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Drug delivery systems based on poly(e caprolactone) for cancer treatment

Drug delivery systems based on poly(e caprolactone) for cancer treatment

As can be concluded, taking into account these very interesting results, the potential of PCL particles loaded with anticancer drugs is evident. However, the majority of the research efforts have been focussed on the use of copolymers due to their better drug loading and release properties, and to a more suitable biodegradation profile 10 . As an example, MePEG/PCL amphiphilic block copolymers (nanoparticle diameter ≈ 100 nm) proved to be able to encapsulate doxorubicin (DOX) in aqueous solutions. Confocal laser scanning microscopy (CLSM) demonstrated that drug-loaded micelles accumulated mostly in cytoplasm instead of cell nuclei, in contrast to free DOX. Furthermore, these drug-loaded particles exhibited time-delayed cytotoxicity in human MCF-7 breast cancer cells 47 . This biodegradable block copolymer has also been surface-functionalized with folic acid to target a folate-binding protein that is overexpressed on the surface of many tumor cells. With this aim, PTX-loaded folate-conjugated MePEG/PCL micelles (50 – 130 nm) were prepared by micelle formation in aqueous medium. The in vitro PTX release profile from the micelles showed no initial burst release but a clear sustained release. Interestingly, these PTX-loaded micelles proved much higher cytotoxicity for cancer cells (e.g., MCF-7 and HeLa cells) than MePEG/PCL micelles non-conjugated to folate. A confocal image analysis revealed that fluorescent PTX-loaded folate-conjugated micelles were endocytosed into MCF-7 cells through the interaction with overexpressed folate receptors on the surface of cancer cells 48 . Furthermore, PEG/PCL nanoparticles were prepared by a dialysis method and further surface- functionalized with folate moieties (via a coupling reaction between the –OH groups of PEG and the –COOH group of folic acid) for the active targeting of 5-FU and PTX to tumors. It was observed an enhanced cytotoxicity of these drug-loaded nanoparticles against folate receptor expressing tumor cells 49 . MePEG/PCL nanoparticles loaded with taxol were prepared by a dialysis procedure 26 . This copolymer was also used in the vehiculization of geldanamycin. In this case, the pharmacokinetic profile of the drug was improved (enhancement in the AUC ≈ 72-fold) and this formulation exhibited a lower systemic toxicity 50 . Finally, MePEG/PCL nanoparticles loaded with cisplatin (entrapment efficiency ≥ 75 %) have shown a significant less toxicity and an enhanced circulation time, compared to the free drug. Cisplatin release occurred in a sustained manner. In vitro cytotoxicity studies proved the efficacy of cisplatin-loaded nanoparticles against BGC823 and H 22 cancer cell
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16613788

16613788

mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) phosphorylation in MCF-7 human breast cancer cells. Pretreatment of cells with the selective phospholipase C (PLC) inhibitor U73122, or incubation of cells in a Ca 2þ -free medium did not alter Cch-stimulated MAPK/ERK phosphorylation. Phosphorylation of MAPK/ERK was mimicked by phorbol 12- myristate acetate (PMA), an activator of protein kinase C (PKC), but Cch-evoked MAPK/ERK activation was unaffected by down- regulation of PKC or by pretreatment of cells with GF109203X, a PKC inhibitor. However, Cch-stimulated MAPK/ERK phos- phorylation was completely blocked by myristoylated PKC- z pseudosubstrate, a specific inhibitor of PKC- z , and high doses of staurosporine. Pretreatment of human breast cancer cells with wortmannin or LY294002, selective inhibitors of phosphoinositide 3- kinase (PI3K), diminished Cch-mediated MAPK/ERK phosphorylation. Similar results were observed when MCF-7 cells were pretreated with genistein, a non-selective inhibitor of tyrosine kinases, or with the specific Src tyrosine kinase inhibitor PP2. Moreover, in MCF-7 human breast cancer cells mAChR stimulation induced an increase of protein synthesis and cell proliferation, and these effects were prevented by PD098059, a specific inhibitor of the mitogen activated kinase kinase. In conclusion, analyses of mAChR downstream effectors reveal that PKC- z , PI3K, and Src family of tyrosine kinases, but not intracellular-free Ca 2þ mobilization or conventional and novel PKC activation, are key molecules in the signal cascade leading to MAPK/ERK activation. In addition, MAPK/ERK are involved in the regulation of growth and proliferation of MCF-7 human breast cancer cells. J. Cell. Physiol. 204: 678–686, 2005. ß 2005 Wiley-Liss, Inc.
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16642065

16642065

The resistance of tumour cells to different antineoplastic agent is an obstacle for cancer chemotherapy. The main mechanism in drug resistance is the multidrug resistance (MDR) phenomenon, which constitutes the reduction of intracellular drug level due to the P-glycoprotein pump function [12]. Animal studies have shown that the use of EMF can enhance drug delivery across biological barriers (rat abdominal skin), using benzoic acid as the drug candidate [13]. It has been reported by various authors that PEMF can produce alterations in antineoplastic drugs cytotoxicity [14 – 17]. In addition, the use of unpulsed magnetic fields has been found to produce alterations in MCF-7 cells. In this way, Harland and Liburdy [18] have observed that 1.2 AT, 60 Hz EMF partially blocked tamoxifen’s inhibitory action on the growth of this human mammary tumour cells in vitro.
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16610763

16610763

Apoptosis in different cell lines (Hisamitsu et al. 1997, Simko´ et al. 1998), variations in cell cycle distribution (Schimmelpfeng & Dertinger 1997), alterations in the potency of anticancer drugs (Liang et al. 1997, Miyagi et al. 2000) and changes in cellular Ca 2þ regulation (Lindstrom et al. 1993), ornithine decarboxylase enzyme activity (Valtersson et al. 1997), RNA synthesis (Greene et al. 1991) and Na þ /K þ – ATPase activities (Blank 1992). Moreover, Ishido et al. (2001) found that a 1.2 mT, 50 Hz sinusoidal magnetic field (MF) inhibits the antipro- liferative action of melatonin on MCF-7 cells. However, Loberg et al. (2000) published that MF exposure (60 Hz, 1 mT, 72 hours) has no effect on cell viability or growth in a battery of breast cancer cell lines, including MCF-7.
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Participación de las GTPasas Rac1 y Rho en la migración e invasión de células de cáncer de mama en respuesta a leptina

Participación de las GTPasas Rac1 y Rho en la migración e invasión de células de cáncer de mama en respuesta a leptina

Previously we observed that leptin induces changes in the morphology and actin cytoskeleton rearrangements on MCF7 and MDA-MB-231 cells. To evaluate the participation of PI3K in leptin-induced actin cytoskeleton rearrangements, the cells were treated with leptin in the presence or absence of Wortmanin, and F-actin fibers were stained with rhodamine-phalloidin. In both cell lines, we observed that Wortmanin-treated cells showed perinuclear accumulation F-actin (Figure 4). In normal conditions MCF-7 cells show an epithelial phenotype, but the leptin-treated cells changes to mesenchymal phenotype, and the PI3K inhibition abrogated these leptin-induced changes, retaining the cells in an epithelial shape similar to control cells (Figure 4A). In MDA-MB-231 cells, leptin treatment induced the formation of narrow protrusions at the front or rear of the cells, inhibition of PI3K resulted in cells with elongated shape cells by extending narrow protrusions in multiple directions; moreover, Wortmanin treatment increased cell spread area in several cells, which had broad lamellipodia spread at the cell periphery (Figure 4B). These changes are similar to the ones previously observed in NSC23766 or C3 transferase-treated cells (Mendoza-Catalán, et al 2012. Submitted).
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Evaluación de la actividad citotóxica de los extractos etanólicos de las plantas Annona muricata, Annona cherimola y Physalis peruviana En la línea célular MCF- 7 de adenocarcinoma de seno

Evaluación de la actividad citotóxica de los extractos etanólicos de las plantas Annona muricata, Annona cherimola y Physalis peruviana En la línea célular MCF- 7 de adenocarcinoma de seno

In the present study the cytotoxic activity of the crude extracts obtained from plants Annona cherimola, Physalis peruviana, Annona muricata and Physalis peruviana against the tumor cell line MCF-7 breast adenocarcinoma, by the MTT assay was evaluated. Concentrations by this method were evaluated from 2 µg/mL to 200μg / mL for 48 h in ethanol extracts of plants Annona muricata, Annona cherimola and Physalis peruviana and compared with the effect of vincristine at a concentration 120 nM. The results showed that at a concentration of vincristine 120Nm of MCF-7 cells have a percentage viability of 28%, and found that at a concentration of 75 μ g/mL the MCF-7 cells showed a low percentage of viability for extracts of Annona muricata seeds, seeds of Annona cherimola, leaves of Annona cherimola and leaves and stems Physalis peruviana with an IC 50 = 9 μ g/mL, IC 50 = 34 μ g/mL, IC 50 = 11 μ g/mL, IC 50 = 8
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Computational and Biological Evaluation of N-octadecyl-N'-propylsulfamide, a Selective PPARα Agonist Structurally Related to N-acylethanolamines.

Computational and Biological Evaluation of N-octadecyl-N'-propylsulfamide, a Selective PPARα Agonist Structurally Related to N-acylethanolamines.

In this study, we initially showed by super-shift experiments that the presence of OEA induced effective PPARa-RXRa heterodi- mers that interacted with the PPRE of the ACOX gene. We also performed in vitro studies with the PPRE (DR1) of human CPT1 gene. Our results showed that the interaction of the co-activator SRC1 with PPARa through a functionally active PPRE in the CPT1 gene was stronger in the presence of either OEA or CC7 compared to CC12. Previously we reported a similar effect using another co-activator, TIF2 [17]. Complementary to the GST pull- down studies with CPT1, we performed additional in vitro studies in transfected cells with CPT1-PPRE (DR1)-luciferase and human PPARa and RXRa. Again, PPARa agonists such as OEA, CC7 and GW7647 induced an increase in luciferase activity by enhancing the interaction between CPT1-PPRE and PPARa- RXRa in presence of SRC1. To investigate how RXRa-PPARa modulated the acetylation status of histones and other factors associated with PPREs of target genes in the presence of these drugs, we transiently transfected MCF-7 cells with expression vectors for PPARa and RXRa in either the presence or absence of the HDAC inhibitor TSA. Our results showed for the first time that PPARa inhibition by co-repressors was completely abolished by TSA in the presence of OEA and other agonists, including CC7
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Biocompatible ELR Based Polyplexes Coated with MUC1 Specific Aptamers and Targeted for Breast Cancer Gene Therapy

Biocompatible ELR Based Polyplexes Coated with MUC1 Specific Aptamers and Targeted for Breast Cancer Gene Therapy

793 ELRs as naturally inspired recombinant polymers are 794 characterized by their biocompatibility in terms of lack of 795 cytotoxicity and immunogenicity. This has been assessed in 796 both in vitro and in vivo assays thus making them appropriate 797 for local and systemic administration. 52,61 Similar results were 798 obtained in in vitro studies involving positively charged ELRs. 41 799 In light of these fi ndings and the physical characterization of the 800 polyplexes, their cytotoxicity with S2.2 and 5TR1 aptamers was 801 evaluated using both cancer lines. The results showed that the 802 cell viability of MCF-7 cells incubated in the presence of 803 polyplexes with di ff erent ratios was clearly higher than 100% 804 and about 100% for HepG2 (Figure 4). A similar increase in 805 viability was previously observed in a murine myoblastoma cell 806 line, 62 human breast cancer cell line, 63 and mesenchymal stem 807 cells, 64,65 when treated with several ELRs and, recently, when 808 C6 rat glioma cells were coincubated with ELR polyplexes, 46 809 thereby demonstrating the friendly nature of these recombinant 810 polymers as well as the supplemental speci fi city conferred by 811 the aptamers on MUC1+ cells. In contrast, a high level of 812 cytotoxicity was found for cells treated with PEI, probably due 813 to the presence of free PEI after formation of polyplexes, which 814 disrupts the plasmatic membrane and causes necrosis. 66,67 815 Although PEI is commonly used in transfection for in vitro 816 assays, it often has a strong cytotoxic e ff ect, depending on the 817 cell line, as reported elsewhere. 66,68 Nowadays research is 818 focusing in decreasing this toxicity by the use of biocompatible 819 molecules such as chitosan or employing PEG as shell. 69,70 In 820 contrast, previous studies with positively charged ELRs 821 incubated with blood components showed the innocuous 822 character of these polymers 46 making them useful for 823 intravenous administration.
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Interacción entre los receptores a estrógenos mitocondriales y la ATP sintasa en células de cáncer de mamaInteraction between mitochondrial estrogen receptors and ATP synthase in breast cancer cells

Interacción entre los receptores a estrógenos mitocondriales y la ATP sintasa en células de cáncer de mamaInteraction between mitochondrial estrogen receptors and ATP synthase in breast cancer cells

Breast cancer is the most frequent cancer type in Mexican women. Growth and survival of healthy and breast cancer cells depend on estradiol (E2), which acts through two estrogen receptor subtypes: ERα and ERβ. Thus, the E2-ERs signaling pathway is important for hormone-sensitive cancer progression. The effects of E2 on mitochondrial structure and function are not clearly elucidated. Recently, the presence of estrogen receptors in the mitochondrion and their E2-dependent transcriptional activity were demonstrated in different cell types. This supports the idea that E2 actions on mitochondria are modulated through resident mitochondrial estrogen receptor (mtERs). Moreover, mitochondrial dysfunction has been associated with cancer and other human diseases. In this study we studied the protein-protein interactions between ERs and ATP synthase in the MCF-7 and BT-474 breast cancer cell lines. Western blotting and co-immunoprecipitation were used to analyze these interactions. We detected an interaction between ERα and ATP synthase in mitochondrial and cytoplasmic fractions of the MCF-7 cell line but not in the BT-474 cell line. Our results are the first to prove that there is an interaction between ERα receptors and the ATP synthase in MCF-7 cells. These novel results could represent a potential therapeutic target for the treatment of hormone sensitive breast cancer
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Efecto de la inhibición de la UCP2 sobre el estrés oxidativo inducido por citotóxicos en líneas de cáncer de mama MCF 7

Efecto de la inhibición de la UCP2 sobre el estrés oxidativo inducido por citotóxicos en líneas de cáncer de mama MCF 7

Peroxid/Peroxidase de Molecular Probes. Se sembraron 15000 células MCF-7 por pocillo en una placa de 96 pocillos y tras 24 horas, al encontrarse a una confluencia del 60%, la mitad de las células fueron sometidas a la inhibición de la UCP2 mediante un siRNA mientras que la otra mitad fue sometida al vehículo (lipofectamida). Pasadas 24 horas, se aplicaron los tratamientos (cisplatino, paclitaxel o tamoxifeno) o bien DMSO en el grupo control. Tras 48 horas de tratamiento, se añadió una cantidad de 50μM del reactivo y 0,1 U/mL de peroxidasa de rábano en tampón Krebbs Ringer (145 mM NaCl, 4.86 mM KCl, 0.54 CaCl 2 ,
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Selección y caracterización de nanoanticuerpos de camélidos Anti-CDH11Selection and characterization of camelids anti-CDH11 Nanobodies

Selección y caracterización de nanoanticuerpos de camélidos Anti-CDH11Selection and characterization of camelids anti-CDH11 Nanobodies

Debido a que los bacteriófagos recombinantes expresan el dominio VHH anti CDH11-EC1, se realizó un ensayo de inmunofluorescencia con el fin de verificar que podrían ser candidatos para la detección de diversas patologías en la cual su característica es la sobreexpresión de cadherina-11. Para esto se realizó el ensayo con dos líneas celulares de cáncer de mama: MCF-7 (Figura 26) y MDA-MB-231 (Figura 27). Esta última es característica por sobreexpresar cadherina-11. Por lo que, se marcaron a los bacteriófagos recombinantes de las rondas 1, 2 y 3 con FITC (verde). Este fluoróforo permite el marcaje debido a que se une a las proteínas del bacteriófago por medio de interacciones con los grupos amino(SIGMA, 1990). De igual manera, se utilizó un anticuerpo primario anti-OB cadherin marcado con un anticuerpo secundario Alexa Fluor 594 (rojo) como control positivo. De acuerdo con la Figura 26, las células MCF-7 presentan núcleos definidos indicando el marcaje correcto por el fluoróforo Hoechst (azul). Por otra parte, es posible notar fluorescencia en rojo, tanto en verde en estas células. La fluorescencia en rojo, puede deberse a diversas razones: La primera, podría indicar la expresión de cadherina-11, sin embargo; esta reportado que la cadherina que comúnmente expresa las células MCF-7 es la E-cadherina (Blaschuk y Devemy, 2009). Sin embargo; la fluorescencia de debida por los bacteriófagos recombinantes de las rondas dos y tres es poca, lo cual es posible que los bacteriófagos recombinantes presenten especificidad hacia alguna cadherina similar.
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Modulación del efecto citotóxico del arsénico por meléculas bioactivas

Modulación del efecto citotóxico del arsénico por meléculas bioactivas

Dicha circunstancia podría causar una inducción intensa, rápida y sostenida de la actividad catalítica, aún durante la recuperación. En cambio, aunque silimarina elevó 1,76 veces la actividad de GGT, no protegió a las células del estrés asociado al cambio de medio. En aquellas tratadas con arsenito, sólo quercetina evitó la inhibición causada por éste, requiriendo al menos dos horas de recuperación. En la línea MCF-7, la enzima fue menos activada por los estresantes (cambio de medio y tratamientos), con baja actividad basal (respecto a ZR-75-1). As incrementó tal parámetro luego del periodo de recuperación; efecto que no fue contrarrestado por ninguno de los dos flavonoides. Así, el nivel constitutivo de expresión de GGT determinaría la modalidad de respuesta ulterior a agentes químicos potencialmente nocivos. Esto estimula una visión alternativa sobre biomarcadores de estrés, cuyo real valor dependería del grado de diferenciación celular y su estado funcional. Como aquí se ha visto, en la línea que presentaba niveles basales altos de GGT (ZR-75-1), el efecto citotóxico se asociaba a su inhibición, apoyando su rol citoprotector y protumoral ( 158 ); mientras que el mismo efecto era observado tras su estimulación en células con nivel iniciales menores (MCF-7 y CHO-K1), ilustrando que un parámetro individual no puede ser evaluado sin considerar el contexto biológico de dónde proviene (ej.: GGT como marcador de progresión neoplásica y, simultáneamente, como marcador de daño oxidativo).
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Expresion génica de SERCA2 y SERCA3 en células MCF-7 y MDA-MB-231 de cáncer de mama tratada cpm butirato de sodio, tricostatina A o 5-aza-2´ dc

Expresion génica de SERCA2 y SERCA3 en células MCF-7 y MDA-MB-231 de cáncer de mama tratada cpm butirato de sodio, tricostatina A o 5-aza-2´ dc

expression is considerably reduced or absent in colon, gastric, breast, choroid plexus, and lung cancers compared to normal epithelial cells of these tissues that express this enzyme at high levels [16–20]. The loss of SERCA3 expression in several types of cancer suggests that abnormal expression of this enzyme is an early event during carcinogenesis [16–21]. The degree of loss in SERCA3 protein expression is proportional to the loss of differentiation in benign and malignant tumors [16–20]. SERCA3 expression has been shown to decrease at early stages of dysplasia in adenomas, and remains low, or becomes absent in advanced stages of cancer [16–21]. In addition, SERCA3 protein expression gradually increases in spontaneously differentiating colon cancer Caco-2 cells after reaching confluence [17]. A different set of experiments showed that treatment of gastric, colon, and lung cancer cells with HDACi, such as sodium butyrate induced a marked expression of SERCA3 protein, whereas SERCA2 protein expression did not change significantly or was reduced [17,19].
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La activación muscarínica estimula la proliferación de células tumorales de mama humana con participación de la óxido nítrico sintasa.

La activación muscarínica estimula la proliferación de células tumorales de mama humana con participación de la óxido nítrico sintasa.

Spoonster y col. (1997) evidenciaron que la activación, del receptor M 5 transfectado establemente en células CHO, con CARB revertía el fenotipo maligno de estas células con capacidad de diseminarse hacia un fenotipo fibroblástico no invasivo. Al estudiar la expresión y función de RCM en líneas celula- res derivadas de adenocarcinomas mamarios murinos de aparición espontánea en ratones de la cepa BALB/c, obtenidas y caracterizadas en el Instituto Roffo (LM2, LM3 y LMM3) observamos que las mismas sobreexpresan RCM en comparación con células de la línea normal del epitelio mamario murino NMuMG (ATCC) (Español, 2002; 2004). Por ensayos de unión y saturación con el antagonista muscarínico tritiado bencilato de quinuclidinilo, así como por Western blot demostramos una expresión mayoritaria de los subtipos M 2 y M 4 en las células LM2 y LM3. Mientras que en las células de la línea LMM3, obtenida de un tumor mamario metastático (MM3) se observó un cambio hacia la sobreexpresión del receptor M 3 (Rim- maudo, 2005). Estos resultados son comparables a los observados por nosotros en las células MCF-7, las que también muestran una expresión significativa del mismo subtipo de receptor. Ye LH y col. (2006) han demostrado que la inoculación de células MCF-7 en ratones inmunosuprimidos SCID, permite de-
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Proceso de Extracción y Modificaciones Químicas de ácido Oleanólico  de Phoradendron Tomentosum y su Uso para Tratar Cáncer

Proceso de Extracción y Modificaciones Químicas de ácido Oleanólico de Phoradendron Tomentosum y su Uso para Tratar Cáncer

Además de los artículos publicados existen numerosas patentes en relación a las modificaciones químicas al ácido oleanólico y el uso de las mismas. El documento CN 1715291/2006 (44) describe la síntesis de ácido oleanólico succinilado. Utiliza 7 veces la cantidad de anhídrido succínico con la catálisis de piridina anhidra 4mL por cada g de reactivo. Esta mezcla de reacción se refluja por 8 horas a 100° C para producir el derivado. En esta invención, la reacción se lava con agua para eliminar el anhídrido y piridina residual y se purifica por medio de recristalización en etanol. El inventor afirma que con esta modificación el compuesto posee mejor solubilidad y dispersión en agua, y mayor biodisponibilidad que el compuesto original. El producto se puede tomar oralmente para tratar daño agudo y crónico al hígado, disminuir los niveles de transaminasas, reducir la fibrosis del hígado e inhibir cambios patológicos en el hígado.
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APUNTES MCF GERMÁN MARTÍNEZ

APUNTES MCF GERMÁN MARTÍNEZ

Estos conocimientos comprenden: Áreas de las figuras planas más simples, volúmenes de algunos poliedros, la relación del teorema de Pitágoras dada para 3, 4 y 5; 6, 8 y 10; [r]

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Acciones protectoras de los estrogenos sobre musculo liso vascular

Acciones protectoras de los estrogenos sobre musculo liso vascular

de útero, células umbilicales y células MCF-7 de cáncer de mama La lI11portancla lisio lógica de los efectos que los estrógenos inducen sobre la membrana y su relación con la función vas[r]

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Caracterización del perfil de sensibilidad de un panel de líneas celulares para valoración de citotoxicidad in vitro.

Caracterización del perfil de sensibilidad de un panel de líneas celulares para valoración de citotoxicidad in vitro.

Se emplearon las líneas celulares derivadas de tumores sólidos humanos MCF-7 (adenocarci- noma de mama), HEp-2 (carcinoma de laringe), HT-29 (adenocarcinoma colorrectal), HeLa y SiHa (carcinoma de cuello uterino), MKN-45 (carcinoma gástrico), obtenidas del banco de células del Laboratorio de Inmunología del Instituto Nacional de Cancerología de Colombia, y U-937 (adherente derivada de linfoma histiocítico), obtenida de la Fundación Instituto de Inmunología. Las líneas celulares se mantuvieron en frascos de cultivo de 75 cm 2 de área, con medio mínimo esencial y

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FGF 1 induces ATP release from spinal astrocytes in culture and opens pannexin and connexin hemichannels

FGF 1 induces ATP release from spinal astrocytes in culture and opens pannexin and connexin hemichannels

Fig. 1. FGF-1 – induced permeabilization of spinal astrocytes is at fi rst mediated by opening of Px HCs; then Cx HCs contribute. (A) LY 2− uptake evaluated as fl uorescence in- tensity normalized to the control value in con fl uent cultures treated with FGF-1 for the indicated times. Representative images are in Fig. S1. (B and C ) Decay in fl uorescence fol- lowing LY injection (LYDF) of isolated cells (images acquired every 2 min). LYDF under control conditions and after 2 h (B) or 7 h (C) FGF-1 treatment show the effect of 1 mM octanol (Oct), a Cx HC blocker, and 200 μ M carbenoxolone (CBX), a Px and Cx HC blocker. Arrows indicate blocker application. Control and FGF-1 – treated cells injected with LY 2− were in sister cultures used on the same day. LY 2− fl uorescence was normalized to initial values. Bar graphs on the Right show quantitation; each point represents one cell. Decay rates and rates after drug application were normalized to rates at onset of measurement. [*P < 0.05, **P < 0.01, ***P < 0.001 vs. control; ## P < 0.01 vs. FGF-1 treatment, 15 cells injected
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APUNTES MCF GERMÁN MARTÍNEZ, LECTURA 4

APUNTES MCF GERMÁN MARTÍNEZ, LECTURA 4

Los resultados de tales condiciones favorables se harán sentir muy pronto, pues en el siglo XVII se verá toda una admirable conjunción del Álgebra y de la Geometría con el[r]

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