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At least 1,387 records · Page 77Linked to original sources
PubMed2006

Interplay between lipoproteins and bee venom phospholipase A2 in relation to their anti-Plasmodium toxicity.

We previously showed that the in vitro intraerythrocytic development of the malarial agent Plasmodium falciparum is strongly inhibited by secreted phospholipases A(2) (sPLA(2)s) from animal venoms. Inhibition is dependent on enzymatic activity and requires the presence of serum lipoproteins in the parasite culture medium. To evaluate the potential involvement of host lipoproteins and sPLA(2)s in malaria, we investigated the interactions between bee venom phospholipase A(2) (bvPLA(2)), human triglyceride-rich lipoproteins, and infected erythrocytes. Even at high enzyme concentration (100x IC(50)), bvPLA(2) binding to Plasmodium-infected or normal erythrocytes was not detected. On the contrary, tight association with lipoproteins was observed through the formation of buoyant bvPLA(2)/lipoprotein complexes. Direct involvement of the hydrolysis lipid products in toxicity was demonstrated. Arachidonic acid (C20:4), linoleic acid (C18:2), and, to a lesser extent, docosahexaenoic acid (C22:6) appeared as the main actors in toxicity. Minimal oxidation of lipoproteins enhanced toxicity of the lipolyzed particles and induced their interaction with infected or normal erythrocytes. Fresh or oxidized lipolyzed lipoproteins induced the parasite degeneration without host cell membrane disruption, ruling out a possible membranolytic action of fatty acids or peroxidation products in the death process. In conclusion, our data enlighten on the capability of secreted PLA(2)s to exert cytotoxicity via the extracellular generation of toxic lipids, and raise the question of whether such mechanisms could be at play in pathophysiological situations such as malaria.

Animals↗
PubMed2006

The glucagon-miniglucagon interplay: a new level in the metabolic regulation.

Miniglucagon (glucagon 19-29) is the ultimate processing product of proglucagon, present in the glucagon-secreting granules of the alpha cells, at a close vicinity of the insulin-secreting beta cells. Co-released with glucagon and thanks to its original mode of action and its huge potency, it suppresses, inside the islet of Langerhans, the detrimental effect of glucagon on insulin secretion, while it leaves untouched the beneficial effect of glucagon on glucose competence of the beta cell. At the periphery, miniglucagon is processed at the surface of glucagon- and insulin-sensitive cells from circulating glucagon. At that level, it acts via a cellular pathway which uses initial molecular steps distinct from that of insulin which, when impaired, are involved in insulin resistence. This bypass allows miniglucagon to act as an insulin-like component, a characteristic which makes this peptide of particular interest from a pathophysiological and pharmacological point of views in understanding and treating metabolic diseases, such as the type 2 diabetes.

Animals↗
PubMed2005

Interplay between the maillard reaction and lipid peroxidation in biochemical systems.

The Maillard reaction and lipid peroxidation are two of the most important chemical reactions that take place in biochemical systems. Both include a whole network of different reactions in which an extraordinarily complex mixture of compounds is produced in very different amounts, with both positive and negative consequences. In addition, both reactions are intimately interrelated, and the products of each reaction influence the other. Furthermore, there are common intermediates and products in both pathways; these products are usually known as advanced glycation end products (AGEs) and advanced lipoxidation end products (ALEs). Moreover, other AGE/ALEs are analogous and participate similarly in both amino acid degradation and amino phospholipid/protein polymerization by identical mechanisms. All these data suggest that the Maillard reaction and lipid peroxidation are so closely interrelated that both reactions should be considered simultaneously to understand the reaction mechanisms, kinetics, and products in the complex mixtures of carbohydrates, lipids, and proteins occurring in biochemical systems. In these systems, lipids and carbohydrates are competing in the chemical modification of amino phospholipids and proteins. Therefore, although there are significant differences between the Maillard reaction and lipid peroxidation, many aspects of both reactions can be better understood if they are included in only one general carbonyl pathway that can be initiated by both lipids and carbohydrates.

Biochemistry↗
PubMed2005

The interplay of chemokines and dendritic cells in the pathogenesis of lupus nephritis.

Lupus nephritis (LN) occurs in more that one-third of patients with systemic lupus erythematosus. Production of nephritogenic autoantibodies, glomerular immune complex deposition, and cytokine overproduction have been postulated to contribute to the pathogenesis of LN. However, overexpression of chemokines and imbalance of dendritic cell (DC) homeostasis may contribute to the development of nephritis in SLE. We present evidence that monocyte chemoattractant protein (MCP)-1 promotes renal disease in experimental glomerulonephritis, while its increased urinary levels reflect the severity of the disease in humans. Although macrophages are the prevalent infiltrating population within the kidney, it has been recently proposed that several chemokines and related receptors expressed by DCs may divide this cell population into myeloid (mDC) and plasmacytoid (pDC) subsets. However, the chemokine receptors expressed by pDCs are not functional, and other molecules are involved in the chemoattraction of these cells. We found increased expression of interleukin (IL)-18 in glomeruli of patients with active LN along with glomerular infiltration by pDCS. Since pDCs bear IL-18 receptor (IL-18R), it is conceivable that circulating pDCs may migrate toward glomeruli by IL-18/IL-18R interactions. Therefore, the relative depletion of circulating pDCs reflects the severity of inflammatory disease in LN.

Cell Movement↗
PubMed1998

Accessible content and accessibility experiences: the interplay of declarative and experiential information in judgment.

Recall tasks render 2 distinct sources of information available: the recalled content and the experienced ease or difficulty with which it can be brought to mind. Because retrieving many pieces of information is more difficult than retrieving only a few, reliance on accessible content and subjective accessibility experiences leads to opposite judgmental outcomes. People are likely to base judgments on accessibility experiences when they adopt a heuristic processing strategy and the informational value of the experience is not called into question. When the experience is considered nondiagnostic, or when a systematic processing strategy is adopted, people rely on accessible content. Implications for the operation of the availability heuristic and the emergence of knowledge accessibility effects are discussed.

Journal Article↗
PubMed1997

A model for developing effective treatments: progression and interplay of theory, research, and practice.

The central thesis of this article is that advances in psychotherapy research for children and adolescents are limited, despite the large number of controlled studies and consistent conclusions about demonstrated effectiveness. The ways in which individual studies are conducted and the lack of an overall plan for the progression of research to identify effective treatments have contributed to the limited conclusions. In this article, I identify steps toward developing effective treatment that entail conceptualization and investigation of clinical problems, processes of change, and conditions that influence treatment outcome. Progress will not only require more systematic accretion of research, but also expansion in the range of questions, outcomes, and models of treatment delivery that are examined. Efforts to improve the knowledge base and to integrate knowledge into clinical practice can also be greatly enhanced by modifying the ways in which clinical work is conducted and specifically by systematically monitoring treatment implementation and patient progress.

Adolescent↗
PubMed2003

The interplay of collagen IV, tumor necrosis factor-alpha, gelatinase B (matrix metalloprotease-9), and tissue inhibitor of metalloproteases-1 in the basal lamina regulates Sertoli cell-tight junction dynamics in the rat testis.

During spermatogenesis, preleptotene and leptotene spermatocytes must translocate across the blood-testis barrier formed by inter-Sertoli cell-tight junctions (TJs) from the basal compartment of the seminiferous epithelium adjacent to the basement membrane to the adluminal compartment at stages VIII-IX for further development. Because of the close proximity between extracellular matrix (ECM) that constitutes the basement membrane and the blood-testis barrier, we sought to investigate the role of ECM in Sertoli cell TJ dynamics. When Sertoli cells were cultured in vitro to initiate the assembly of the Sertoli cell TJ-permeability barrier, the presence of an anticollagen IV antibody indeed perturbed the barrier. Because ECM is known to maintain a pool of cytokines and TNFalpha has been shown to regulate TJ dynamics in other epithelia, we investigated whether TNFalpha can regulate Sertoli cell TJ function via its effects on collagen alpha3(IV) and other proteins that maintain the homeostasis of ECM. As expected, recombinant TNFalpha perturbed the Sertoli cell TJ-barrier assembly in vitro dose dependently. TNFalpha also inhibited the timely induction of occludin, which is known to associate with the Sertoli cell TJ-barrier assembly. Furthermore, TNFalpha induced the expression of Sertoli cell collagen alpha3(IV), gelatinase B (matrix metalloprotease-9, MMP-9) and tissue inhibitor of metalloproteases-1 but not gelatinase A (matrix metalloprotease-2), and promoted the activation of pro-MMP-9. These results thus suggest that the activated MMP-9 induced by TNFalpha is used to cleave the existing collagen network in the ECM, thereby perturbing the TJ-barrier. This in turn creates a negative feedback that causes TNFalpha to induce collagen alpha3(IV) and tissue inhibitor of metalloproteases-1 expression so as to replenish the collagen network in the disrupted TJ-barrier and limit the activity of MMP-9. Taken collectively, these observations strengthen the notion that ECM is involved in the regulation of junction dynamics in addition to its structural role in the testis.

Animals↗
PubMed2003

Adhering junction dynamics in the testis are regulated by an interplay of beta 1-integrin and focal adhesion complex-associated proteins.

During spermatogenesis, the movement of developing germ cells across the seminiferous epithelium associates with extensive restructuring of cell-cell actin-based adherens junctions (AJs), such as ectoplasmic specialization (ES, a testis-specific AJ junction), between Sertoli and germ cells. Although this event of germ cell movement is essential to the completion of spermatogenesis, the mechanism(s) that regulates AJ restructuring is largely unknown. Using Sertoli-germ cells cocultured in vitro to study the regulation of AJ assembly, it was shown that this event associated with a transient induction of beta 1-integrin, vinculin, p-FAK-Tyr(397), and phosphatidylinositol 3-kinase (PI3K) but not the nonphosphorylated form of focal adhesion kinase (FAK), paxillin, and p130 Cas. Furthermore, p-FAK-Tyr(397) was shown to coimmunoprecipitate with beta 1-integrin, vinculin, and c-Src both in vitro and in vivo using Sertoli-germ cell cocultures and seminiferous tubules, respectively. These results seemingly suggest that the testis is using constituent proteins of the focal adhesion complex (FAC) found in other epithelia between cell and extracellular matrix to regulate AJ dynamics. To further confirm that p-FAK, a putative FAC protein in other epithelia, is indeed present at the site of ES, immunohistochemistry and immunofluorescent microscopy were used. The p-FAK-Tyr(397) and p-FAK-Tyr(576) were found to localize almost exclusively at the site of apical ES with weak staining at the basal ES in the seminiferous epithelium in a stage-specific manner, being highest at stages VI-VIII. In contrast, FAK was largely restricted to the basal compartment but with weak staining at the apical compartment. When rats were treated with 1-(2,4-dichlorobenzyl)-indazole-3-carbohydrazide (AF-2364) to perturb Sertoli-germ cell AJs, an induction of beta 1-integrin, vinculin, p-FAK-Tyr(397), PI3K, and p130 Cas but not the nonphosphorylated form of FAK and paxillin was also detected in the testis, coinciding with the time spermatids began to deplete from the epithelium, indicating their involvement in AJ disassembly. Thereafter, the levels of vinculin, p-FAK-Tyr(397), PI3K, and p130 Cas in the testis plunged, coinciding with the declining events of AJ disruption when virtually all spermatids were depleted from the epithelium. Taken collectively, these results suggest a bifunctional role of p-FAK, being involved in the events of Sertoli-germ cell AJ assembly and disassembly. In summary, the events of AJ dynamics in the testis, in particular at the site of ES, are regulated, at least in part, by proteins that are found in the FAC in other epithelia, such as beta1-integrin, vinculin, and FAK utilizing the integrin/pFAK/PI3K/p130 Cas signaling pathway.

Adherens Junctions↗
PubMed1985

Interplay of nutrients and hormones in the regulation of glucagon release.

The role of nutrients and hormones in the regulation of glucagon release is investigated in pancreatic A cells purified by autofluorescence-activated cell sorting. Purified A cells lack secretory activity in 1-h incubation at 1.4 mM glucose. Their release mechanism can be activated by arginine, alanine, and glutamine, alone or in combination. Glucose inhibits amino acid-induced glucagon release through a direct insulin-independent action upon pancreatic A cells. Nutrient-induced glucagon release is suppressed by somatostatin and amplified by (Bu)2cAMP or epinephrine. The epinephrine stimulus is inhibited by 10(-11) M somatostatin and abolished by 10(-10) M of this peptide. The effects of somatostatin and epinephrine are associated with parallel changes in cellular cAMP levels, which is not the case for the variations induced by amino acids or glucose. It is confirmed that calcium is an essential requirement for glucagon release. In contrast to its exquisite sensitivity for somatostatin, the glucagon release process is relatively insensitive to insulin during a 1-h exposure. The hormone affects solely epinephrine-induced glucagon release and its inhibitory action is partial and only observed at 10(-7) M. This suppressive effect of insulin is not attributable to variations in glucose handling but appears associated with the stimulatory effect of epinephrine. It is concluded that a nutrient-induced signal interacts with a hormone-inducible cAMP signal to activate the secretory process in pancreatic A cells.

Alanine↗
PubMed1985

Interplay of nutrients and hormones in the regulation of insulin release.

Single pancreatic B cells are purified by autofluorescence-activated cell sorting, and their secretory activity is measured after overnight culture. Compared to intact islets, the isolated cells release 2-fold more insulin under basal conditions and 5-fold less during nutrient stimulation. Their secretory activity can be induced by glucose, leucine, or arginine, but only 0.3-1.7% of their hormone content is liberated at 20 mM nutrient concentrations. This poor nutrient-induced insulin release from purified B cells is attributed to their low cAMP levels and is markedly increased after addition of (Bu)2cAMP, of glucagon, or of pancreatic A cells. These results strongly support the concept that the potent in vivo insulin-releasing action of glucose and leucine is not only dependent on their fuel capacity in pancreatic B cells but also on the concurrent cAMP levels in these cells. In isolated islets, endogenously released glucagon apparently determines the cAMP production in B cells and thus participates in the nutrient-induced secretory process. Somatostatin and epinephrine were shown to exert their suppressive effects via the glucagon-dependent messenger system. It is concluded that nutrients and hormones interact with two different messenger systems which amplify each others' stimulatory effect upon insulin release. cAMP might represent the hormone-induced messenger which sets the B cell's sensitivity and secretory capacity for nutrient stimuli such as glucose. The higher insulin secretory response observed after reaggregation of single B cells could not be attributed to an altered activity in the nutrient or hormonal regulatory units, raising the possibility that the aggregated state of the cells is rather responsible for a better organization or cooperation of the secretory effector unit.

Amino Acids↗
PubMed2003

The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression.

The inflammatory response is a highly regulated physiological process that is critically important for homeostasis. A precise physiological control of inflammation allows a timely reaction to invading pathogens or to other insults without causing overreaction liable to damage the host. The cellular signaling pathways identified as important regulators of inflammation are the signal transduction cascades mediated by the nuclear factor-kappaB and the activator protein-1, which can both be modulated by glucocorticoids. Their use in the clinic includes treatment of rheumatoid arthritis, asthma, allograft rejection, and allergic skin diseases. Although glucocorticoids have been widely used since the late 1940s, the molecular mechanisms responsible for their antiinflammatory activity are still under investigation. The various molecular pathways proposed so far are discussed in more detail.

Gene Expression Regulation↗
PubMed2006

Review: Insulin and endothelin: an interplay contributing to hypertension development?

CONTEXT: The aim of this article was to review the existing data on the interactions among insulin, insulin resistance, and endothelin and how those contribute to the development of hypertension in insulin-resistant states. EVIDENCE ACQUISITION: A literature search of MEDLINE database was performed to identify English-language articles published during the last 20 yr. Search terms used were endothelin, insulin, insulin resistance, and hyperinsulinemia in combination with blood pressure and hypertension. Reference lists of retrieved articles were also evaluated for relevant information. EVIDENCE SYNTHESIS: Several mechanisms connect insulin resistance and compensatory hyperinsulinemia with blood pressure elevation in the context of the metabolic syndrome, i.e. sodium retention, sympathetic activation, and impairment of endothelial nitric oxide production. Accumulating evidence suggests that activation of the endothelin system seems to be another important, yet less discussed, mechanism. In vitro studies have shown that insulin stimulates both endothelin-1 production and action on the vascular wall. In vivo, high levels of insulin result in increase in circulating endothelin-1 in healthy individuals, and this effect is also seen in insulin-resistant subjects, a relationship not observed with nitric oxide production. Moreover, endothelin receptor antagonism effectively reduces blood pressure in animal models of insulin resistance and hypertension. On the other hand, elevation of endothelin-1 levels can further increase insulin resistance, forming possibly a deleterious circle. CONCLUSIONS: Endothelin-1 may play a crucial role in the pathogenesis of hypertension in insulin-resistant states. Future research should examine the potential of endothelin receptor antagonism to help blood pressure control in patients with insulin resistance.

Animals↗
PubMed1983

The effect of cortisol, progesterone, and transcortin on phytohemagglutinin-stimulated human blood mononuclear cells and their interplay.

The effect of transcortin on [3H]thymidine incorporation into phytohemagglutinin-stimulated human peripheral blood mononuclear cells and its influence on the well known suppressive effect of cortisol were investigated. Human transcortin by itself had no effect on thymidine incorporation between the concentrations of 0.25-1 X 10(-6) M. When transcortin was added to cortisol, the suppressive effect of cortisol decreased in proportion to the decrease in the protein-unbound cortisol concentration. We also investigated the influence of progesterone on transcortin-bound cortisol. When 0.5 and 1 X 10(-6) M transcortin, which contained 1 and 2 X 10(-7) M cortisol as a transcortin-bound form, were added to 5 X 10(-6) M progesterone, greater suppression of thymidine incorporation was observed that than produced by progesterone alone (86.1% and 81.3 for 0.5 and 1 X 10(-6) M transcortin, respectively). Moreover, when 5 X 10(-7) M transcortin containing the same amount of cortisol was added with 1, 2, and 5 X 10(-6) M progesterone, a greater suppression (92.6%, 74.1%, and 32.4% of control for 1, 2, and 5 x 10(-6) M progesterone) was demonstrated than that caused by progesterone alone (95.1%, 75.8%, and 49.5% of control for the corresponding concentrations of progesterone). This increased suppression was accompanied by an increase in the percentage of protein-unbound cortisol. These results indicate that unbound cortisol, whose concentration increases in the presence of progesterone, may be biologically active. The interaction between progesterone and cortisol may be modulated in part by the transcortin concentration.

Cells, Cultured↗