Biomedical subjects

Fang Wang

Publications and source records attributed to Fang Wang.

At least 145 records · Page 8Linked to original sources

PubMed2005

Measuring dynamics of caspase-3 activity in living cells using FRET technique during apoptosis induced by high fluence low-power laser irradiation.

BACKGROUND AND OBJECTIVES: Low-power laser irradiation (LPLI) has been used for therapies such as curing spinal cord injury, healing wound etc. Yet, the mechanism of LPLI remains unclear. In order to determine the effects of high fluence LPLI on cell growth and caspase-3 activity, we have measured the dynamics of caspase-3 activity during cell apoptosis induced by high fluence LPLI treatment. STUDY DESIGN/MATERIALS AND METHODS: He-Ne laser was used to irradiate human lung adenocarcinoma cells (ASTC-a-1). Cell Counting Kit-8 was used for cytotoxicity assay. A fluorescent microscope was used to perform fluorescence resonance energy transfer (FRET) imaging. A luminescence spectrometer was used to acquire the fluorescent emission spectrum. Statistical analysis was performed with Student's paired t-test. RESULTS: Cytotoxicity assay showed that when light irradiation fluence exceeded 60 J/cm2, LPLI treatment induced ASTC-a-1 cell apoptosis in a fluence-dependent manner. FRET imaging and spectrofluorometric analysis demonstrated that caspase-3 was activated during high fluence LPLI-induced cell apoptosis. CONCLUSIONS: Using FRET technique, we have reported that high fluence LPLI can induce human lung adenocarcinoma cells (ASTC-a-1) apoptosis. The activation of caspase-3 plays an important role in the apoptotic process.

Adenocarcinoma↗

PubMed2005

Changes in soil properties after establishment of Artemisia halodendron and Caragana microphylla on shifting sand dunes in semiarid Horqin Sandy Land, northern China.

In the semiarid Horqin sandy land of northern China, establishment of artificial sand-fixing shrubs on desertified sandy lands is an effective measure to control desertification and improve the regional environment. Caragana microphylla Lam. and Artemisia halodendron Turcz. ex Bess. are two of the dominant native shrub species, which are adapted well to windy and sandy environments, and thus, are widely used in revegetation programs to control desertification in Horqin region. To assess the effects of artificially planting these two shrub species on restoration of desertified sandy land, soil properties and plant colonization were measured 6 years after planting shrubs on shifting sand dunes. Soil samples were taken from two depths (0-5 cm and 5-20 cm) under the shrub canopy, in the mid-row location (alley) between shrub belts, and from nonvegetated shifting sand dune (as a control). Soil fine fractions, soil water holding capacity, soil organic C and total N have significantly increased, and pH and bulk density have declined at the 0-5-cm topsoil in both C. microphylla and A. halodendron. At the 5-20 cm subsurface soil, changes in soil properties are not significant, with exception of bulk density and organic C concentration under the canopy of A. halodendron and total N concentration under the canopy of C. microphylla. Soil amelioration processes are initiated under the shrub canopies, as higher C and N concentrations were found under the canopies compared with alleys. At the same time, the establishment of shrubs facilitates the colonization and development of herbaceous species. A. halodendron proved to have better effects in fixing the sand surface, improving soil properties, and restoring plant species in comparison to C. microphylla.

Aluminum Silicates↗

PubMed2005

Asymmetric reduction of ethyl 4-chloro-3-oxobutanoate to ethyl (R)-4-chloro-3-hydroxybutanoate with two co-existing, recombinant Escherichia coli strains.

Two recombinant strains, E. coli M15 (pQE30-alr0307) and E. coli M15 (pQE30-gdh0310), which were constructed to express, respectively, an NADPH-dependent aldehyde reductase gene and a glucose dehydrogenase gene, were mixed in an appropriate ratio and used for the asymmetric reduction of ethyl 4-chloro-3-oxobutanoate to ethyl (R)-4-chloro-3-hydroxybutanoate. The former strain acted as catalyst and the latter functioned in NADPH regeneration. The biotransformation was completed effectively without any addition of glucose dehydrogenase or NADP+/NADPH. An optical purity of 99% (ee) was obtained and the product yield reached 90.5% from 28.5 mM: substrate.

Acetoacetates↗

PubMed2005

Neutralization of muscarinic receptor autoantibodies by intravenous immunoglobulin in Sjögren syndrome.

Autoantibodies that inhibit M3 muscarinic receptor (M3R)-mediated neurotransmission and cause bladder and bowel dysfunction have been reported in patients with Sjögren syndrome and belong to a family of functional autoantibodies that includes the thyroid-stimulating hormone receptor antibody present in Graves disease. We have recently reported that antiidiotypic antibodies present in pooled immunoglobulin (Ig) G or IgG from healthy individuals neutralize anti-M3R antibody-mediated inhibition of smooth muscle contraction in vitro. Here we extend these studies to the clinic by examining whether therapeutic doses of intravenous immunoglobulin (IVIG) provided to patients with autoimmune diseases neutralize anti-M3R activity in vivo and improve bladder and bowel symptoms. Three patients with primary Sjögren syndrome, dermatomyositis, and celiac disease, respectively, all of whom had anti-M3R activity on a functional bladder contractile assay, were provided a single course of IVIG at a dose of 400 mg/kg per day for 5 days. Anti-M3R activity was neutralized at 4 weeks after IVIG infusion, whereas levels of specific autoantibodies (anti-La, anti-Jo-1, and anti-tissue transglutaminase) were unchanged. Bladder and bowel scores revealed variable improvement after IVIG. Neutralization of anti-M3R activity by IVIG in vivo, presumably as a result of antiidiotypic antibodies directed specifically against anti-M3R autoantibodies, provides a clinical correlate of our in vitro findings. This offers a rationale for IVIG as a treatment for parasympathetic dysfunction in patients with autoantibodies inhibiting postganglionic cholinergic neurotransmission. We suggest the presence of a network of naturally occurring antiidiotypic antibodies that regulate the expression of functional autoantibodies against neuronal receptors and ion channels.

Adult↗

PubMed2005

Ana o 3, an important cashew nut (Anacardium occidentale L.) allergen of the 2S albumin family.

BACKGROUND: Cashew nut allergy is the second most commonly reported tree nut allergy in the United States. We have previously cloned and characterized major cashew allergens belonging to the vicilin and legumin families of seed storage proteins. OBJECTIVE: Here we set out to describe a third major cashew allergen, a 2S albumin. METHODS: The recombinant cashew 2S albumin was amplified from a cDNA library by means of PCR, sequenced, and expressed in Escherichia coli. Immunoblotting was used to screen for reactivity with patients' sera, and inhibition immunoblotting was used to identify the corresponding native cashew nut proteins. The mass of affinity-purified native allergen was determined by means of matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectroscopy. Patients' sera were used to probe solid-phase 2S albumin peptides to identify linear epitopes. RESULTS: The cloned allergen, designated Ana o 3, was identified as 2S albumin. MALDI-TOF mass spectroscopy of native Ana o 3 yielded a molecular mass of 12,598 d. Immunoblot analysis showed 21 (81%) of 26 sera from patients with cashew allergy were reactive. Three native Ana o 3 large-subunit isoforms with molecular weights ranging from approximately 6 to 10 kd were identified. Probing of overlapping synthetic Ana o 3 peptides with patients' sera identified 16 reactive peptides, 4 of which gave strong signals and one of which positionally overlaps linear epitopes in mustard and walnut allergenic 2S albumins. The overlapping cashew and walnut epitopes also share considerable homology. CONCLUSIONS: We conclude that this 2S albumin protein is a major allergen in cashew nut and demonstrates a possible basis for cross-reactivity with walnut 2S albumin.

Adolescent↗

PubMed2005

Disruption of palladin results in neural tube closure defects in mice.

Palladin is a newly identified actin-associated protein which was proposed to be involved in actin cytoskeleton organization and nervous system development. Here, we show that inactivation of palladin leads to embryonic lethality due to severe defects of cranial neural tube closure and herniation of liver and intestine. It was found that palladin(-/-) embryos died around E15.5 and developed cranial neural tube closure defects (NTDs) with 100% penetrance. Whole mount in situ hybridization revealed that expression of palladin in early wild type embryos (E8.5) was specifically restricted in the elevating cranial neural folds where the neural tube closure is initiated. Palladin expression closely mirrors the phenotypic defects observed in palladin(-/-) mutants. While in E 9.5 and E10.5 embryos palladin was ubiquitously expressed. In vitro study revealed that formation of stress fibers in cytoplasm, cell adherent ability to extra-cellular matrix protein fibronectin and cell migration were dramatically disturbed in palladin(-/-) murine embryonic fibroblast cells (MEFs). Our findings suggest that palladin plays important roles in actin stress fiber formation, cell adhesion and migration. We propose that palladin is required for the initiation of neural tube closure and provides an important new candidate that may be implicated in the etiology of human NTDs.

Animals↗

PubMed2005

Resveratrol induces apoptosis and differentiation in acute promyelocytic leukemia (NB4) cells.

Resveratrol (3,5,4'-trihydroxy-trans-stilbene) is a naturally occurring phytoalexin found in grapes and wine, and has been reported to exert a variety of important pharmacological effects. We have investigated the activity of resveratrol on proliferation and differentiation of the acute promyelocytic leukemia cell line NB4. The growth inhibitory properties of resveratrol appear to be due to its induction of apoptotic cell death, as determined by morphological changes, DNA fragmentation, increased proportion of the subdiploid cell population and decreased mitochondrial transmembrane potential (Deltapsi(m)). Colorimetric assay for activity of caspase-3 showed an obvious increase in caspase-3 activity in cells after treatment with resveratrol. However, the expression levels of protein Bcl-2 and Bax show no significant change in response to resveratrol treatment. These results suggest that apoptosis of NB4 cells induced by resveratrol requires caspase-3 activation and is related to the mitochondrial transmembrane potential. The combination of resveratrol and all-tran-retinoic acid (ATRA) induced 100% of the NB4 cells to become NBT-positive, whereas only a small part of cells became positive for NBT after a similar exposure to either resveratrol or ATRA alone. Thus, resveratrol may be useful in treating acute promyelocytic leukemia.

Anticarcinogenic Agents↗

PubMed2005

Anti-angiogenic activity of resveratrol, a natural compound from medicinal plants.

Resveratrol (3,4',5-trihydroxy-trans-stilbene), a naturally occurring phytoalexin found in grapes and wine, possesses cancer-preventive activity. Angiogenesis is a crucial step in the growth and metastasis of cancers. We have investigated the effect of resveratrol on angiogenesis in vitro and ex vivo, and found that resveratrol directly inhibited human umbilical vein endothelial cell growth and decreased the gelatinolytic activities of matrix metalloproteinase-2. Tube formation was inhibited by treatment with resveratrol after plating endothelial cells on Matrigel. Resveratrol treatment also inhibited endothelial cell attachment to basement membrane components fibronectin and laminin, and displays similar behavior on cell chemotaxis. In addition, resveratrol has been found to be an angiogenesis inhibitor in the rat aorta matrix culture model. Therefore, inhibition of angiogenesis associated with cancer may be a novel mechanism for the anticancer activity of resveratrol.

Angiogenesis Inhibitors↗

PubMed2005

PVD following plasmin but not hyaluronidase: implications for combination pharmacologic vitreolysis therapy.

PURPOSE: To study whether intravitreal injection of plasmin + hyaluronidase safely induces posterior vitreous detachment (PVD). METHODS: Rabbits were randomized into three groups: (A) 20 rabbits, intravitreal injection of plasmin 1 U + hyaluronidase 20 U in balanced salt solution (BSS) 0.1 mL into one eye; (B) 12 rabbits, plasmin alone; (C) 12 rabbits, hyaluronidase alone. The fellow eye of each rabbit was injected BSS 0.1 mL. In Group A, scanning electron microscopy (SEM) was done in four rabbits at 0.5 hour and in four rabbits at 1 hour. After 7 days, all the remaining 36 rabbits received electroretinography, SEM was examined in eight of each group, and immunohistochemistry was done in four of each group. RESULTS: SEM disclosed the eyes of Group A had complete PVD (8/8), Group B partial PVD (7/8), and Group C (8/8) and all the control eyes (24/24) no PVD after 7 days. Partial PVD was found in 4/4 at 0.5 hour and complete PVD was seen in 3/4 at 1 hour in Group A. Immunohistochemistry showed that the amounts of laminin and fibronectin in the vitreoretinal interface were decreased in Group A and B versus the control eyes (P <0.001), but not in Group C versus the control eyes (P >0.05). Electroretinography showed no changes in any group (P >0.05). CONCLUSION: Vitreous injection of plasmin + hyaluronidase induced complete PVD with no obvious toxicity. Plasmin induced partial PVD, but hyaluronidase had no effects.

Animals↗

PubMed2005

Induction of mucosal and systemic immune response by single-dose oral immunization with biodegradable microparticles containing DNA encoding HBsAg.

The purpose of this work was to assess the ability of plasmid DNA encoding hepatitis B virus (HBV) HBsAg encapsulated in poly(DL-lactide-co-glycolic acid) (PLGA) microparticles to induce local and systemic HBsAg-specific immunity following a single dose of oral immunization. RT-PCR analysis demonstrated prolonged transcription of plasmid DNA, consistent with the sustained expression and presentation of target antigen observed by confocal laser scanning microscopy, in gut-associated lymphocyte tissue (GALT) from mice immunized orally with plasmid DNA encapsulated into PLGA microparticles. Oral administration of PLGA-DNA microparticles induced a long-lasting and stable antigen-specific antibody response, both serum total antibody and intestinal IgA, in BALB/c mice. Mice immunized orally exhibited antigen-specific gamma interferon production and cytotoxic T lymphocyte responses in spleen and GALT after restimulation in vitro with HBsAg or tumour cells stably expressing HBsAg. In contrast, naked DNA vaccines given by intramuscular injection induced only systemic cellular and humoral responses to HBsAg, which were much lower than the responses elicited by oral DNA encapsulated in PLGA microparticles at equivalent doses. The results are encouraging with regard to obtaining good compliance and vaccination coverage with candidate plasmid DNA vaccines, especially in developing countries.

Administration, Oral↗

PubMed2005

Enhancement of glutamate uptake mediates the neuroprotection exerted by activating group II or III metabotropic glutamate receptors on astrocytes.

We investigated whether the activation of astroglial group II and III metabotropic glutamate receptors (mGluRs) could exert neuroprotective effects and whether the neuroprotection was related to glutamate uptake. Our results showed that the activation of astroglial group II or III mGluRs exerted neuroprotection against 1-methyl-4-phenylpyridinium (MPP+) astroglial conditioned medium-induced neurotoxicity in midbrain neuron cultures. Furthermore, MPP+ decreased glutamate uptake of primary astrocytes and C6 glioma cells, which was recovered by activating group II or III mGluRs. Specific group II or III mGluRs antagonists completely abolished the neuroprotective effects and the enhancement of glutamate uptake of their respective agonists. Our results showed that the primary cultured rat astrocytes and C6 glioma cells expressed receptor proteins for group II mGluR2/3, group III mGluR4, mGluR6 and mGluR7. C6 glioma cells expressed mRNA for group II mGluR3, group III mGluR4, mGluR6, mGluR7 and mGluR8. In conclusion, we confirmed that the activation of astroglial mGluRs exerted neuroprotection, and demonstrated that the mechanism underlying this protective role was at least partially related to the enhancement of glutamate uptake.

1-Methyl-4-phenylpyridinium↗

PubMed2005

Detection of mutations in the COL4A5 gene by analyzing cDNA of skin fibroblasts.

BACKGROUND: Alport syndrome is a progressive hereditary glomerulonephritis that is characterized by hematuria, sensorineural deafness, ocular lesions, and progressive renal failure. The majority of cases (about 85%) are caused by mutations in the COL4A5 gene on the X chromosome which encodes the type IV collagen alpha5 chain (X-linked Alport syndrome). METHODS: In this study we performed a systematic analysis of the entire coding region of COL4A5 mRNA in 31 unrelated Chinese X-linked Alport syndrome patients and four controls by using reverse transcription-polymerase chain reaction (RT-PCR) and direct sequencing methods. The mRNA analyzed was isolated from cultured skin fibroblasts of Alport syndrome patients. RESULTS: The entire sequences of mRNA of the controls corresponded exactly to the published sequence. There were 28 variants detected by analyzing mRNA of COL4A5 in 28/31 patients. Of those, a total of 25 functionally significant COL4A5 mutations was confirmed in 25/31 patients by using RT-PCR method and subsequently confirmed at genomic DNA level, which included seven different mutations described in previous reports, and 18 novel mutations. The mutation detection rate was 80.6% (25/31), which is comparable with the highest previous detection sensitivity of COL4A5 mutations in evident X-linked Alport syndrome using genomic DNA. Furthermore, three splicing mutations that occurred at the cryptic splice sites and would be overlooked or simply considered as intronic sequence variations by solely analyzing genomic DNA were identified in this study. CONCLUSION: RT-PCR and direct sequencing using cultured skin fibroblasts RNA is a practical approach with high sensitivity for genetic analysis in X-linked Alport syndrome patients.

Chromosomes, Human, X↗

PubMed2005

A highly epothilone B-resistant A549 cell line with mutations in tubulin that confer drug dependence.

A 95-fold epothilone B (EpoB)-resistant, but not dependent, A549 human lung carcinoma cell line, A549.EpoB40 (EpoB40), has a Gln to Glu mutation at residue 292 that is situated near the M-loop of betaI-tubulin. Further selection of this cell line with higher concentrations of EpoB produced A549.EpoB480 (EpoB480), which is approximately 900-fold resistant to EpoB. This cell line, like EpoB40, exhibits cross-resistance to Taxol and extreme sensitivity to vinblastine, but in contrast to EpoB40 it is unusually dependent on EpoB, requiring a minimum of 125 nmol/L EpoB to maintain normal growth. Sequence analysis of the beta-tubulin and Kalpha1-tubulin genes in EpoB480 showed that, in addition to the beta292 mutation, beta60 was mutated from Val to Phe and alpha195 was mutated from Leu to Met. Mass spectrometry indicated that both the Val(60)Phe and Leu(195)Met mutations in betaI- and Kalpha1-tubulin, respectively, were expressed at the protein level. Molecular modeling indicated that beta60 is located at the end of the H1-S2 loop that has been implicated as a principal partner of the M-loop for contacts between protofilaments. A mutation at beta60 could inhibit the lateral contacts between protofilaments, thereby destabilizing microtubules. alpha195 is located at the external surface of the microtubule that has been proposed as the domain that interacts with a variety of endogenous proteins, such as stathmin and microtubule-associated protein 4. A mutation at alpha195 could modulate the interactions between tubulin and regulatory proteins. We propose that the betaVal(60)Phe mutation plays a critical role in the drug-dependent phenotype of EpoB480 cells.

Cell Line, Tumor↗

PubMed2005

Transforming growth factor-alpha inhibits the intrinsic pathway of c-Myc-induced apoptosis through activation of nuclear factor-kappaB in murine hepatocellular carcinomas.

Nuclear factor-kappaB (NF-kappaB) plays an important role during liver neoplastic development through transcriptional regulation of prosurvival genes, which then counteract the death-inducing signals elicited by the host immune response. The c-Myc proto-oncogene is frequently deregulated in liver tumors. Furthermore, enforced expression of c-Myc in the liver promotes the development of hepatocellular carcinomas, a process that is accelerated by coexpression with transforming growth factor-alpha (TGF-alpha). TGF-alpha/c-Myc-derived hepatocellular carcinomas display reduced apoptotic levels compared with those of single c-Myc transgenic hepatocellular carcinomas, suggesting that TGF-alpha provides a survival advantage to c-Myc-transformed hepatocytes. Given that TGF-alpha/c-Myc hepatocellular carcinomas display constitutive NF-kappaB activity, here, we have tested the hypothesis that enforced expression of TGF-alpha results in constitutive NF-kappaB activation and enhanced cell survival using TGF-alpha/c-Myc-derived hepatocellular carcinoma cell lines. We show that TGF-alpha induces NF-kappaB through the phosphatidylinositol 3-kinase/Akt axis in these bitransgenic hepatocellular carcinomas. Furthermore, we found that adenovirus-mediated inhibition of NF-kappaB activity impairs the ability of TGF-alpha/c-Myc-derived tumor cells to grow in an anchorage-independent fashion due to sensitization to c-Myc-induced apoptosis. Lastly, we show that NF-kappaB inhibits c-Myc-induced activation of caspase-9 and caspase-3 through up-regulation of the antiapoptotic target genes Bcl-X(L) and X-linked inhibitor of apoptosis (XIAP). Overall, these results underscore a crucial role of NF-kappaB in disabling apoptotic pathways initiated by oncogenic transformation.

Animals↗

PubMed2005

Expression of human beta-defensin-2 with multiple joined genes in Escherichia coli.

Human beta-defensin (HBD)-2 is a small cationic peptide with a broad range of antimicrobial activity. In this study, multiple copies of the hBD2 gene were linked in tandem, and a number of different Escherichia coli expression vectors were evaluated, including pQE-30, pBV220, pET-28a(+), and pGEX-4T-2. No expression of multiple joined genes was detectable in the pQE-30 expression system, whereas in pBV220 with one or two joined hBD2 genes and in pET-28a(+) with one, two, or four copies, target proteins were expressed at a low level. Only when pGEX-4T-2 was applied as expression plasmid with one or two joined hBD2 genes were target proteins expressed in high level, and the expressed fusion proteins account for 26 and 16% of the total insoluble proteins, respectively. In the pGEX-4T-2 and pET-28a(+) expression systems, the effects of multiple joined genes on the growth of host strains and plasmid stability were examined. Host cells containing plasmid carrying fewer copies of hBD2 genes were faster in cell growth. Plasmid stability decreased with an increase in multiple joined genes, which was especially noticeable in the pET-28a(+) system. Furthermore, the presence of glucose in culture medium brought about a positive effect on plasmid stability when using pET28-nhBD2 as expression vectors.

Blotting, Western↗

PubMed2005

[Protective effect of phenolic alkaloids from Menispermum dauricum on myocardial cerebral ischemia/reperfusion injury in rabbits].

OBJECTIVE: To explore the mechanism underlying the effects of phenolic alkaloids abstracted from Menispermum dauricum(PAMd) on concurrent myocardial and cerebral ischemia/reperfusion injury in rabbits. METHODS: Both left anterior descending coronary artery and bilateral carotid arteries were ligated to induce myocardial and cerebral ischemia/reperfusion injury at the same time in rabbits. At 30 minutes after ischemia, the occlusion was released to allow return of circulation, and 2 ml of blood was collected from the femoral vein 10 minutes before ischemia, 1, 10, 30 minutes after ischemia, and 1,10, 30, 60, 120, 180, 240 minutes after reperfusion. All rabbits were sacrificed at the end of reperfusion, and the left ventricle, hippocampus, cortex, and cerebellum were removed for examination. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. RESULTS: At 10 minutes after reperfusion, MDA content in serum was significantly higher and SOD activity was significantly lower in ischemia/reperfusion group than those of control group (both P<0.05). In rabbits with administration of PAMd, MDA content was lower and SOD activity was higher in serum compared with ischemia/reperfusion group(P<0.05). Similar results as in the blood in regard to MDA content and SOD activity were obtained in tissues. CONCLUSION: PAMd could attenuate the injury induced by lipid peroxidation and enhance the activity of SOD, thus it might play a protective role in concurrent myocardial-cerebral ischemia/reperfusion injury.

Alkaloids↗

PubMed2005

[The effect of freezing and low molecular weight heparin treatment on the production of hepatocyte growth factor of human RPE cells].

OBJECTIVE: This study is to investigate the human hepatocyte growth factor (HGF) level and proliferation of cultured human retinal pigment epithelial cells (RPE), treated with freezing, or Tedelparin (low molecular weight heparin), or both. METHOD: Cultured human RPE cells were placed at -80 degrees C freezer for 15 and 60 seconds respectively. One group of freezing-treated cells was kept in culture for another 3 d or 6 d, with or without Tedelparin (25 microl/ml). Another group of freezing-treated cells was injected into the vitreous of rabbits immediately, and 3 d or 6 d later the vitreous of injected rabbits were harvested and put into the medium of cultured human RPE cells, with or without Tedelparin (25 microl/ml). The level of HGF in culture medium and vitreous was measured by ELISA, and the cell proliferation was examined by MTT assay. RESULTS: The HGF concentration was increased on day 3 in culture medium of freezing-treated human RPE cells (F = 27.36, P < 0.01), and in the rabbit vitreous injected with freezing-treated human RPE cells (F = 6.24, P < 0.01). Tedelparin can reduce the HGF concentration in culture medium of freezing-treated human RPE cells at day 3 and 6 (F = 179.50, P < 0.01). The rabbit vitreous injected with freezing-treated RPE cells can promote the proliferation of normal RPE cells (P < 0.01), which was suppressed by 48 h treatment of Tedelparin (F = 44.90, P < 0.05). CONCLUSION: Freezing may increase the expression of HGF, or promote the proliferation of RPE cells. Tedelparin may suppress the proliferation of RPE cells by inhibiting HGF production.

Animals↗

PubMed2005

[Involvement of MAPKs and NF-kappaB pathways in Pseudomonas pyocyanin-induced interleukin-8 expression by human airway epithelial cells].

To investigate the molecular mechanisms of signaling transduction by which Pseudomonas pyocyanin induces IL-8 expression in human airway epithelial cells, A549 and SPC-A-1 cells were challenged with P. aeruginosa conditioned medium or pyocyanin. Chemokine interleukin-8 (IL-8) release from the challenged cells was measured by ELISA, and Western blot was performed to analyze the degradation of IkappaB-alpha and the phosphorylation of MAPKs (mitogen-activated protein kinases) in the extracts from cells stimulated with pyocyanin. Both of P. aeruginosa conditioned medium and pyocyanin remarkably increased IL-8 expression by human airway epithelial cells. Degradation of IkappaB-alpha was found shortly after A549 cells were stimulated with pyocyanin. Western hybridization analysis also demonstrated that pyocyanin caused phosphorylation of MAPKs including ERK1/2, p38 and JNK in A549 cells. Pretreatment of A549 cells with U0126 (10 micromol/L), a selective inhibitor of MEK1/2 (ERK1/2 kinase) or with SB203580 (10 micromol/L), a specific inhibitor of p38 MAPK, diminished the pyocyanin-induced IL-8 production. These findings suggest that Pseudomonas pyocyanin can increase IL-8 expression by human airway epithelial cells through MAPKs signaling pathways and the activation of NF-kappaB is also involved in this process.

Butadienes↗