid ceramide in astrocytes. Here, we show that Abeta42 induced mitochondrial fragmentation in wild type astrocytes, but not in nSMase2-deficient cells or astrocytes treated with Fumonisin B1 (FB1), an inhibitor of ceramide synthases. Unexpectedly, ceramide depletion was concurrent with rapid movements of mitochondria, indicating an unknown function of ceramide for mitochondria. Using immunocytochemistry and super resolution microscopy we detected ceramide-enriched and mitochondria-associated membranes (CEMAMs) that were codistributed with microtubules. Interaction of ceramide with tubulin was confirmed by cross-linking to pacFACer, a bifunctional ceramide analog, and binding of tubulin to ceramide-linked agarose beads. Ceramide-associated tubulin (CAT) translocated from the perinuclear region to peripheral CEMAMs and mitochondria, which was prevented in nSMase2-deficient or FB1-treated astrocytes. Proximity ligation and coimmunoprecipitation assays showed that ceramide depletion reduced association of tubulin with voltage-dependent anion channel 1 (VDAC1), an interaction known to block mitochondrial ADP/ATP transport. Ceramide-depleted astrocytes contained higher levels of ATP, suggesting that ceramide-induced CAT formation leads to VDAC1 closure, thereby reducing mitochondrial ATP release, and potentially motility and resistance to Abeta42. Our data also indicate that inhibiting ceramide generation may protect mitochondria in Alzheimers disease.

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Evolution of Voltage-Dependent Anion Channel Function: From Molecular Sieve to Governator to Actuator of Ferroptosis.

The voltage-dependent anion channel (VDAC) is well known as the pathway for passive diffusion of anionic hydrophilic mitochondrial metabolites across the outer membrane, but a more complex functionality of the three isoforms of VDAC has emerged, as addressed in theResearch Topic on "Uncovering the Function of the Mitochondrial Protein VDAC in Health and Disease: from Structure-Function to Novel Therapeutic Strategies." VDAC as the single most abundant protein in mitochondrial outer membranes is typically involved in isoform-specific interactions of the mitochondrion with its surroundings as, for example, during mitochondria-dependent pathways of cell death. VDAC closure can also act as an adjustable limiter (governator) of global mitochondrial metabolism, as during hepatic ethanol metabolism to promote selective oxidation of membrane-permeant acetaldehyde. In cancer cells, high free tubulin inhibits VDAC1 and VDAC2, contributing to suppression of mitochondrial function in the Warburg phenomenon. Erastin, the canonical inducer of ferroptosis, opens VDAC in the presence of tubulin and hyperpolarizes mitochondria, leading to mitochondrial production of reactive oxygen species, mitochondrial dysfunction, and cell death. Our understanding of VDAC function continues to evolve.

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Protonation state of glutamate 73 regulates the formation of a specific dimeric association of mVDAC1.

The voltage-dependent anion channel (VDAC) is the most abundant protein in the outer mitochondrial membrane and constitutes the primary pathway for the exchange of ions and metabolites between the cytosol and the mitochondria. There is accumulating evidence supporting VDAC's role in mitochondrial metabolic regulation and apoptosis, where VDAC oligomerization has been implicated with these processes. Herein, we report a specific pH-dependent dimerization of murine VDAC1 (mVDAC1) identified by double electron-electron resonance and native mass spectrometry. Intermolecular distances on four singly spin-labeled mVDAC1 mutants were used to generate a model of the low-pH dimer, establishing the presence of residue E73 at the interface. This dimer arrangement is different from any oligomeric state previously described, and it forms as a steep function of pH with an apparent pKof 7.4. Moreover, the monomer-dimer equilibrium affinity constant was determined using native MS, revealing a nearly eightfold enhancement in dimerization affinity at low pH. Mutation of E73 to either alanine or glutamine severely reduces oligomerization, demonstrating the role of protonated E73 in enhancing dimer formation. Based on these results, and the known importance of E73 in VDAC physiology, VDAC dimerization likely plays a significant role in mitochondrial metabolic regulation and apoptosis in response to cytosolic acidification during cellular stress.

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Picroside II Exerts a Neuroprotective Effect by Inhibiting mPTP Permeability and EndoG Release after Cerebral Ischemia/Reperfusion Injury in Rats.

Mitochondrial membrane permeability is closely related to cerebral ischemia/reperfusion (I/R) injury. This paper explored the neuroprotective effect of picroside II (Picr), which inhibits the permeability of mitochondrial permeability transition pore (mPTP) and endonuclease G (EndoG) release from mitochondria into cytoplasm after cerebral I/R in rats. After 2 h of cerebral ischemia and 24 h of reperfusion in rats with different intervention measures, the neurobehavioral function, infarction volume, and reactive oxygen species (ROS) content in brain tissues were observed by modified neurological severity scale (mNSS), triphenyl tetrazolium chloride (TTC) staining, and enzyme-linked immunosorbent assay, respectively. The permeability of mPTP was assayed using spectrophotometry. The morphology and apoptotic cells of brain tissues were observed by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase dUTP nick end labeling assay, respectively. The expressions of EndoG and voltage-dependent anion channel 1 (VDAC1) were determined by immunohistochemical assay and western blot. The Picr group exhibited clear decreases in mNSS scores, ROS content, number of apoptotic cells, mPTP permeability and expression of VDAC1, and EndoG in cytoplasm and nuclei, and the morphology of brain tissue was improved as compared with the model group (P < 0.05). Picr could attenuate cerebral I/R injury by downregulating the expression of VDAC1 and decreasing the permeability of mPTP, thereby inhibiting EndoG release from mitochondria into cytoplasm.

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WDR26/MIP2 interacts with VDAC1 and regulates VDAC1 expression levels in H9c2 cells.

MIP2, one of WDR26 isoforms, encodes a 498 amino acid protein with an amino-terminal CTLH domain and five carboxyl-terminal WD40 motifs. MIP2 is localized to the mitochondria and protects cardiomyocytes against oxidative stress; however, nothing is known about how MIP2 confers its cytoprotection. Using co-immunoprecipitation (co-IP) method to isolate MIP2-protein complex from Sprague -Dawley rat heart, followed by mass spectrometry analysis, we have identified VDAC1, a protein located at mitochondria, as a novel MIP2-interacting protein in the myocardium of rat hearts as well as H9c2 cells. This interaction was further confirmed by co-IP assays in the myocardial tissues and H9c2 cardiomyocytes, and by protein overlay assay (POA) in vitro. It was shown that MIP2 overexpression alleviated the HO-induced increase of VDAC1 and cell damage, and MIP2 deficiency aggravated the increase of VDAC1 and cell damage in HO-treated H9c2 cells. Our research suggests that the protective effect of MIP2 on the cardiomyocytes against oxidative stress is partly associated with its interaction with VDAC1 and thus inhibiting its expression.

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ROS-mediated oligomerization of VDAC2 is associated with quinocetone-induced apoptotic cell death.

Quinocetone (QCT) has been approved and widely used as an animal feed additive in China since 2003. However, investigations indicate that QCT shows potential toxicity both in vitro and in vivo. Although voltage dependent anion channel 1 (VDAC1) involved in regulating QCT-induced apoptotic cell death has been established, the role of voltage dependent anion channel 2 (VDAC2) in QCT-induced toxicity remains unclear. In this study, we showed that QCT-induced cell death was coupled to VDAC2 oligomerization. Moreover, VDAC inhibitor 4, 4'-diisothiocyano stilbene-2, 2'-disulfonic acid (DIDS) alleviated QCT-induced cell death and VDAC2 oligomerization. Meanwhile, overexpression VDAC2 aggravated QCT-induced VDAC2 oligomerization. In addition, caspase inhibitor Z-VAD-FMK and reactive oxidative species (ROS) scavenger N-acetyl-l-cysteine (NAC) apparently blocked QCT-induced cell death and VDAC2 oligomerization. Finally, overexpression N-terminal truncated VDAC2 attenuated QCT-induced VDAC2 oligomerization but had no influence on its localization to mitochondria when comparing to the full length of VDAC2. Taken together, our results reveal that ROS-mediated VDAC2 oligomerization is associated with QCT-induced apoptotic cell death. The N-terminal region of VDAC2 is required for QCT-induced VDAC2 oligomerization.

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Upregulation of Spinal Voltage-Dependent Anion Channel 1 Contributes to Bone Cancer Pain Hypersensitivity in Rats.

Voltage-dependent anion channel 1 (VDAC1) is thought to contribute to the progression of tumor development. However, whether VDAC1 contributes to bone cancer pain remains unknown. In this study, we found that the expression of VDAC1 was upregulated in the L2-5 segments of the spinal dorsal horn at 2 and 3 weeks after injection of tumor cells into the tibial cavity. Intrathecal injection of a VDAC1 inhibitor significantly reversed the pain hypersensitivity and reduced the over-expression of Toll-like receptor 4 (TLR4). Intrathecal injection of minocycline, an inhibitor of microglia, also attenuated the pain hypersensitivity of rat models of bone cancer pain. These results suggest that VDAC1 plays a significant role in the development of complicated cancer pain, possibly by regulating the expression of TLR4.

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VDAC1 and SERCA3 Mediate Progesterone-Triggered Ca2Signaling in Breast Cancer Cells.

Progesterone is a biphasic hormone whose confounding role in breast cancer cells involves an initial proliferative surge, followed by sustained growth arrest. Recently we reported that progesterone induces a time- and concentration-dependent release of reactive oxygen species and thus regulates the antiproliferative activity in the breast cancer cell line. Furthermore, the expression of p27, a crucial cell cycle control protein, was regulated by binding of progesterone on progesterone receptor B, thus leading to antiproliferative signaling via multiple signaling pathways including p53, PTEN, and antioxidant systems. Here, we performed an LC-MS/MS analysis of three different breast cancer cell lines. Bioinformatics data analysis and functional classification of proteins revealed a role of progesterone in calcium signaling in MCF-7 cells, and the major differentially expressed calcium regulators were S100A11, S100A10, calreticulin, VDAC1, SERCA3, and SERCA1. Later on we confirmed it by a cell-line-based system having a calcium cameleon sensor targeted at endoplasmic reticulum and found moderate calcium efflux from endoplasmic reticulum upon progesterone treatment. Real-time PCR, Western blot, and TMRM staining confirmed the role of calcium signaling regulators VDAC1 and SERCA3 in progesterone response. Taking together all of these results with our previous studies, we suggest that progesterone, by regulating important proteins involved in calcium signaling and transport, can modulate cell proliferation and cell death. Furthermore, our research may open new avenues for the hypothesis that surgery conducted during the luteal phase of the menstrual cycle might facilitate improved patient survival.

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