Biomedical subjects

B Pipy

Publications and source records attributed to B Pipy.

At least 37 records · Page 2Linked to original sources

PubMed1998

Fenspiride inhibits histamine-induced responses in a lung epithelial cell line.

Using the human lung epithelial WI26VA4 cell line, we investigated the capacity of fenspiride, an anti-inflammatory drug with anti-bronchoconstrictor properties, to interfere with histamine-induced intracellular Ca2+ increase and eicosanoid formation. Histamine and a histamine H1 receptor agonist elicited a rapid and transient intracellular Ca2+ increase (0-60 s) in fluo 3-loaded WI26VA4 cells. This response was antagonized by the histamine H1 receptor antagonist, diphenhydramine, the histamine H2 receptor antagonist, cimetidine, having no effect. Fenspiride (10(-7)-10(-5) M) inhibited the histamine H1 receptor-induced Ca2+ increase. In addition, histamine induced a biphasic increase in arachidonic acid release. The initial rise (0-30 s), a rapid and transient arachidonic acid release, was responsible for the histamine-induced intracellular Ca2+ increase. In the second phase release (15-60 min), a sustained arachidonic acid release appeared to be associated with the formation of cyclooxygenase and lipoxygenase metabolites. Fenspiride (10(-5) M) abolished both phases of histamine-induced arachidonic acid release. These results suggest that anti-inflammatory and antibronchoconstrictor properties of fenspiride may result from the inhibition of these effects of histamine.

Arachidonic Acid↗

PubMed1998

Involvement of calcium and arachidonate metabolism in acetylated-low-density-lipoprotein-stimulated tumor-necrosis-factor-alpha production by rat peritoneal macrophages.

We show that lipopolysaccharide-free actetylated low-density lipoprotein (LDL), but not native LDL, stimulates tumor-necrosis factor-alpha (TNF-alpha) secretion by rat peritoneal macrophages and the signal-transduction pathways involved. The role of the scavenger receptor (SR) in this response was suggested by the absence of an effect induced by native LDL, signal coupling involving pertussis-toxin-dependent guanine-nucleotide-binding regulatory (G) protein, and the complete inhibition of this response by SR ligands [poly(I) and dextran sulfate]. Acetylated LDL induces rapid Ca2+ release from inositol-phosphate-sensitive Ca2+ stores mediated by pertussis-sensitive G proteins and a sustained Ca2+ rise mediated by Ca2+ influx and by Ca2+ release from ryanodine-sensitive Ca2+ stores. Acetylated LDL-induced Ca2+ influx and TNF-alpha production were abolished by inhibitors of phospholipase C (U73122) and phospholipase A2 (bromophenacyl bromide), but were not affected by an inhibitor of protein kinase C (calphostine C). Therefore, Ca2+ influx induced by acetylated LDL is dependent on Ca2+ store depletion. Arachidonate released by acetylated LDL acts as a second messenger to activate TNF-alpha secretion via Ca2+ influx. While the Ca2+ signal was not modified by an inhibitor of protein tyrosine kinases (PTK; herbimycin A), this inhibitor completely blocked TNF-alpha production, suggesting the involvement of PTK downstream of the Ca2+ signal. These results suggest that a sustained elevation of intracellular Ca2+, mediated through Ca2+ influx via the phospholipase-A2-dependent pathway, is essential for induction of TNF-alpha secretion. The type of SR class involved in these pathways remains to be identified.

Animals↗

PubMed1998

IL-13 induces tyrosine phosphorylation of phospholipase C gamma-1 following IRS-2 association in human monocytes: relationship with the inhibitory effect of IL-13 on ROI production.

Here we analysed the involvement of tyrosine phosphorylation in the regulation of the initial molecular events induced by IL-13 to modulate TPA-triggered reactive oxygen intermediates (ROI) production. Our data indicate that treatment of monocytes with a protein tyrosine kinase inhibitor (herbimycin A) prevents IL-13-induced cAMP accumulation and subsequent ROI inhibition. We have previously demonstrated that cAMP accumulation depends on inositol phosphates hydrolysis (InsPs) and intracellular Ca2+ mobilisation. The inhibition of InsPs and intracellular Ca2+ release by herbimycin A suggests a primary role of tyrosine kinases upstream PLC activation. We further specify that IL-13 stimulates PLC-gamma 1 and IRS-2 tyrosine phosphorylation in human monocytes. We demonstrate for the first time that IL-13 induces the association of IRS-2 with PLC-gamma 1. We proposed here that PLC-gamma 1 is a new candidate recruited by IRS-2.

Benzoquinones↗

PubMed1998

Metabolism and cytotoxicity of chlorpropham (CIPC) and its essential metabolites in isolated rat hepatocytes during a partial inhibition of sulphation and glucuronidation reactions: a comparative study.

The changes in metabolism and cytotoxicity of chlorpropham (CIPC) and its major metabolites, 4-hydroxychlorpropham (4-OH CIPC), 3-chloroaniline, and 3-chloroacetanilide were investigated in isolated rat hepatocyte suspensions after a partial inhibition of sulphation and glucuronidation and the two reactions combined in an attempt to assess the part of each of them in the enhanced CIPC toxicity observed in vivo after D-galactosamine treatment. With sulphation and glucuronidation effective, CIPC has a cytolytic effect and reduces intracellular ATP and K+ level while 4-OH CIPC has a weak cytolytic effect but modifies ATP and K+ level in a greater extent than CIPC. Inhibition of sulphation does not affect the cytotoxicity of CIPC or 4-OH CIPC because there is a compensatory increase in the amount of 4-OH CIPC glucuronide formed and the level of free 4-OH CIPC always remain low. In contrast, when incubations are carried out with either CIPC or 4-OH CIPC, the presence of D-galactosamine leads to a decrease of glucuronide and sulphate conjugates accompanied, respectively, by a 3.6-fold and 6. 9-fold increase of the free 4-OH CIPC level in the culture medium. This alteration of the metabolism is followed by a marked reduction of ATP synthesis with a concomitant modification of cell permeability. The cytolytic effect is due to CIPC itself, whereas the effect on energy supply was attributed to free 4-OH CIPC. The results demonstrate a combined effect of free 4-OH CIPC and D-galactosamine on intracellular ATP level that could account for the partial inhibition of sulphation. This change in the CIPC metabolism could explain the increased CIPC toxicity observed in vivo after D-galactosamine pretreatment.

Acetanilides↗

PubMed1998

Immunocytochemical characterization of lung macrophage surface phenotypes and expression of cytokines in acute experimental silicosis in mice.

The expression of the surface phenotypical profile and the cytokines TNF-alpha and IL-1beta from murine lung macrophages was studied in parenchymal lung tissue and bronchoalveolar fluid of mice, over a 2-week period, following a single intratracheal instillation of silica. The acute inflammatory reaction, confirmed by a significant augmentation of four times the control values of the number of macrophages recovered by lavage from experimental animals, was followed by organized granulomas in the interstitium. The immunohistochemical analysis of lung tissue sections after silica instillation demonstrated the increased alveolar and interstitial tissue expression of all surface antigens and cytokines studied, mainly Mac-1, F4/80 antigens, TNF-alpha and IL-1beta, which were occasionally observed in normal uninjected and saline-treated mice. These findings show that, after silica instillation, the expression of surface phenotypical markers of lung macrophages increased, and this change was concomitantly associated with an increased expression of the cytokines TNF-alpha and IL-1beta. These changes support the conclusion that an influx of the newly recruited and activated macrophage population, with a different phenotype, is induced by treatment during inflammation. The populational changes involve difference in functional activity and enhance TNF-alpha and IL-1beta expression. These cytokines, produced in the silicosis-induced inflammatory process, are associated with the development of fibrosis and may contribute to disease severity.

Acute Disease↗

PubMed1998

Effects of characterised Pseudomonas aeruginosa exopolysaccharides on adherence to human tracheal cells.

This study evaluated, in vitro, the role of different Pseudomonas aeruginosa exopolysaccharides (EPS) in mediating adherence to human respiratory epithelial cells. Two mucoid and non-mucoid isogenic pairs of P aeruginosa strains isolated from patients with cystic fibrosis (CF) and bronchiectasis were used. Adherence was tested with human tracheal epithelial cell lines from CF and normal fetuses. The CF cells bound significantly more bacteria than the normal cells. The strain from the bronchiectasis patient was significantly more adherent than that from the CF patient and this difference was consistently most marked with the non-mucoid variant and with normal epithelial cells. The differing behaviour of mucoid CF and non-mucoid bronchiectasis strains reflected the chemical composition of their EPS: mainly alginate in the former and neutral polysaccharides in the latter. Additive inhibition experiments with chemically characterised EPS indicated that neutral polysaccharides associated with alginate may act as ligands for the adherence of P. aeruginosa to CF epithelial cells.

Alginates↗

PubMed1998

IgA nephropathy complicating diabetic glomerulosclerosis.

A retrospective study was done on 66 diabetic patients who had renal biopsies performed during 1979-1994. This review shows 10 patients who presented IgA nephropathy associated with diabetic nephropathy. Six patients had insulin-dependent diabetes mellitus and 4 patients non-insulin-dependent diabetes mellitus. All patients presented with proteinuria and 7 had hematuria. Four patients presented with renal impairment. Histologic evaluation disclosed the presence of thickened glomerular basement membranes and increased mesangial matrix in all cases, associated with nodular sclerosis in 8 cases. By immunofluorescence, diffuse mesangial IgA deposits were observed in all cases. The high incidence of the coexistence of IgA nephropathy and diabetes seems not merely coincidental. Structural and/or functional abnormalities of the glomerular basement membranes might facilitate the development of immune complex glomerular diseases. In patients with diabetes, the appearance of urinary abnormalities and/or deterioration in renal function altered the clinical history of diabetic nephropathy. The disorders are clinically suggestive of the presence of nondiabetic renal disease and raised the possibility of another pathogenetic mechanism.

Adult↗

PubMed1998

Metallothionein expression in human lung and its varying levels after lung transplantation. Toulouse Lung Transplantation Group.

The aim of this study was to determine the lung levels of metallothionein (MT), a free radical scavenger, because oxygen-derivated free radicals (ODFRs) have been involved both in reperfusion injury of transplanted lungs and in cardiac or renal allograft destruction. First, MT localization was evaluated in 14 normal human lung biopsy specimens. Then, in lung transplant recipients, MT content in BAL fluid (BALF) and its transcription rate in alveolar macrophages (AMs) were determined. The BALFs of 69 patients were separated into six groups: lung transplant recipients in clinically stable condition (CSR), those with acute rejection (AR), asymptomatic cytomegalovirus infection (ACMV), cytomegalovirus pneumonitis (CMVP), bronchiolitis obliterans syndrome (BOS), and patients without transplants who served as control subjects (NTCs). In normal lungs, 83% of AMs were positively stained. MT staining was also observed in pleural endothelial cells and basal cells from bronchial epithelium. In lung transplant recipients, MT levels in BALF were significantly higher in patients with CSR, AR, ACMV, and CMVP compared with NTCs, while during BOS, MT had a significantly lower level compared with other lung transplant groups. However, no difference among groups was found concerning MT-II messenger RNA expression in AMs, showing that, as in normal lung, AMs are not the only cells that produce MT. These data report for the first time to our knowledge MT cell distribution in human lung with specific emphasis on its enhanced levels after lung transplantation, even in the absence of complication. Possible correlation among MT levels, ODFRs, cytokine levels, and corticosteroid treatment during complications of lung transplantation are discussed.

Acute Disease↗

PubMed1997

Effect of interleukin-4 on allergen-induced arachidonic acid metabolism of rat peritoneal macrophages during immediate hypersensitivity reactions.

The aim of this study was to investigate the [3H]arachidonic acid metabolism of rat peritoneal macrophages, induced by allergen (ovalbumin) and the impact of interleukin-4 on this process. We established that ovalbumin induces an increase of [3H]arachidonic acid mobilisation from membrane lipids and of [3H]arachidonic acid catabolism, principally by the 5-lipoxygenase pathway, when the macrophages are sensitized and when serum is present. The allergen effect is not modified by the presence of interleukin-4 in the culture medium of macrophages 15 h before the allergen challenge. We also showed that, whereas the basal [3H]arachidonic acid metabolism of macrophages from control and actively sensitized rats is not different, interleukin-4 increases the [3H]arachidonic acid mobilisation and catabolism by cyclooxygenase and 5-lipoxygenase pathways in macrophages from control rats although it does not in macrophages from actively sensitized rats. In macrophages from control rats, the interleukin-4 effect is diminished by the addition of IgEs to their culture medium. In summary, interleukin-4 has an enhancer effect on the macrophage arachidonic acid catabolism that depends on the sensitization condition of the cell but that has no consequences on the further increased arachidonic acid metabolism induced by the allergen.

Allergens↗

PubMed1997

Implication of neutral polysaccharides associated to alginate in inhibition of murine macrophage response to Pseudomonas aeruginosa.

There is evidence that exopolysaccharides (EPS) contribute to the persistence of Pseudomonas aeruginosa in cystic fibrosis lung. However, the relationship between the chemical composition of EPS and the modulation of phagocytic cells is poorly understood. In order to evaluate the role of the chemical composition of EPS in macrophage behavior changes, we pretreated macrophages with characterized EPS and assessed P. aeruginosa phagocytosis and reactive oxygen intermediate (ROI) production. The results showed that alginate and neutral polysaccharides are involved in phagocytic impairment of P. aeruginosa. Moreover, alginates were able to prime macrophages for increased P. aeruginosa-induced macrophage oxidative burst as determined by chemiluminescence. In contrast, neutral polysaccharides are responsible for the decrease of ROI by a scavenging effect evaluated by the xanthine-xanthine oxidase system. This study showed that the content of P. aeruginosa EPS in alginate, but also in neutral polysaccharides, influences the behavior of strains towards phagocytosis and macrophage oxidative burst.

Alginates↗

PubMed1996

Reactive oxygen intermediates as regulators of TNF-alpha production in rat lung inflammation induced by silica.

Exposure to mineral dusts such as silica has been associated with progressive pulmonary inflammation and fibrosis. There is evidence that the release of reactive oxygen intermediates (ROI) and cytokines by alveolar macrophages (AM) is involved in lung injury associated with silica exposure. However, the chronology and relationship between these two mediators are poorly understood. In this study, an animal model of silicosis has been used, allowing simultaneous follow-up of lung histopathologic state, AM TNF-alpha production at the protein (biologic assay) and mRNA (reverse transcriptase-PCR) levels, and the release of ROI (luminol-dependent chemiluminescence), after bronchoalveolar lavages. In particular, it has been shown that intratracheal instillation of silica (50 mg/kg) in rats led to fibrosis characterized by cellular interstitial infiltrates with granulomas, and in AM, it led to 1) an early and continuous increase in 12-O-tetradecanoylphorbol-13-acetate- or zymosan-triggered ROI production (days 1, 3, 14, and 28 post-treatment), and 2) a rise of TNF-alpha mRNA expression and protein secretion on days 3 and 14. A free radical scavenger pretreatment (N-ter-butyl-alpha-phenylnitrone) reversed lung histopathologic changes and decreased AM ROI production and TNF-alpha expression at the level of mRNA. These findings suggest that ROI production is an important primary event determining the silica-induced inflammatory process. ROI may act in an autocrine or paracrine manner and regulate TNF-alpha production by a mechanism promoting gene expression. The critical role of this cytokine in the pathogenesis of silicosis was confirmed by anti-TNF-alpha Ab treatment.

Animals↗

PubMed1996

Involvement of calcium in macrophage leukotriene release during experimental cirrhosis.

The aim of the present study was to assess the mechanism of 5-lipoxygenase metabolites (LT) secretion by peritoneal macrophages in rats wih CC14 induced cirrhosis. After stimulation with calcium ionophore A23187 or opsonized zymosan, [3H] arachidonic acid labeled macrophages from cirrhotic rats presented a significantly greater secretion of LT than macrophages from healthy controls. In addition, the phorbol ester TPA (protein kinase C activator) increased LT production only in macrophages from cirrhotic animals and not in controls. Although Ca2+ is thought to be involved in 5 lipoxygenase activation, the role of Ca2+ in LT production was studied. The use of a Ca2+-free medium as well as the addition of TMB-8 (an inhibitor of intra-cellular Ca2+ movements and of plasma membrane Ca2+ fluxes) resulted in a fall in LT production greater for macrophages from cirrhotic animals than for controls. The measurement of cytosolic Ca2+ concentration by cytofluorimetry showed that Fluo-3 loaded macrophages from cirrhotic rats had a greater cytosolic CA2+ concentration than macrophages from control animals both in basal conditions and after A23187 stimulation. Study of 45Ca2+ uptake suggest, that extra-cellular Ca2+ is implicated in the elevated cytosolic Ca2+ observed in macrophages from cirrhotic animals as compared to healthy controls. The greater Ca2+ concentration observed in macrophages from cirrhotic rats was not related to a difference in phospholipase C activation because inositol phosphate production did not differ between macrophages from healthy and cirrhotic animals. Taken together these results suggest that as compared to healthy animals, the greater LT production during cirrhosis could be dependent upon a difference in 5-lipoxygenase activation related to a rise in cytosolic Ca2+ concentration independently of inositol phosphates generation.

Analysis of Variance↗

PubMed1996

TNF-alpha enhances Toxoplasma gondii cyst formation in human fibroblasts through the sphingomyelinase pathway.

The cystogenesis event of Toxoplasma gondii is poorly understood. In order to throw light on it, the effect of tumor necrosis factor-alpha (TNF-alpha) was studied in the Prugniaud strain of the organism. This showed that TNF-alpha increased the number of cysts formed in vitro in human MRC5 fibroblasts. The sphingomyelinase pathway may be involved in mediating the TNF effect, since ceramide (natural form in permeabilized cells or cell-permeable analogue) could mimic the action of TNF. More precisely, our results strongly suggest the involvement of an acidic sphingomyelinase in mediating the effect of TNF; indeed, D609 inhibited both the TNF effect and cyst formation, while arachidonic acid had no effect. Moreover, protein kinase (PKC) seems also to play a role in the process, since phorbol-12-myristate-13-acetate (PMA) enhanced the cyst formation. However, chelerythrine chloride did not prevent the TNF effect, suggesting that several host-cell pathways can affect the cystogenesis event. Taken together, these results suggest the active participation of host-cell components in the cystogenesis of Toxoplasma gondii.

Alkaloids↗

PubMed1996

Nitric oxide and superoxide anion production during endothelial cell proliferation.

We have previously reported that nitric oxide (NO) synthase activity, protein, and mRNA are increased in proliferating compared with postconfluent bovine aortic endothelial cells (BAEC). Because superoxide anion inactivates NO, in the present study, we have assessed the effect of proliferation on superoxide anion production by use of cytochrome c reduction. The superoxide anion production in proliferating cells was increased about threefold compared with postconfluent cells in both basal and calcium ionophore-stimulated conditions and exceeded the amount of released nitrite and nitrate (NOx) in all cases. A-23187 (1 microM) stimulated the superoxide anion production about twofold at all stages of confluence. Because superoxide anion can inactivate NO, we then assessed the effect of proliferation on NO bioactivity released in the conditioned medium, by use of RFL-6 cells (reporter cells very rich in guanylate cyclase, which on activation by NO generates guanosine 3',5'-cyclic monophosphate, second messenger of NO). In the absence of added superoxide dismutase (SOD) in the conditioned medium, the guanylate cyclase-stimulating activities evoked by A-23187 from proliferating and growth-arrested cells were similar, despite a greater NOx release in the former. When SOD (100 U/ml) was added in the conditioned medium, the guanylate cyclase-stimulating activity evoked by 1 microM A-23187 was increased approximately 10-fold and closely paralleled NOx release (i.e., was greater in supernatant of proliferating cells than in that of growth-arrested cells). Thus BAEC release more superoxide anion extracellularly than NO at all stages of confluence. Endothelium-derived superoxide anion is a major determinant of the breakdown of NO.

Animals↗

PubMed1996

Henoch-Schönlein purpura and membranoproliferative-like glomerulonephritis.

A 17-year-old man presented Henoch-Schönlein purpura with renal impairment, nephrotic syndrome needing transitory hemodialysis and hematuria. By light microscopy, the renal biopsy revealed membranoproliferative-like lesion associated with massive subendothelial deposits, some subepithelial deposits, hyalin thrombi and intracapillary neutrophils. By immunofluorescence, intense nodular and segmental deposits of IgG, IgM, IgA, C3, fibrinogen and C1q were found to be present in the intracapillary area and the mesangium. By electron microscopy, large subendothelial and rare subepithelial deposits were observed. A skin biopsy demonstrated leukocytoclastic skin vasculitis with IgA deposits in the arterial walls. Treatment with corticosteroids resulted in return renal to normal renal function but persistent proteinuria and hematuria. A second renal biopsy, performed after 2 months, showed a marked decrease in lesions and deposits. Fifteen months later, the patient presented normal serum creatinine level but proteinuria and hematuria persisted. At this time, a third renal biopsy was performed and showed segmental mesangial sclerosis and the decrease of disappearance of deposits. Two years after the first hospitalization, no abnormal serum creatinine or urinalysis were present. This report describes a detailed study of a case presented with Henoch-Schönlein purpura and morphologic features consistent with membranoproliferative-like lesion, who recovered normal renal function and urinalysis; repeat biopsies performed at intervals of 2 months and 1 year confirmed the disappearance of mesangial proliferation, double contours and deposits.

Adolescent↗

PubMed1996

Tumour necrosis factor-alpha gene expression by alveolar macrophages in human lung allograft recipient with recurrence of sarcoidosis. Toulouse Lung Transplantation Group.

Recurrence of sarcoidosis in lung allografts is an interesting model to study the pathogenesis of this disease. We report a case of sarcoidosis recurrence in a single lung allograft recipient 2 years after transplantation. The expression of tumour necrosis factor-alpha (TNF-alpha) gene by alveolar macrophages was monitored. The TNF-alpha gene was not expressed at the time of recurrence of sarcoidosis, but only later when prominent granulomas were observed.

Adult↗

PubMed1995

Acetylated low density lipoprotein inhibits the incorporation of arachidonic acid in phospholipids with a concomitant increase of cholesterol arachidonate in rat peritoneal macrophages.

The aim of our work was to evaluate the influence of native low density lipoproteins (LDL) and LDL chemically modified by acetylation (acLDL) on incorporation and release of arachidonic acid (AA) in rat peritoneal macrophages. Compared to a control group without treatment, 100 micrograms/ml of acLDL for 15 h considerably increased the incorporation of [3H]AA in cholesterol-ester (CE) of rat peritoneal macrophages and induced a decrease of 3H-labeled membrane phospholipids (PL). No effect was shown with LDL treatment. In the presence of acLDL, LS3251 (100 nM), an acyl-coenzyme A:cholesterol acyltransferase (ACAT) inhibitor, inhibited the [3H]AA incorporation into CE in macrophages. [3H]AA-prelabeled macrophages cultured for 15 h with acLDL (compared to macrophages untreated or treated with LDL) showed an increase of labeled CE and a decrease of labeled PL and of cyclooxygenase and lipoxygenase eicosanoid production. After zymosan stimulation of macrophages prelabeled with [3H]AA and treated with or without LDL or acLDL, AA release and eicosanoid production increased in all groups of macrophages. The inhibition of eicosanoid production in foam cells does not seem to be linked to an inhibition of phospholipase but rather paralleled to an increase of the cholesterol [3H]arachidonate. A significant portion of cellular arachidonate released from phospholipids, in particular from phosphatidylcholine, could serve as a substrate to ACAT in this foam cell.

Acetylation↗

PubMed1995

Interleukin-13 inhibits protein kinase C-triggered respiratory burst in human monocytes. Role of calcium and cyclic AMP.

Interleukin-13 (IL-13), a novel cytokine produced by activated lymphocytes modulates some monocyte functions, but no data is available concerning the signal transduction pathway. We show here, the inhibitory effect of IL-13 on 12-O-tetradecanoylphorbol-13-acetate (TPA)-triggered reactive oxygen intermediate production in human monocytes and the signals involved in this response. Our results show that IL-13 produces rapid and transient phosphoinositide hydrolysis and intracellular Ca2+ mobilization. Furthermore, IL-13 induces intracellular cAMP accumulation through inositol 1,4,5-trisphosphate-dependent Ca2+ mobilization. Metabolic inhibitors were used to relate the first steps in signaling pathways to the inhibitory effect of IL-13 on TPA-triggered reactive oxygen intermediate production. Indeed, inhibitors of phospholipase C (neomycin), intracellular Ca2+ mobilization (8-[N,N-diethylamino]-octyl 3,4,5-trimethoxybenzoate hydrochloride), adenylate cyclase (delta 9-tetrahydrocannabinol), and protein kinase A (N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide) impair the IL-13 inhibitory response. Altogether these observations indicate that modulatory effect of IL-13 on the TPA-induced oxidative burst is the result of the intracellular cAMP accumulation through an inositol 1,4,5-trisphosphate-induced Ca2+ mobilization-dependent pathway.

Animals↗