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At least 523 records · Page 29Linked to original sources
PubMed2006

Modulation of cell proliferation during palatogenesis by the interplay between Tbx3 and Bmp4.

During secondary palate development, two shelves are elevated to a horizontal position above the tongue through a process involving many cellular mechanisms, including proliferation. In particular, the expression patterns of Tbx3 and Bmp4, which are colocalized at embryonic day 13.5 (E13.5) and have unique expression patterns in specific regions at E14.5, have been investigated in early mouse palatogenesis. Tbx3 expression is reported to be associated with Bmp4 signaling during the process of organogenesis in other areas, such as limb development. However, the function of Tbx3 and the relationship between Tbx3 and Bmp4 in palate development have not been determined. We have examined the gene expression pattern and cell proliferation in order to understand the mutual interactions and function of Tbx3 and Bmp4. An electroporation method was used to investigate the altered pattern of these genes after their over-expression in organ cultures. NOGGIN protein-soaked beads were also implanted into the cultured palate to determine the function of Bmp4 in palatogenesis. After electroporation and NOGGIN bead implantation, the number of PCNA-positive cells was counted. The results showed that Tbx3 and Bmp4 strongly up- and down-regulated each other in order to control the proliferation of the palatal shelf. Thus, Tbx3 expression is induced by Bmp4 in the mesenchyme of the anterior palatal shelves, whereas mesenchymal expression of Tbx3 down-regulates Bmp4 expression in the mesenchyme of the palate. The harmonization between Tbx3 and Bmp4 therefore controls cell proliferation to regulate secondary palate development.

Animals↗
PubMed2004

Limitations on reproductive success in endemic Aquilegia viscosa (Ranunculaceae) relative to its widespread congener Aquilegia vulgaris: the interplay of herbivory and pollination.

Plant reproduction can be strongly affected by herbivory and different features of pollination ecology, such as pollinator visitation rates and capacity for self-pollination. The purpose of this study is to compare the relative impact of herbivory and pollination on maternal reproductive success in endemic Aquilegia viscosa and its widespread congener Aquilegia vulgaris. We conducted herbivore exclusion experiments in two populations of each species in 2 different years and showed that the maternal fertility of A. viscosa was significantly more limited by floral predation and pre-dispersal seed predation than its widespread congener. In the absence of herbivory, A. viscosa retained significantly lower maternal fertility than A. vulgaris. Experimental pollinations in an insect-free glasshouse showed that the two species have an equal seed/ovule ratio both in the absence of pollinators and in the presence of non-limiting outcross pollination. Pollinator visitation rates were significantly higher in populations of A. vulgaris than in populations of A. viscosa. In addition, path analyses showed that spur length, an important trait for pollinator attraction in Aquilegia, and, indirectly sepal and petal width, contribute positively to the seed/ovule ratio in A. vulgaris, but not in A. viscosa. These results indicate that maternal fertility of endemic A. viscosa is strongly reduced by flower and seed predation despite low rates of pollinator visitation, and that pollen or resource limitation in the wild may further reduce maternal fertility. Finally, floral trait variation appears to be decoupled from fertility variation in endemic A. viscosa, which possibly constrains the evolution of reproductive traits in this species.

Analysis of Variance↗
PubMed2006

The interplay between shifts in biomass allocation and costs of reproduction in four grassland perennials under simulated successional change.

When perennial herbs face the risk of being outcompeted in the course of succession, they are hypothesized to either increase their biomass allocation to flowers and seeds or to invest more in vegetative growth. We tested these hypotheses in a 3-year garden experiment with four perennials (Hypochaeris radicata, Cirsium dissectum, Succisa pratensis and Centaurea jacea) by growing them in the midst of a tall tussock-forming grass (Molinia caerulea) that may successionally replace them in their natural habitat. In all species except for the short-lived H. radicata, costs of sexual reproduction were significant over the 3 years, since continuous bud removal enhanced total biomass or rosette number. To mimic succession we added nutrients, which resulted in a tripled grass biomass and higher death rates in the shorter-lived species. The simulated succession resulted also in a number of coupled growth responses in the survivors: enhanced plant size as well as elevated seed production. The latter was partly due to larger plant sizes, but mostly due to higher reproductive allocation, which in turn could be partly explained by lower relative somatic costs and by lower root-shoot ratios in the high-nutrient plots. Our results suggest that perennial plants can increase both their persistence and their colonization ability by simultaneously increasing their vegetative size and reproductive allocation in response to enhanced competition and nutrient influxes. These responses can be very important for the survival of a species in a metapopulation context.

Asteraceae↗
PubMed2003

The interplay of stress, gender and cognitive style in depressive onset.

Major depression is more common in women than men, but the reasons for this difference have not been completely understood. We examine recent evidence investigating whether sex differences in exposure or response to stressful life events play an explanatory role in the sex differences found in onset of depression. We also explore the possibility that sexual dimorphism in depressive prevalence and response to events is related to sex differences in cognitive style. We conclude that differences between women and men in response to stressful life events and cognitive style are relevant to understanding sex differences in the onset of depression.

Adult↗
PubMed2007

An intimate interplay between precocious, migrating pericytes and endothelial cells governs human fetal brain angiogenesis.

In order to better understand the process of angiogenesis in the developing human brain, we have examined the spatial relationship and relative contributions of endothelial cells and pericytes, the two primary cell types involved in vessel growth, together with their relation with the vascular basement membrane. Pericytes were immunolocalized through use of the specific markers nerve/glial antigen 2 (NG2) proteoglycan, endosialin (CD248) and the platelet-derived growth factor receptor beta (PDGFR-beta), while endothelial cells were identified by the pan-endothelial marker CD31 and the blood brain barrier (BBB)-specific markers claudin-5 and glucose transporter isoform 1 (GLUT-1). The quantitative analysis demonstrates that microvessels of the fetal human telencephalon are characterized by a continuous layer of activated/angiogenic NG2 pericytes, which tightly invest endothelial cells and participate in the earliest stages of vessel growth. Immunolabelling with anti-active matrix metalloproteinase-2 (aMMP-2) and anti-collagen type IV antibodies revealed that aMMP-2 producing endothelial cells and pericytes are both associated with the vascular basement membrane during vessel sprouting. Detailed localization of the two vascular cell types during angiogenesis suggests that growing microvessels of the human telencephalon are formed by a pericyte-driven angiogenic process in which the endothelial cells are preceded and guided by migrating pericytes during organization of the growing vessel wall.

Basement Membrane↗
PubMed2005

Apoptosis in UV-C light irradiated p53 wild-type, apaf-1 and p53 knockout mouse embryonic fibroblasts: interplay of receptor and mitochondrial pathway.

Mouse embryonic fibroblasts (MEFs) deficient for the transcription factor p53 are hypersensitive to UV-C light. They also show a reduced recovery from UV-C induced replication blockage and are unable to repair UV-C photoproducts. In this study, we utilized wild-type (wt), Apaf-1 deficient (apaf-1(-/-)) and p53 deficient (p53(-/-)) MEFs in order to elucidate the role of non-repaired UV-C lesions in apoptotic signalling. Corresponding with the cellular sensitivity determined by the WST assay, p53(-/-) cells displayed the highest level of apoptosis, whereas wt cells showed moderate apoptosis after UV-C irradiation. Apaf1(-/-) cells were most resistant. In wt cells apoptosis was executed both via the mitochondrial and the receptor-mediated pathway, as shown by Bcl-2 decline, induction of fasR and activation of caspases-3,8,9. In apaf-1(-/-) (p53(+/+)) cells, the mitochondrial pathway was blocked downstream of Bcl-2, indicating that in this case apoptosis was mediated via the induction of fasR and caspase-3,8 activation. In p53 deficient cells, non-repaired UV-C induced DNA lesions triggered sustained up-regulation of fas ligand (fasL) mRNA, which was not seen in wt and apaf-1(-/-) cells. Therefore, in p53(-/-) MEFs, the receptor/ligand triggered pathway appeared to be dominant. This was confirmed by significant reduction of apoptosis after DN-FADD transfection. As opposed to wt and apaf-1(-/-) cells, p53 deficient MEFs showed no induction of Fas receptor and no Bcl-2 decline. Nevertheless, the resulting caspase-8 and -3 activation was stronger compared to wt and apaf-1(-/-) cells. The data indicate that UV-C light activates in MEFs both the Fas (CD95, Apo-1) receptor and the mitochondrial damage pathways. In p53(-/-) cells, however, the high level of non-repaired DNA damage forces signalling by fasL upregulation, leading to enhanced UV-C-induced apoptosis.

Animals↗
PubMed2006

The interplay between pro-death and pro-survival signaling pathways in myocardial ischemia/reperfusion injury: apoptosis meets autophagy.

INTRODUCTION: Programmed cell death of cardiac myocytes occurs following a bout of ischemia/reperfusion (I/R), which results in reduced function of the heart. Numerous studies, including in vivo, have shown that cell death occurs via necrosis and apoptosis following I/R. Recently, autophagy has emerged as a powerful mediator of programmed cell death, either opposing or enhancing apoptosis, or acting as an alternative form of programmed cell death distinct from apoptosis. AIM: Here we review the apoptotic and autophagic signaling pathways, their influences on each other, and we discuss the relevance of autophagy in the heart.

Apoptosis↗
PubMed2006

Mechanistic study of the cellular interplay of transport and metabolism using the synthetic modeling method.

PURPOSE: The aims of this study were 1) to demonstrate a new modeling strategy that uses experimental computational models built by the synthetic method and 2) to study the consequences of spatial alignment, or lack thereof, of P-glycoprotein (Pgp) and CYP3A4 on the transport and metabolism of drug-like compounds and the influence of competitive inhibition by metabolites on the transport and metabolism of those compounds. METHODS: The synthetic method of modeling and simulation was used to construct discrete-event, discrete-space models. Within a framework designed for experimentation, object-oriented software components were assembled into devices representing the efflux transport and metabolism mechanisms within cell monolayers in Caco-2 transwell systems. RESULTS: Conditions for transport and metabolism synergism (and lack thereof) were identified. Simulations showed how spatial alignment altered the coordinated influences of Pgp and CYP3A4 on absorption of a series of drug-like compounds. Within those experiments, when the metabolites were also substrates of Pgp, the metabolite levels produced were insufficient to give evidence of a competitive inhibitory effect on either transport or metabolism. CONCLUSIONS: The results provide evidence of the potential value of using this class of models to improve our understanding of how complex cellular processes influence the transport and absorption of compounds, and the consequences of interventions.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1987

The interplay between endogenous catecholamines and induced ventricular tachycardia during electrophysiologic testing.

Plasma epinephrine and norepinephrine concentrations were measured before, during, and shortly after induced ventricular tachycardia (VT) in 22 selected patients. Sustained, unimorphic VT was induced by programmed ventricular stimulation and terminated after 45 to 384 seconds by overdrive pacing in all patients. In no patient did VT result in loss of consciousness. The baseline plasma catecholamine concentrations did not correlate with the baseline right ventricular effective refractory period, the cycle length of induced VT, or the number of extrastimuli required to induce VT. Induced VT was not associated with a significant increase in the mean plasma epinephrine concentration. In contrast, the plasma norepinephrine concentration increased from a mean baseline level of 317 +/- 136 pg/ml (mean +/- standard deviation) to 418 +/- 220 pg/ml during VT (p less than 0.01) and increased further to 569 +/- 387 pg/ml shortly after VT (p less than 0.01). The plasma norepinephrine concentration shortly after VT correlated with the rate and duration of VT and with the magnitude of decrease in mean blood pressure during VT (p less than 0.05 for each). In eight patients the same configuration of VT was induced on two sequential attempts; in five patients the same number of extrastimuli were required for the second induction of VT as for the first, whereas in three patients fewer extrastimuli were required. Plasma catecholamine concentrations were not higher in patients requiring fewer extrastimuli to induce the second episode of VT, either shortly after the first episode of VT or shortly after the second episode of VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Atrial natriuretic factor release during rapid ventricular pacing: interplay between autonomic and hemodynamic stimulants.

Plasma levels of atrial natriuretic factor (ANF) and norepinephrine are markedly elevated during episodes of ventricular tachycardia. Although atrial distention appears to be the major stimulus for ANF release, reflex changes in autonomic tone might also contribute. Plasma ANF and norepinephrine levels, sinus node cycle length, systolic blood pressure, and mean right atrial pressure were therefore assessed during rapid right ventricular pacing at 150 beats/min for 10 minutes. In five patients (group 1) observations were made without autonomic blockade, and another five patients (group 2) had ventricular pacing after cardiac autonomic blockade. In group 1 systolic blood pressure fell during ventricular pacing from 122 +/- 4 to 105 +/- 5 mm Hg (p < 0.02), norepinephrine levels increased from 195 +/- 26 to 411 +/- 71 pg/ml (p < 0.02), and sinus node cycle length decreased from 936 +/- 99 to 688 +/- 58 msec (p < 0.02). Right atrial pressure was elevated from 2.6 +/- 0.6 to 7.4 +/- 0.6 mm Hg (p < 0.02), and ANF levels increased from 161 +/- 23 to 240 +/- 26 pg/ml (p < 0.05). Whereas systolic blood pressure, norepinephrine, sinus cycle length, and right atrial pressure returned promptly to baseline levels when ventricular pacing was stopped, ANF levels continued to rise (296 +/- 37 pg/ml; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Interplay between hydroxylamine, metarhodopsin II and GTP-binding protein in bovine photoreceptor membranes.

The decay reactions of metarhodopsin II and the dissociation of the complex between rhodopsin (in the metarhodopsin II state) and the GTP-binding protein (G-protein) (in its inactive, GDP-binding form) have been compared at various concentrations of hydroxylamine. The reactions of the chromophore were measured by absorption changes in the visible range, the complex dissociation by changes in the near-infrared scattering. An additional monitor of the complex was given by the G-protein-dependent equilibrium between metarhodopsin I and metarhodopsin II. For all measurements, fragments of isolated bovine rod outer segments in suspension were used. In the absence of hydroxylamine, the rhodopsin-G-protein complex dissociated within 20-30 min at room temperature. The presence of hydroxylamine greatly accelerated (e.g., 5-fold at 1 mM NH2OH) the dissociation. Under all conditions, the free, dissociated G-protein can reassociate to metarhodopsin II produced by subsequent bleaching. Dissociation of the metarhodopsin II-G-protein complex required the decay of photoproducts with a maximal absorbance of 380 nm, but was not affected by the simultaneous presence of metarhodopsin III or metarhodopsin III - like photoproducts with a maximal absorbance between 450 and 470 nm. Despite the acceleration of metarhodopsin II-G-protein dissociation by NH2OH, metarhodopsin II-G-protein was relatively stabilized as compared to free metarhodopsin II. The ratio of the decay rates of free metarhodopsin II and metarhodopsin III-G-protein was increased as much as 10-fold in the presence of 25 mM NH2OH. The results indicate a mutual interdependence of retinal, opsin and G-protein.

Animals↗