Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HeLa Cells”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

[The comparison of sensitivity of BGM cells, HeLa cells, HEL cells and A 549 cells to herpes simplex virus-1].

This study was undertaken to compare sensitivity of buffulo green monkey (BGM) cells, Hela cells, human embryo lung (HEL) cells and A549 cells to herpes simplex virus-1. The plague forming unit (PFU) technique was used to measure the four cell lines simultaneously. The results showed that BGM cells were superior to the Hela cells, HEL cells, A549 cells in terms of both sensitivity and rapidity of appearance of cytopathic effect (CPE). It indicates that BGM cells constitute a new, sensitive and valuable cell line used for the detection of HSV-1 in cell culture.

Animals↗

Comparison of the sensitivity of human embryo kidney cells, HeLa cells, and WI38 cells for the primary isolation of viruses from the eye.

A comparison has been made of the efficiency of human embryo kidney (HEK) cills, HeLa cells, and WI38 cells for the isolation of viruses from the eyes of patients suffering from acute conjunctivitis or keratoconjunctivitis. From a total of 99 specimens 21 adenoviruses (serotypes 3, 4, 7, 8, and 13) were isolated in HEK cells, eight (serotypes 3 and 8) in HeLa cells, and four (serotype 3) in WI38 cells. Of the ten herpes simplex viruses isolated nine were recovered in HEK cells, seven in WI38 cells, and none in HeLa cells. The combination of HeLa cells and WI38 cells is not considered an adequate alternative to the difficult-to-obtain HEK cells for the isolation of viruses from the eye.

Adenoviridae↗

The Na+,K+,2Cl- -cotransport system in HeLa cells and HeLa cell mutants exhibiting an altered efflux pathway.

We have investigated the characteristics of a transport system in HeLa cells, which turned out to be very similar to a previously described Na+, K+, 2Cl- -cotransport system. For further understanding about the physiological role of the cotransporter, we have mutagenized HeLa cells and selected progeny cells for growth in low potassium (0.2 mM) medium. The selected HeLa cells (LK1) exhibited alterations in the Na+,K+,2Cl- -cotransport system. LK1 cells showed a remarkable reduction of 86Rb+ efflux via the cotransporter when compared to the parental HeLa cells. In contrast, bumetanide-sensitive potassium influx, measured by 86Rb+ uptake, was increased in the LK1 cells (increase in Vmax). Km values of the cotransporter in HeLa cells and LK1 mutants revealed similar properties for 86Rb+ and 22Na+ uptake. In addition, (3H)-bumetanide binding studies were carried out on intact HeLa cells; 1.7 pmol/mg protein (3H)-bumetanide was specifically bound to HeLa parental cells, which could be calculated to a number of 103,000 binding sites/cell. LK1 cells present, 1.44 pmol/mg protein, specifically bound (3H)-bumetanide and, respectively, 137,000 binding sites/cell. The LK1 cells also exhibited an increase in the number of (3H)-ouabain binding sites as well as an increase in the activity of the Na+,K+-ATPase, expressed as a function of ouabain-sensitive 86Rb+ uptake. Furthermore, LK1 cells were different in the concentrations of intracellular Na+ (increases) and K+ (decreases) when compared to the HeLa parental cells. When grown in low K+ medium (0.2 mM K+), protein content and cell volume were increased in the LK1 cells, while the DNA content was not significantly different between both cell lines.

Biological Transport↗

[Experimental study on adenovirus-mediated transfer of p53 or adenovirus- mediated transfer of p53 combined with radiotherapy for human cervical cancer cell line HeLa cells].

OBJECTIVE: To evaluate the therapeutic efficiency of adenovirus-mediated transfer of p53(Ad-p53) or Ad-p53 combined with radiotherapy for human cervical cancer cell line HeLa cells. METHODS: HeLa cells were either transfected with Ad-p53 alone or with Ad-p53 combining with radiotherapy. Reverse transcription polymerase chain reaction(RT-PCR), the cell growth, morphological changes, cell cycle, apoptosis and molecular changes were measured using cell counting, microscopy, flow cytometry, DNA ladder, and in vivo therapy experiments to evaluate the therapeutic efficiency of the regimens. RESULTS: Ad-p53 could be transfected into HeLa cells and p53 mRNA could be expressed more in the targeted HeLa cells. Ad-p53 transfer had strong therapeutic effects to HeLa cells in vitro and in vivo (the inhibition rates were 61.8% and 54.8%, respectively), moreover, the combined administration of Ad-p53 and radiotherapy had stronger therapeutic effects in vitro and in vivo (the inhibition rate was 85.5% in vitro, and the inhibition rate was 77.4% in vivo). The inhibition rate by radiotherapy alone was 44.6% in vitro and 58.4% in vivo. Massive apoptosis of HeLa cells was induced by these regimens. Cell cycle analysis demonstrated that all these regimens could arrested HeLa cells in G(2)-M. CONCLUSIONS: After introduced into HeLa cells, Ad-p53 shows therapeutic efficiency for HeLa cells both in vitro and in vivo. Moreover, Ad-p53 could enhance therapeutic efficiency for HeLa cells when combined with radiotherapy.

Adenoviridae↗

[DNA repair of CHL cells and HeLa cells after DNA damage induced by different oxidative agents].

OBJECTIVE: To investigate DNA repair in CHL cells and HeLa cells after DNA damage induced by different oxidative agents. METHODS: CHL cells and HeLa cells were exposed to various damaging agents, CHL cells: H(2)O(2) for 25 min, K(2)Cr(2)O(7) for 105 min, doxorubicin (Dox) for 75 min HeLa cells: H(2)O(2) for 25 min, K(2)Cr(2)O(7) for 105 min; then cells were continuously cultured for 0-3 h after washing. Alkaline single cell gel electrophoresis (ASCGE) assay was used to detect DNA strand breaks. RESULT: (1) DNA strand breaks were induced in CHL cells after exposure to H(2)O(2) K(2)Cr(2)O(7) or Dox, which were repaired evidently after continuous culture for 1 h(P<0.01). The damages induced by H(2)O(2) or K(2)Cr(2)O(7) were repaired completely after culture for 2-3 h. However, the demage induced by Dox was repaired incompletely. (2) DNA strand breaks were induced also in HeLa cells after exposure to H(2)O(2) or K(2)Cr(2)O(7), which were repaired evidently after continuous culture for 0.5 h(P<0.01),and completely after culture for 1 h. (3) The regression coefficient related to the rate of comet cells and repair time was statistically different (P<0.05) between CHL cells and HeLa cells. CONCLUSION: DNA damage induced by Dox is repaired more difficult than that induced by H(2)O(2) or K(2)Cr(2)O(7). The repair initiates immediately after DNA damage in both of cells, but more rapidly in HeLa cells than in CHL cells.

DNA↗

Dephosphorylation of nitrobenzylthioinosine 5'-monophosphate by ecto 5'-nucleotidase of HeLa cells.

HeLa cells as well as human and mouse erythrocytes possess membrane sites which bind the inhibitor of nucleoside transport, nitrobenzylthioinosine (NBMPR), reversibly but tightly (KD, 10(-9)-10(-10) M). Site-specific binding of the ligand correlates with inhibition of nucleoside transport. The present study showed that the 5'-phosphate of NBMPR, NBMPR-P, was not transport inhibitory. Upon exposure to [35S]NBMPR-P or [G-3H]NBMPR-P, HeLa cells retained the isotopic labels virtually exclusively in the form of NBMPR. The dephosphorylation of [G-3H]NBMPR-P by HeLa cells, assayed by the production of extracellular [G-3H]NBMPR, was competitively inhibited by AMP, but was not affected by the presence of 5 microM NBMPR, a concentration sufficient to completely occupy the transport inhibitory sites. Thus, the sites at which dephosphorylation of NBMPR occurs in HeLa cells are separate from and function independently of the high affinity sites which bind NBMPR.

5'-Nucleotidase↗

Properties of DNA ligase from uninfected and virus-infected HeLa cells.

HeLa cells contain a high M.W. form of DNA ligase which can be completely converted to a low M.W. form. Stokes radius, frictional ratio, sedimentation coefficient, molecular weight, pH dependence, and heat inactivation rate of the two forms have been studied. The major properties of the two forms of DNA ligase in HeLa cells (in particular molecular weights and pH dependence) resemble those of the "dimer" and "monomer" structures described in cultured human cells (Pedrali, G., Spadari, S., Ciarrocchi, G., Pedrini, M., Falaschi, A. (1973) Eur. J. Biochem., 39 343) . In synchronized HeLa cells, the DNA ligase shows a two fold increase during S phase and parallels the increase in the DNA synthesis rate. DNA ligase increases in parallel with viral DNA synthesis after infection of HeLa cells with vaccinia and Herpes virus but its cofactor requirements and physical properties (including the dimer leads to monomer conversion) are unchanged, suggesting that the newly formed ligase is not virus-coded.

HeLa Cells↗

Effect of extracts of trichosanthes root tubers on HepA-H cells and HeLa cells.

AIM: To investigate the cytotoxic activity of extracts of trichosanthes root tubers (EOT) on HepA-H cells and HeLa cells compared with trichosanthin (TCS), and to explore the possible mechanism of growth inhibitory effect of EOT on HeLa cells. METHODS: Tumor cells were cultured in vitro, and then microculture tetrzoalium assay (MTT) was used to investigate drugs' cytotoxic activity. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to observe ultrastructural changes of cells, and electrophoresis was performed to detect changes of biochemical characteristics of intercellular DNA. RESULTS: TCS and EOT had no obvious effects on HepA-H cells (P>0.05), but had remarkable effects on HeLa cells in a time and dose dependent manner (r>0.864, P<0.05 or P<0.01). The inhibitory rate of EOT was much higher than that of TCS (P<0.01). Median inhibitory rates (IC50) of TCS and EOT on HeLa cells were 610.9 mg/L and 115.6 mg/L for 36 h, and 130.7 mg/L and 33.4 mg/L for 48 h respectively. Marked morphologic changes were observed including microvillus disappearance or reduction, cell membrane bledding, cell shrinkage, condensation of chromosomes and apoptotic bodies with complete membranes. Meanwhile, apoptosis of HeLa cells was confirmed by DNA ladder formation on gel electrophoresis. CONCLUSION: TCS and EOT have no obvious effects on HepA-H cells, but have significant inhibitory effects on HeLa cells, indicating that EOT is superior to TCS in anti-tumor activity.

Cell Division↗

Overexpression of manganese-superoxide dismutase prevents methylmercury toxicity in HeLa cells.

HeLa cells were stably transformed with plasmid constructs that allowed constitutive expression of antioxidant enzymes such as catalase, glutathione peroxidase (GSH-Px), Cu,Zn-superoxide dismutase (Cu,Zn-SOD) or Mn-superoxide dismutase (Mn-SOD) to examine the involvement of reactive oxygen generation in methylmercury toxicity. Overexpression of catalase, GSH-Px or Cu,Zn-SOD did not affect the sensitivity of HeLa cells against methylmercury. However, the sensitivity of HeLa cells against methylmercury was decreased by overexpression of Mn-SOD, an enzyme localized in matrix of mitochondria and which decomposes superoxide anions. These results suggest that formation of superoxide anions in the mitochondria might be involved in the mechanism of the cytotoxicity of methylmercury.

Catalase↗

Properties of beta-adrenergic receptors in untreated and butyrate-treated Hela cells.

HeLa cells contain receptors on their surface which are beta-adrenergic in nature. The binding of (-)-[3H]dihydroalprenolol is rapid, reversible, stereospecific and of relatively high affinity. The HeLa cells also contain an adenylate cyclase which is activated by (-)-isoproterenol greater than (-)-epinephrine greater than (-)-norepinephrine. The adenylate cyclase of HeLa is also activated by guanyl-5'-ylimidodophosphate (Gpp(NH)p), a nonhydrolyzable analogue of GTP. Inclusion of both (-)-isoproterenol and Gpp(NH)p leads to approximately additive rather than synergistic activation of adenylate cyclase. After treatment of HeLa cells with 5mM sodium butyrate there is an increase in the number of beta-adrenergic receptors, but not in their affinity, which is reflected in an increased ability of (-)-isoproterenol to activate adenylate cyclase. Other properties of the beta-adrenergic receptor including association and dissociation rates, temperature optimum of adenylate cyclase and response to Gpp(NH)p are relatively unaffected by butyrate pretreatment of the cells.

Adenylyl Cyclases↗

Nucleophosmin/B23 (NPM) oligomer is a major and stable entity in HeLa cells.

HeLa cell extract was separated by 7% polyacrylamide gel electrophoresis without SDS and subsequently stained with anti-nucleophosmin/B23 (NPM) antibody in a Western blot analysis. Two immunobands were obtained. The major band with a slower electromobility (RF = 0.23) is the NPM oligomer, while the fast-moving minor band is the monomer (RF = 0.56). The oligomer constitutes about 95% of total NPM. The oligomer sedimented faster (10 s) than the monomer in sucrose density gradient centrifugation. Three oligomer bands were identified. NPM oligomer is not affected by treatments with DNase. RNase, 10 mM EDTA, 1 M NaCl, and lyophilization. However, 3 M urea causes reversible dissociation of NPM oligomer into monomer. The level of NPM oligomer remains unchanged in HeLa cells after treatment with the cytotoxic agents, actinomycin D, toyocamycin and camptothecin. These results indicate that NPM oligomer is the major and stable NPM entity in HeLa cells.

Biological Transport↗

Reconstitution of RNAase P activity using inactive subunits from E. coli and HeLa cells.

HeLa cell RNAase P activity found in the flow-through of anti-Sm affinity columns can be separated into inactive RNA and protein components. These components can be used to reconstitute active hybrid enzyme complexes with purified subunits from E. coli RNAase P. The RNA in the HeLa cell fractions employed is enriched for species between 85 and 115 nucleotides long. This reconstitution assay is a convenient means of purifying the functional RNA and protein of HeLa cell RNAase P. Probes derived from the genes for the subunits of E. coli RNAase P hybridize to genomic DNA of gram-negative prokaryotic organisms, but no positive signals are seen with genomic DNA from a variety of eukaryotic organisms.

Endoribonucleases↗

Glucocorticoid hormone receptor mediated induction of metallothionein synthesis in HeLa cells.

HeLa cells grown in chemically defined medium lacking glucocorticoids synthesize metallothioneins, low molecular-weight heavy-metal binding proteins. Dexamethasone and hydrocortisone increase the rate of metallothionein synthesis five- to ten-fold. Maximal induction is achieved with 10(-8)M dexamethasone and 10 (-7)M hydrocortisone. Half-maximal induction is achieved at 5 X 10(-9)M dexamethasone and 5 X 10(-8)M hydrocortisone. Although carried for many generations in the absence of any glucocorticoids, HeLa cells (clone S) contain 25,000 specific 3H-dexamethasone receptors that translocate into the nucleus after one hour of incubation. 3H-dexamethasone binds to a single class of receptors with an apparent Kd = 18.8 nM. A variety of steroids can be classified into three classes, based on their effect on metallothionein synthesis: (a) full agonists (optimal inducers), (b) intermediate effectors which have either partial agonist or antagonist activities, and (c) inactive steroids. There is a correlation between the effects on metallothionein synthesis of different steroids and their ability to compete with 3H-dexamethasone binding. We conclude that metallothionein is induced in HeLa cells by a glucocorticoid receptor mediated mechanism.

Dexamethasone↗

Biophysical characterization of gap-junction channels in HeLa cells.

HeLa cells seem not to be junctionally coupled when probed with techniques such as Lucifer yellow spreading and/or ionic coupling measured with three inserted microelectrodes. When investigated with double whole-cell patch-clamp measurements, HeLa cells in monolayer cultures were electrically coupled in 39% of the cases with very low transjunctional conductances (average one to five open channels). These gap-junction channels had a single-channel conductance gamma = 26 +/- 6 pS and were voltage-gated with an equivalent gating charge z = 3.1 +/- 1.5 for a voltage of half-maximal inactivation Uo = 49 +/- 10 mV. The voltage-dependent component represents only 31 +/- 8% of the total junctional conductance. The voltage-insensitive conductance is characterized by a residual open probability po (infinity) = 0.34 +/- 0.12, which corresponds to a ratio Gmin/Gmax = 0.50 +/- 0.12. Dissociation of monolayer cells into cell pairs yielded about 58% coupled cell pairs with no notably altered single-channel properties.

Connexins↗

Characterization of a transferrin-independent uptake system for iron in HeLa cells.

HeLa cells incubated in serum-free medium accumulated 59Fe ("non-transferrin iron") when incubated with either 59Fe-citrate, 59Fe-nitrilotriacetate, or 59Fe dissolved in Tricine ascorbate. Accumulation of iron was time-, concentration-, and Ca2+-dependent and was saturable. Uptake of non-transferrin (non-Tf) iron was transferrin-independent because of the fact that uptake occurred at pH 5.5, a pH at which transferrin binds iron poorly and at which transferrin is not internalized by cells. Uptake of non-Tf iron was less affected than uptake of transferrin iron by 1) exposure of cells to trypsin, a maneuver that cleaves Tf receptors, or 2) incubation of cells with phenylarsine oxide, an agent that inhibits both fluid- and receptor-mediated internalization. After exposure of cells to non-Tf iron at 37 degrees C, most of the cell-associated radioactivity was recovered in heme and ferritin, demonstrating that iron gained access to intracellular compartments and was not simply adsorbed to the cell surface. Uptake of non-Tf iron could be partially blocked by Cu2+ in a dose-dependent manner, while the accumulation of transferrin-bound iron was unaffected by Cu2+. Other transition metals, such as Zn2+, Cd2+, and Mn2+ were able to inhibit the uptake of non-Tf iron to different degrees. The accumulation of 109Cd was inhibited by incubation of cells with non-Tf iron, Cu2+, or Mn2+. The extent of inhibition was concentration- and metal-dependent. A number of cultured cell lines including HeLa, human skin fibroblasts, and Chinese hamster ovary cells demonstrated uptake of non-Tf iron and 109Cd. Additionally, an endosome acidification mutant of Chinese hamster ovary cells, which exhibited an increase in non-Tf iron uptake, also exhibited an increase in the uptake of Cd2+. These observations suggest that the characteristics of the non-Tf iron transport system in HeLa cells are similar if not identical to those reported for perfused rat liver (Wright, T. L., Brissot, P., Ma, W.-L., and Weisiger, P. A. (1986) J. Biol. Chem. 261, 10909-10914) and suggest the existence of a family of transition metal transport systems, each with a different metal specificity.

Arsenicals↗

Heparan sulfate at the surface of HeLa cells.

HeLa cells, labeled with Na235SO4, release into the culture medium 35SO4 bound to plasma membrane vesicles next to 35SO4-glycoproteins and free 35SO4. Plasma membrane vesicles, experimentally produced by treatment with formaldehyde, contain 35SO4 and their surface can be stained with high iron diamine. Scanning of chromatograms of the trypsinate from labeled cells demonstrates radioactivity on the spot of heparan sulfate. It is concluded that HeLa cells synthesize heparan sulfate, which is incorporated at the plasma membrane and released by shedding of small vesicles.

Cell Membrane↗