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Hong Cao

Publications and source records attributed to Hong Cao.

At least 37 records · Page 2Linked to original sources

Caveolin-1 interacts directly with dynamin-2.

Caveolin is the principal component of caveolae in vivo. In addition to a structural role, it is believed to play a scaffolding function to organize and inactivate signaling molecules that are concentrated on the cytoplasmic surface of caveolar membranes. The large GTPase dynamin has been shown to mediate the scission of caveolae from the plasma membrane, although it is unclear if dynamin interacts directly with caveolin or via accessory proteins. Therefore, the goal of this study was to test whether dynamin associates with caveolae via a direct binding to the caveolin 1 (Cav1) protein. Immunoelectron microscopy of lung endothelium or a cultured hepatocyte cell line stained with antibodies for Dyn2 and Cav1 shows that these proteins co-localize to caveolae. To further define this interaction biochemically, in vitro experiments were performed using glutathione-S-transferase (GST)-Dyn2 and GST-Cav1 fusion proteins, which demonstrated a direct interaction between these proteins. This interaction appears to be mediated by the proline-arginine-rich domain (PRD) of Dyn2, as a GST-PRD fragment binds Cav1 while GST-Dyn2DeltaPRD does not. Further, in vitro binding studies using two Dyn2 spliced forms and Cav1 peptides immobilized on paper identify specific domains of Cav1 that bind Dyn2. Interestingly, these Cav1-binding domains differ markedly between two spliced variant forms of Dyn2. In support of these distinctive physical interactions, we find that the different Dyn2 forms, when expressed as GTPase-defective mutants, exert markedly different inhibitory effects on caveolae internalization, as assayed by cholera toxin uptake. These studies provide the first evidence for a direct interaction between dynamin and the caveolin coat, and demonstrate a selectivity of one Dyn2 form toward the caveolae-mediated endocytosis.

Amino Acid Sequence↗

Actin and Arf1-dependent recruitment of a cortactin-dynamin complex to the Golgi regulates post-Golgi transport.

Cortactin is an actin-binding protein that has recently been implicated in endocytosis. It binds directly to dynamin-2 (Dyn2), a large GTPase that mediates the formation of vesicles from the plasma membrane and the Golgi. Here we show that cortactin associates with the Golgi to regulate the actin- and Dyn2-dependent transport of cargo. Cortactin antibodies stain the Golgi apparatus, labelling peripheral buds and vesicles that are associated with the cisternae. Notably, in vitro or intact-cell experiments show that activation of Arf1 mediates the recruitment of actin, cortactin and Dyn2 to Golgi membranes. Furthermore, selective disruption of the cortactin-Dyn2 interaction significantly reduces the levels of Dyn2 at the Golgi and blocks the transit of nascent proteins from the trans-Golgi network, resulting in swollen and distended cisternae. These findings support the idea of an Arf1-activated recruitment of an actin, cortactin and Dyn2 complex that is essential for Golgi function.

ADP-Ribosylation Factor 1↗

Dissecting RNA-interference pathway with small molecules.

RNA interference (RNAi) is a process whereby short-interfering RNAs (siRNA) silence gene expression in a sequence-specific manner. We have screened a chemical library of substituted dihydropteridinones and identified a nontoxic, cell permeable, and reversible inhibitor of the RNAi pathway in human cells. Biochemical and fluorescence resonance-energy transfer experiments demonstrated that one of the compounds, named ATPA-18, inhibited siRNA unwinding that occurred within 6 hr of siRNA transfection. Extracts prepared from ATPA-18-treated cells also exhibited a decrease in target RNA cleavage by activated RNA-induced silencing complex (RISC*). Interestingly, when activated RISC*, which harbors unwound antisense siRNA, was treated with ATPA-18 in vitro, target RNA cleavage was not affected, indicating that this compound inhibited siRNA unwinding or steps upstream of unwinding in the RNAi pathway. Our results also establish the timing of siRNA unwinding and show that siRNA helicase activity is required for RNAi. ATPA-18 analogs will therefore provide a new class of small molecules for studying RNAi mechanisms in a variety of model organisms and deciphering in vivo genetic functions through reverse genetics.

Cell Line↗

Identification of two neutralizing regions on the severe acute respiratory syndrome coronavirus spike glycoprotein produced from the mammalian expression system.

The Spike (S) protein of the severe acute respiratory syndrome-associated coronavirus (SARS-CoV) plays important roles in viral pathogenesis and potentially in the development of an effective vaccine against this virulent infectious disease. In this study, the codon-optimized S gene of SARS-CoV was synthesized to construct DNA vaccine plasmids expressing either the full-length or segments of the S protein. High titer S-specific immunoglobulin G antibody responses were elicited in rabbits immunized with DNA against various segments of the S protein. Two neutralizing domains were identified on the S protein, one at the N terminus (Ser12-Thr535) and the other near the C terminus (Arg797-Ile1192).

Animals↗

Pharmacodynamic comparison of pantoprazole enantiomers: inhibition of acid-related lesions and acid secretion in rats and guinea-pigs.

Pantoprazole is an irreversible proton pump inhibitor that is administered as a racemic mixture clinically. The effects of pantoprazole sodium (PAN.Na) enantiomers on acid-related lesions were compared using models of pylorus ligation induced ulcer, histamine induced ulcer and reflux oesophagitis in rats and guinea-pigs. Compared with (+)-PAN.Na and (+/-)-PAN.Na, (-)-PAN.Na showed much stronger inhibitory effects on pylorus ligation induced and histamine induced ulcers, but similar effects on reflux oesophagitis. The doses of (-)-PAN.Na, (+)-PAN.Na and (+/-)-PAN.Na required for 50% inhibition (ID50) of acid-related lesions were 1.28, 5.03 and 3.40 mg kg(-1) against pylorus ligation induced ulcer, 1.20, 4.28 and 3.15 mg kg(-1) against histamine induced ulcer, and 2.92, 3.56 and 3.70 mg kg(-1) against reflux oesophagitis, respectively. The inhibitory effects of PAN.Na enantiomers on basal gastric acid output were compared in rats with acute fistula. In contrast to inhibitory rates of 89.3% and 83.6% on gastric acid output by (-)-PAN.Na and (+/-)-PAN.Na at 1.5 mg kg(-1), (+)-PAN.Na had an inhibitory rate of only 24.7% at the same dose. The above results indicate that (-)-PAN.Na is more potent than (+)-PAN.Na at inhibiting acid-related lesions owing to its stronger inhibition of acid secretion.

2-Pyridinylmethylsulfinylbenzimidazoles↗

Postoperative analgesia after spinal blockade in infants and children undergoing cardiac surgery.

The aim of this prospective, randomized, controlled clinical trial was to define the opioid analgesic requirement after a remifentanil (REMI)-based anesthetic with spinal anesthetic blockade (SAB+REMI) or without (REMI) spinal blockade for open-heart surgery in children. We enrolled 45 patients who were candidates for tracheal extubation in the operating room after cardiac surgery. Exclusion criteria included age <3 mo and >6 yr, pulmonary hypertension, congestive heart failure, contraindication to SAB, and failure to obtain informed consent. All patients had an inhaled induction with sevoflurane and maintenance of anesthesia with REMI and isoflurane (0.3% end-tidal). In addition, patients assigned to the SAB+REMI group received SAB with tetracaine (0.5-2.0 mg/kg) and morphine (7 mug/kg). After tracheal extubation in the operating room, patients received fentanyl 0.3 mug/kg IV every 10 min by patient-controlled analgesia for pain score = 4. Pain scores and fentanyl doses were recorded every hour for 24 h or until the patient was ready for discharge from the intensive care unit. Patients in the SAB+REMI group had significantly lower pain scores (P = 0.046 for the first 8 h; P =0.05 for 24 h) and received less IV fentanyl (P = 0.003 for the first 8 h; P = 0.004 for 24 h) than those in the REMI group. There were no intergroup differences in adverse effects, including hypotension, bradycardia, highest PaCO(2), lowest pH, episodes of oxygen desaturation, pruritus, and vomiting.

Anesthesia, Spinal↗

Pre- or postinsult administration of lidocaine or thiopental attenuates cell death in rat hippocampal slice cultures caused by oxygen-glucose deprivation.

UNLABELLED: Lidocaine and thiopental improve recovery when administrated during hypoxia and ischemia; however, the effect of pre- or postinsult treatment alone is unknown. We applied either lidocaine or thiopental to hippocampal slice cultures from 20-day-old rats either before or after 10 min of oxygen-glucose deprivation (OGD). Propidium iodide (PI) fluorescence was used as an indicator of neuronal death for 7 days after OGD. OGD-induced neuronal death, in both the Cornus Ammonis 1 (CA1) and the dentate gyrus regions, peaked the first day after ischemia. Preinsult administration of either lidocaine (10, 100 microM) or thiopental (250, 600 microM) significantly reduced the damage measured on the first and second days after OGD; these drugs also significantly decreased the summed daily post-OGD PI fluorescence in both regions. Postinsult administration of lidocaine (10, 100 microM) or thiopental (250, 600 microM) significantly decreased the PI fluorescence on the first day after OGD; postinsult administration of these drugs also attenuated the summed daily post-OGD PI. These data indicate that the administration of lidocaine or thiopental either before or directly after OGD reduced neuronal damage in this in vitro model of cerebral ischemia. Postischemic administration is frequently the first opportunity for treatment. IMPLICATIONS: Lidocaine or thiopental applied either 10 min before or 10 min directly after oxygen-glucose deprivation reduced neuronal cell death in rat hippocampal slice cultures. Postinsult administration is often the first opportunity for treatment after stroke; lidocaine and thiopental reduced damage caused by oxygen-glucose deprivation, an in vitro model of stroke.

Animals↗

[Serum leptin level in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To investigate the effect of uvulopalatopharyngoplasty on changes of serum leptin levels in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). METHODS: Sixty-one patients with OSAHS diagnosed by polysomnography were treated with uvulopalatopharyngoplasty. Pretreatment and post-uppp serum leptin concentrations in patients with OSAHS and in BMI-matched controls were measured by radioimmunoassay. Correlations between leptin concentrations and AHI, BMI were analyzed. RESULTS: The concentrations of leptin in patients with OSAHS were higher than that in controls (P < 0.05). Mean levels (x+/-s) of leptin were (9.8+/-2.1) microg/L, (14.2+/-6.7) microg/L, and (19.3+/-7.9) microg/L in patients with severe, mediate and mild obstructive sleep apnea, respectively. Serum leptin levels correlated positively with the degree of OSAHS as reflected by AHI (r = 0. 68, P < 0.01). The leptin concentration of 51 responders after 6 months were significantly decreased (P < 0.01) than that of pre-operation. However, the difference of leptin concentration between pre-operation and post operation was not significant in 9 nonresponders (P > 0.05). CONCLUSIONS: There are higher leptin concentrations in patients with OSAHS, which are significantly correlated to the severity of disease. Serum leptin levels in responders decreased significantly after uvulopalatopharyngoplasty. OSAHS may influence the leptin system, resulting in increased serum leptin level.

Adult↗

[The separation and identification of the flavonoids from the leaves of Bryophyllum pinnatum].

This study investigated the separation of the effective compositions containing quercetin derivatives from the leaves of Bryophyllum pinnatun by solvent extraction of methanol, polar adsorption by porous polymetric resins, mixed solvent extraction of methanol with chloroform and polyamide chromatography. The results indicated that the yield of product containing 51.23% quercetin in the form of quercetin derivatives was 0.2% (W/W). Through the NMR, Mass spectrum, Infrared spectrum, we try to identify the chemical structure of the flavonoids LEF. As a result we can conclude that the chemical structure of the flavonoids from the leaves of Bryophy Ilum pinnatum is C26H28O15 (quercetin3-alpha-L-rha-beta-D-xyl), molecular weight is 580.

Chromatography, High Pressure Liquid↗

Modulating HIV-1 replication by RNA interference directed against human transcription elongation factor SPT5.

BACKGROUND: Several cellular positive and negative elongation factors are involved in regulating RNA polymerase II processivity during transcription elongation in human cells. In recruiting several of these regulatory factors to the 5' long terminal repeat (LTR) promoter during transcription elongation, HIV-1 modulates replication of its genome in a process mediated by the virus-encoded transactivator Tat. One particular cellular regulatory factor, DSIF subunit human SPT5 (hSpt5), has been implicated in both positively and negatively regulating transcriptional elongation but its role in Tat transactivation in vivo and in HIV-1 replication has not been completely elucidated. RESULTS: To understand the in vivo function of hSpt5 and define its role in Tat transactivation and HIV-1 replication, we used RNA interference (RNAi) to specifically knockdown hSpt5 expression by degrading hSpt5 mRNA. Short-interfering RNA (siRNA) designed to target hSpt5 for RNAi successfully resulted in knockdown of both hSpt5 mRNA and protein levels, and did not significantly affect cell viability. In contrast to hSpt5 knockdown, siRNA-mediated silencing of human mRNA capping enzyme, a functionally important hSpt5-interacting cellular protein, was lethal and showed a significant increase in cell death over the course of the knockdown experiment. In addition, hSpt5 knockdown led to significant decreases in Tat transactivation and inhibited HIV-1 replication, indicating that hSpt5 was required for mediating Tat transactivation and HIV-1 replication. CONCLUSIONS: The findings presented here showed that hSpt5 is a bona fide positive regulator of Tat transactivation and HIV-1 replication in vivo. These results also suggest that hSpt5 function in transcription regulation and mRNA capping is essential for a subset of cellular and viral genes and may not be required for global gene expression.

Gene Expression Regulation, Viral↗

Dynamin 2 binds gamma-tubulin and participates in centrosome cohesion.

Dynamin 2 (Dyn2) is a large GTPase involved in vesicle formation and actin reorganization. In this study, we report a novel role for Dyn2 as a component of the centrosome that is involved in centrosome cohesion. By light microscopy, Dyn2 localized aside centrin and colocalized with gamma-tubulin at the centrosome; by immunoelectron microscopy, however, Dyn2 was detected in the pericentriolar material as well as on centrioles. Exogenously expressed green fluorescent protein (GFP)-tagged Dyn2 also localized to the centrosome, whereas glutathione S-transferase (GST)-tagged Dyn2 pulled down a protein complex(es) containing actin, alpha-tubulin and gamma-tubulin from liver homogenate. Furthermore, gel overlay and immunoprecipitation indicated a direct interaction between gamma-tubulin and a 219-amino-acid middle domain of Dyn2. Reduction of Dyn2 protein levels with small-interfering RNA (siRNA) resulted in centrosome splitting, whereas microtubule nucleation from centrosomes was not affected, suggesting a role for Dyn2 in centrosome cohesion. Finally, fluorescence recovery after photobleaching (FRAP) analysis of a GFP-tagged Dyn2 middle domain indicated that Dyn2 is a dynamic exchangeable component of the centrosome. These findings suggest a novel function for Dyn2 as a participant in centrosome cohesion.

Actins↗

Visualizing a correlation between siRNA localization, cellular uptake, and RNAi in living cells.

RNA interference (RNAi) is the process by which short-interfering RNA (siRNA) target a specific mRNA for degradation through interactions with an RNA-induced silencing complex (RISC). Here, a clear correlation between siRNA localization, cellular uptake, and RNAi activity was discovered by delivering siRNA into cells using siRNA-TAT(47-57) peptide, siRNA-TAT(47-57)-derived oligocarbamate conjugates, or nanoparticles. For successful RNAi, the localization of siRNA was distinctly perinuclear, suggesting that siRNA is targeted to these regions for interactions with RISC to induce RNAi. siRNA sequence variation and the presence of the target mRNA apparently did not change the subcellular localization pattern of siRNA. Intriguingly, siRNA conjugated to TAT(47-57) peptide or TAT(47-57)-derived oligocarbamate resulted in efficient RNAi activity and perinuclear localization of siRNA that was distinctly different from nonconjugated free TAT peptide nucleolar localization. These results suggest that interactions with RISC dictate siRNA localization even when siRNA is conjugated to TAT(47-57) peptide.

Base Sequence↗

Inhibition of human immunodeficiency virus type 1 replication by RNA interference directed against human transcription elongation factor P-TEFb (CDK9/CyclinT1).

The human positive transcription elongation factor P-TEFb is composed of two subunits, cyclin T1 (hCycT1) and CDK9, and is involved in transcriptional regulation of cellular genes as well as human immunodeficiency virus type 1 (HIV-1) mRNA. Replication of HIV-1 requires the Tat protein, which activates elongation of RNA polymerase II at the HIV-1 promoter by interacting with hCycT1. To understand the cellular functions of P-TEFb and to test whether suppression of host proteins such as P-TEFb can modulate HIV infectivity without causing cellular toxicity or lethality, we used RNA interference (RNAi) to specifically knock down P-TEFb expression by degrading hCycT1 or CDK9 mRNA. RNAi-mediated gene silencing of P-TEFb in HeLa cells was not lethal and inhibited Tat transactivation and HIV-1 replication in host cells. We also found that CDK9 protein stability depended on hCycT1 protein levels, suggesting that the formation of P-TEFb CDK-cyclin complexes is required for CDK9 stability. Strikingly, P-TEFb knockdown cells showed normal P-TEFb kinase activity. Our studies suggest the existence of a dynamic equilibrium between active and inactive pools of P-TEFb in the cell and indicate that this equilibrium shifts towards the active kinase form to sustain cell viability when P-TEFb protein levels are reduced. The finding that a P-TEFb knockdown was not lethal and still showed normal P-TEFb kinase activity suggested that there is a critical threshold concentration of activated P-TEFb required for cell viability and HIV replication. These results provide new insights into the regulation of P-TEFb function and suggest the possibility that similar mechanisms for monitoring protein levels to modulate the activity of proteins may exist for the regulation of a variety of other enzymatic pathways.

Cell Line↗

Selective binding of TAR RNA by a Tat-derived beta-peptide.

[structure: see text] The interaction between the HIV-1 Tat protein and the TAR RNA element in the nascent viral genomic transcript is required for viral replication. An 11-residue beta-peptide (1), an all-beta homologue of the Arg-rich region Tat 47-57, binds TAR RNA with K(d) = 29 +/- 4 nM. A control beta-peptide (2) in which all Arg side chains are replaced by Lys side chains shows increased affinity but decreased specificity for wild-type vs bulge-deleted TAR RNA, as do the alpha-peptide analogues of 1 and 2.

Amino Acid Sequence↗

Discovery of a small molecule Tat-trans-activation-responsive RNA antagonist that potently inhibits human immunodeficiency virus-1 replication.

Antiretroviral therapy to treat AIDS uses molecules that target the reverse transcriptase and protease enzymes of human immunodeficiency virus, type 1 (HIV-1). A major problem associated with these treatments, however, is the emergence of drug-resistant strains. Thus, there is a compelling need to find drugs against other viral targets. One such target is the interaction between Tat, an HIV-1 regulatory protein essential for viral replication, and trans-activation-responsive (TAR) RNA. Here we describe the design and synthesis of an encoded combinatorial library containing 39,304 unnatural small molecules. Using a rapid high through-put screening technology, we identified 59 compounds. Structure-activity relationship studies led to the synthesis of 19 compounds that bind TAR RNA with high affinities. In the presence of a representative Tat-TAR inhibitor (5 microM TR87), we observed potent and sustained suppression of HIV replication in cultured cells over 24 days. The same concentration of this inhibitor did not exhibit any toxicity in cell cultures or in mice. TR87 was also shown to specifically disrupt Tat-TAR binding in vitro and inhibit Tat-mediated transcriptional activation in vitro and in vivo, providing a strong correlation between its activities and inhibition of HIV-1 replication. These results provide a structural scaffold for further development of new drugs, alone or in combination with other drugs, for treatment of HIV-1-infected individuals. Our results also suggest a general strategy for discovering pharmacophores targeting RNA structures that are essential in progression of other infectious, inflammatory, and genetic diseases.

Animals↗

Photoinduced intramolecular electron transfer and triplet energy transfer in a steroid-linked norbornadiene-carbazole dyad.

Bichromophoric compound 3 beta-((2-(methoxycarbonyl)bicyclo[2.2.1]hepta-2,5-diene-3-yl)carboxy)androst-5-en-17 beta-yl-[2-(N-carbazolyl)acetate] (NBD-S-CZ) was synthesized and its photochemistry was examined by fluorescence quenching, flash photolysis, and chemically induced dynamic nuclear polarization (CIDNP) methods. Fluorescence quenching measurements show that intramolecular electron transfer from the singlet excited state of the carbazole to the norbornadiene group in NBD-S-CZ occurs with an efficiency (Phi SET) of about 14 % and rate constant (kSET) of about 1.6 x 10(7) s-1. Phosphorescence and flash photolysis studies reveal that intramolecular triplet energy transfer and electron transfer from the triplet carbazole to the norbornadiene group proceed with an efficiency (TET + TT) of about 52 % and rate constant (kTET + kTT) of about 3.3 x 10(5) s-1. Upon selective excitation of the carbazole chromophore, nuclear polarization is detected for protons of the norbornadiene group (emission) and its quadricyclane isomer (enhanced absorption); this suggests that the isomerization of the norbornadiene group to the quadricyclane proceeds by a radical-ion pair recombination mechanism in addition to intramolecular triplet sensitization. The long-distance intramolecular triplet energy transfer and electron transfers starting both from the singlet and triplet excited states are proposed to proceed by a through-bond mechanism.

Androstenes↗

Dynamin 3 is a component of the postsynapse, where it interacts with mGluR5 and Homer.

The dynamins comprise a large family of mechanoenzymes known to participate in membrane modeling events. All three conventional dynamin genes (Dyn1, Dyn2, Dyn3) are expressed in mammalian brain and produce more than 27 different dynamin proteins as a result of alternative splicing. Past studies have suggested that Dyn1 participates in specialized neuronal functions such as rapid synaptic vesicle recycling, while Dyn2 may mediate the conventional clathrin-mediated uptake of surface receptors. Currently, the distribution, expression, and function of Dyn3 in neurons, or in any other cell type, are completely undefined. Here, we demonstrate that Dyn1 and Dyn3 localize differentially in the synapse. Dyn1 concentrates within the presynaptic compartment, while Dyn3 localizes to dendritic spine tips. Within the postsynaptic density (PSD), we found Dyn3, but not Dyn1, to be part of a biochemically isolated complex comprised of Homer and metabotropic glutamate receptors. Finally, although dominant-negative Dyn3 did not seem to inhibit receptor endocytosis, overexpression of a specific Dyn3 spliced variant in mature neurons caused a marked remodeling of dendritic spines. These data suggest that Dyn3 is a postsynaptic dynamin and, like its binding partner Homer, plays a significant role in dendritic spine morphogenesis and remodeling.

Amino Acid Sequence↗

Cryptosporidium parvum invasion of biliary epithelia requires host cell tyrosine phosphorylation of cortactin via c-Src.

BACKGROUND & AIMS: Cryptosporidium parvum invasion of epithelia requires polymerization of host cell actin at the attachment site. We analyzed the role of host cell c-Src, a cytoskeleton-associated protein tyrosine kinase, in C. parvum invasion of biliary epithelia. METHODS: In vitro models of biliary cryptosporidiosis using a human biliary epithelial cell line were used to assay the role of c-Src signaling pathway in C. parvum invasion. RESULTS: c-Src and cortactin, an actin-binding protein and a substrate for c-Src, were recruited to the parasite-host cell interface during C. parvum invasion. Tyrosine phosphorylation of cortactin in infected cells was also detected. Inhibition of host cell c-Src significantly blocked C. parvum -induced accumulation and tyrosine phosphorylation of cortactin and actin polymerization at the attachment sites, thereby inhibiting C. parvum invasion of biliary epithelial cells. A triple mutation of tyrosine of cortactin in the epithelia also diminished C. parvum invasion. In addition, proteins originating from the parasite were detected within infected cells at the parasite-host cell interface. Antiserum against C. parvum membrane proteins blocked accumulation of c-Src and cortactin and significantly decreased C. parvum invasion. No accumulation of the endocytosis-related proteins, dynamin 2 and clathrin, was found at the parasite-host cell interface; also, inhibition of dynamin 2 did not block C. parvum invasion. CONCLUSIONS: C. parvum invasion of biliary epithelial cells requires host cell tyrosine phosphorylation of cortactin by a c-Src-mediated signaling pathway to induce actin polymerization at the attachment site, a process associated with microbial secretion but independent of host cell endocytosis.

Actins↗