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PubMed1975

Stimulus-secretion coupling in platelets. Effects of drugs on secretion on adenosine 5'-triphosphate.

The mechanism of stimulus-secretion coupling in platelets was investigated by observing the effects of drugs on the kinetics on ATP secretion induced by either thrombin or the divalent cation ionophore A23187. The actual secretion is the same with either of these agents, since the rate constants and activation energies of secretion are the same and since drugs that affect the final, enzyme-independent steps of thrombin-induced secretion have the same effect on ionophore-induced secretion. Drugs that affect early steps of thrombin-induced secretion have no effect on ionophore-induced secretion. Drugs that act through cAMP (PGE1, theophylline, dibutyryl-cAMP) slow an early step in the mechanism of thrombin-induced secretion and completely block at higher levels, with the required concentration of inhibitor dependent on thrombin concentration. The inhibition of rate appears to be all-or-none, with no intermediate rates observed. By replacing thrombin with trypsin, which makes it possible to observe a complete change in rate-determining step from an enzyme-dependent to an enzyme-independent platelet step, it was found that these drugs slow the rate only when the enzyme-independent step is rate determining. These drugs have no effect on A23187-induced secretion. It was concluded that cAMP inhibits at a step after the enzyme step but before the final step by interfering with transmission of the stimulus-secretion coupling signal. Disruption of microfilament function by cytochalasin B (10 muM) accelerates the rate of secretion induced by either thrombin or ionophore. The microtubule agents colchicine, vinblastine, and vincristine had effects only at concentrations above those usually considered necessary for the specific inhibition of microtubule function. Drugs that inhibit prostaglandin synthesis (aspirin, indomethacin, eicosatetraynoic acid), drugs that block ATP production (antimycin A, deoxyglucose), or several other drugs previously reported to inhibit platelet function had no effect on secretion.

Adenosine Triphosphate↗
PubMed1998

Effect of sham feeding and acute suppression of acid secretion on human gastric lipase secretion.

OBJECTIVE: Gastric lipase and gastric acid are secreted simultaneously. The aim of this study was to investigate whether the acid interferes with the lipase secretion. The secretion of human gastric lipase was studied during blockade of gastric acid secretion and modified sham feeding to estimate the impact of these conditions on both gastric lipase enzyme activity and immunoreactivity. METHODS: Eight healthy volunteers were intubated with a nasogastric tube. We examined gastric aspirates for the amount and activity of lipase secretion during basal conditions, after blockade of acid secretion with a proton pump inhibitor (omeprazole iv. infusion), and in response to sham feeding (chewing gum) during the blockade. RESULTS: The amount of secreted gastric lipase was unaffected by blockade of acid secretion and increased significantly after sham feeding (169.9+/-35.7 microg/15 min to 348.1+/-79.2 microg/15 min; p < 0.01). Likewise, the output of enzyme activity increased after sham feeding (0.63+/-0.09 kU/15 min to 1.52+/-0.36 kU/15 min; p < 0.03). The concentration of enzyme activity remained unchanged by blockade of acid secretion, whereas the output of enzyme activity was decreased, probably because of reduced volume secretion or denaturation and conformational changes of the enzyme. Plasma concentrations of gastrin increased in response to blockade of acid secretion (basal 9.6+/-1.4 pmol/L to 13.3+/-2.9 pmol/L; p < 0.02). CONCLUSIONS: Gastric acid secretion is not a prerequisite for gastric lipase secretion. Lipase enzyme activity, though, is sensitive to anacidic conditions.

Adult↗
PubMed2002

Coordinated regulation of gastric chloride secretion with both acid and alkali secretion.

Gastric secretion of hydrochloric acid requires protons and chloride, yet the mechanisms and regulation of gastric chloride secretion remain unclear. We developed an in vivo technique to simultaneously measure acid/base and chloride secretion into the gastric lumen of anesthetized rats. The cannulated stomach lumen was perfused with weakly pH-buffered chloride-free solution containing a chloride-sensitive fluorophore [5 microM N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide (MQAE)]. Gastric acid and chloride secretion was detected in gastric effluents by 1) flow-through pH electrode and 2) MQAE fluorescence. Gastric effluent was also collected at 1-min intervals for independent determination of chloride amount by chloridometer. In all conditions, both optical and chemical determinations of chloride report similar amounts of secreted chloride. During luminal perfusion with pH 5 solution, net acid and chloride secretion into the lumen was observed. Pentagastrin stimulated both secretions. In contrast, proton pump inhibition (omeprazole) caused alkalinization of the gastric effluent, but chloride secretion was not diminished. During luminal pH 3 perfusion, net alkali secretion was observed, and chloride secretion at luminal pH 3 was greater than pH 5. When tissue is pretreated with omeprazole at luminal pH 3, the addition of prostaglandin E2 synchronously stimulates both alkali and chloride secretion. Results suggest that both acid and alkali secretions are separately coupled with chloride secretion.

Alkalies↗
PubMed1978

Macromolecular secretion by isolated gastric mucosa: fundamental differences in pepsinogen and intrinsic factor secretion.

The secretion of pepsinogen and intrinsic factor (IF) in response to various known stimulators and inhibitors of gastric acid secretion was examined in isolated rabbit gastric mucosa maintained in organ culture. Acetylcholine (10(-8) M) stimulated stimulated both pepsinogen (P less than 0.01) and IF (P less than 0.01) secretion and this stimulation was blocked by atropine. Parasympatholytic agents did not alter unstimulated (basal) secretion of pepsinogen even at high concentrations (atropine, 10(-2) M or propanthelene bromide, 5 X 10(-3) M), however, at these concentrations basal IF secretion was abolished. Histamine (10(-4) and 10(-2) M) had no effect on pepsinogen secretion but stimulated IF secretion (P less than 0.001). Antagonism of H2 receptors by cimetidine reduced both basal and histamine-stimulated IF secretion, but pepsinogen secretion remained unaltered. Under the conditions of the above experiments the gastric mucosal surface was not exposed to HCl but was constantly buffered by culture medium at pH 7.4. When we applied 50 mN HCl to the mucosal surface of the biopsies, pepsinogen secretion doubled (P less than 0.001) but IF secretion was abolished. These studies have clearly documented that: (1) fundamental differences exist in the responses of pepsin and IF secreting cells; (2) H+ ions bathing the mucosal surface of the stomach may influence the results of experiments designed to examine the mechanisms of gastric mucosal macromolecular secretion.

Acetylcholine↗
PubMed2005

ExsE, a secreted regulator of type III secretion genes in Pseudomonas aeruginosa.

Type III secretion systems are toxin delivery systems that are present in a large number of pathogens. A hallmark of all type III secretion systems studied to date is that expression of one or more of their components is induced upon cell contact. It has been proposed that this induction is controlled by a negative regulator that is itself secreted by means of the type III secretion machinery. Although candidate proteins for this negative regulator have been proposed in a number of systems, for the most part, a direct demonstration of their role in regulation is lacking. Here, we report the discovery of ExsE, a negative regulator of type III secretion gene expression in Pseudomonas aeruginosa. Deletion of exsE deregulates expression of the type III secretion genes. We provide evidence that ExsE is itself secreted by means of the type III secretion machinery and physically interacts with ExsC, a positive regulator of the type III secretion regulon. Taken together, these data demonstrate that ExsE is the secreted negative regulator that couples triggering of the type III secretion machinery to induction of the type III secretion genes.

Bacterial Proteins↗
PubMed1973

Amylase secretion by the perfused cat pancreas in relation to the secretion of calcium and other electrolytes and as influenced by the external ionic environment.

1. Amylase secretion from the perfused pancreas consists of two components: a small continuous basal secretion and a stimulated secretion in response to acetylcholine or cholecystokinin-pancreozymin. The response to small doses of either stimulant was repeatable over several hours.2. The calcium concentration of pancreatic juice, always less than that of the perfusate, was normally constant above secretory rates of 0.15 g/10 min. However, when the concentration of enzymes in the juice rose, either after stimulation or at very low secretory rates, the calcium concentration rose in parallel, suggesting that this calcium is bound to, or is a component of, pancreatic enzymes.3. Elevation of the perfusate calcium concentration resulted in a parallel increase in the calcium concentration of the pancreatic juice.4. Calcium-free solutions initially caused a small reduction in basal and stimulated amylase secretion and, after prolonged periods of perfusion, abolished stimulated secretion and caused a reduction in electrolyte secretion. The latter was completely reversed by calcium-rich perfusates but the effects on enzyme secretion were only partially reversible.5. Calcium-rich perfusates had no effect on the rate of electrolyte secretion but potentiated submaximally stimulated amylase secretion.6. Barium did not substitute for calcium in supporting pancreatic secretion.7. Alterations in the extracellular concentrations of sodium, potassium and magnesium had no direct effect on amylase secretion.8. The local anaesthetic tetracaine inhibited amylase secretion at a lower concentration than that required to inhibit electrolyte secretion.9. It is concluded (a) that calcium is secreted into the pancreatic juice in two fractions, one associated with enzymes and the other with the electrolyte component of the juice; and (b) that calcium ions play an important role in the stimulus-secretion coupling of pancreatic acinar cells, but that the effects of calcium depletion on electrolyte secretion may principally be due to alterations in the permeability of the duct system.

Acetylcholine↗
PubMed1998

The Caulobacter crescentus paracrystalline S-layer protein is secreted by an ABC transporter (type I) secretion apparatus.

Caulobacter crescentus is a gram-negative bacterium that produces a two-dimensional crystalline array on its surface composed of a single 98-kDa protein, RsaA. Secretion of RsaA to the cell surface relies on an uncleaved C-terminal secretion signal. In this report, we identify two genes encoding components of the RsaA secretion apparatus. These components are part of a type I secretion system involving an ABC transporter protein. These genes, lying immediately 3' of rsaA, were found by screening a Tn5 transposon library for the loss of RsaA transport and characterizing the transposon-interrupted genes. The two proteins presumably encoded by these genes were found to have significant sequence similarity to ABC transporter and membrane fusion proteins of other type I secretion systems. The greatest sequence similarity was found to the alkaline protease (AprA) transport system of Pseudomonas aeruginosa and the metalloprotease (PrtB) transport system of Erwinia chrysanthemi. The prtB and aprA genes were introduced into C. crescentus, and their products were secreted by the RsaA transport system. Further, defects in the S-layer protein transport system led to the loss of this heterologous secretion. This is the first report of an S-layer protein secreted by a type I secretion apparatus. Unlike other type I secretion systems, the RsaA transport system secretes large amounts of its substrate protein (it is estimated that RsaA accounts for 10 to 12% of the total cell protein). Such levels are expected for bacterial S-layer proteins but are higher than for any other known type I secretion system.

ATP-Binding Cassette Transporters↗
PubMed1989

Endogenous inhibin suppresses only basal follicle-stimulating hormone secretion but suppresses all parameters of pulsatile luteinizing hormone secretion in the diestrous female rat.

The purpose of these studies was to ascertain which parameters of pulsatile gonadotropin secretion are regulated by endogenous inhibin in the intact diestrous female rat. This was determined by examining the changes in the secretion parameters of FSH and LH that resulted from immunoneutralizing endogenous inhibin in diestrous I female rats. Passive immunoneutralization of endogenous inhibin was achieved using specific, high titer ovine antiserum generated against the alpha-subunit of the recently described inhibin molecule. The optimal times after inhibin immunoneutralization to observe the changes in FSH secretion were determined in initial experiments. Pulsatile secretion of both FSH and LH was observable in the diestrous female. Two hours after inhibin immunoneutralization, the mean trough level, mean peak level, and overall mean level of FSH began to increase. The maximal increase and plateau of these parameters were observed 5 h after antiserum injection. During the period of increase, mean FSH pulse amplitude was also increased, but returned to the level observed in control (normal sheep serum-injected) animals when the parameters of trough, peak, and overall mean FSH reached their plateau levels. FSH pulse frequency was not changed at any time. These results indicate that endogenous inhibin affects only the basal parameters of FSH secretion without affecting pulsatile FSH secretion. The transient increase in FSH pulse amplitude resulted from FSH pulses being superimposed on the increasing basal FSH secretion. In contrast, immunoneutralization of endogenous inhibin rapidly increased all parameters (i.e. pulse amplitude and frequency, mean trough and peak levels, and mean plasma levels) of LH secretion. In addition, pituitary sensitivity to an exogenous LHRH challenge was increased in inhibin-immunoneutralized females in terms of stimulated LH secretion. As a result of the already increased rate of basal secretion, the actual quantity of FSH released in response to the LHRH challenge was greatly increased in the inhibin-immunoneutralized rats compared with the normal sheep serum-injected controls; however, the increase in the rate of FSH secretion stimulated by the LHRH challenge was the same in both groups. The observations from these studies collectively demonstrate that inhibin acts endogenously to suppress those parameters of gonadotropin secretion that are regulated by LHRH.

Animals↗
PubMed2002

Pulsatile leptin secretion is independent of luteinizing hormone secretion in prepubertal sheep.

Many studies have suggested that leptin modulates the gonadal axis. A synchronicity of luteinizing hormone (LH) and leptin has been described in humans, suggesting that leptin may modulate the episodic secretion of LH. The objective of this study was to establish whether episodic leptin secretion depends on the episodic LH secretion in prepubertal sheep. We used two different approaches. The first consisted of blocking the release of LH using a long-acting LH-releasing hormone (LHRH) agonist and analyzing the episodic LH and leptin secretions. The second method stimulated the pituitary gland with pulses of LHRH and again LH and leptin secretions were analyzed. Spring-born 20-wk-old Suffolk ewe lambs (n = 5) received intramuscularly a long-acting LHRH agonist (Decapeptyl). Treatment was repeated at 24 and 28 wk of age. Control lambs (n = 6) received the vehicle of Decapeptyl. Diurnal and nocturnal pulsatilities of LH and leptin were studied at 20 (before Decapeptyl injection), 26, and 30 wk. Blood samples were taken at 10-min intervals for 6 h, beginning at 10:00 AM (diurnal sampling) and at 10:00 PM (nocturnal sampling). In all samples, LH and leptin were measured by radioimmunoassay, and pulsatile hormone secretion characteristics were assessed by the CLUSTER program. To characterize further the synchronicity between LH and leptin pulses, LHRH (10 ng/kg body wt) was injected at 60-min intervals, six times, to another five 30-wk-old ewe lambs, for the same time period as the pulsatility study. In the control group, LH secretion did not change between lambs of 20 and 30 wk of age. In LHRH agonist-treated lambs, LH secretion diminished from 20 to 30 wk of age and was lower than in control lambs at 26 and 30 wk of age (p < 0.05). The transversal mean (ng/[mL x 6 h]) of leptin concentrations was different between control lambs of 20 wk of age and 26 and 30 wk of age (p < 0.01). Contrary to the findings in LH secretion, in LHRH agonist-treated lambs, mean plasma leptin concentrations did not decrease. Furthermore, the mean diurnal and nocturnal leptin concentrations and the pulse amplitude were higher at 26 and 30 wk than at 20 wk in LHRH agonist-treated lambs (p < 0.05). There were no differences between diurnal and nocturnal parameters of leptin secretion in both groups. There was no synchronicity between LH and leptin pulses. LHRH pulses significantly increased plasma LH concentrations, producing discernible LH pulses; however, leptin amplitude and leptin pulse frequency were not modified by the exogenous LHRH pulses, exhibiting no coincidence with LH pulses. The data suggest that pulsatile leptin secretion is independent of LH secretion in ewe lambs.

Aging↗
PubMed1990

Biosynthesis and secretion of M- and Z-type alpha 1-proteinase inhibitor by human monocytes. Effect of inhibitors of glycosylation and of oligosaccharide processing on secretion and function.

The biosynthesis and secretion of M-type and Z-type alpha 1-antitrypsin was studied in human monocytes. In monocytes of PiMM individuals alpha 1-antitrypsin represented 0.08% of the newly synthesized proteins and 0.44% of the secreted proteins. Two molecular forms of alpha 1-antitrypsin could be identified: a 51-kDa intracellular form, susceptible to endoglucosaminidase H, thus representing the high-mannose type precursor form and a 56-kDa form resistant to endoglucosaminidase H which was secreted into the medium. Inhibition of de novo glycosylation by tunicamycin impaired the secretion of M-type alpha 1-antitrypsin by about 75% whereas inhibition of oligosaccharide processing by the mannosidase II inhibitor swainsonine did not alter the secretion of M-type alpha 1-antitrypsin. alpha 1-Antitrypsin secreted by human monocytes was functionally active as measured by complex formation with porcine pancreatic elastase. Even unglycosylated alpha 1-antitrypsin secreted by human monocytes treated with tunicamycin formed a complex with elastase. In monocytes of PiZZ individuals the secretion of alpha 1-antitrypsin was decreased. 72% of newly synthesized M-type alpha 1-antitrypsin, but only 35% of newly synthesized Z-type alpha 1-antitrypsin were secreted during a labeling period of 3 h with [35S]methionine. The 51-kDa form of Z-type alpha 1-antitrypsin accumulated intracellularly, whereas the 56-kDa form was secreted. Inhibition of oligosaccharide processing by swainsonine did not alter the decreased secretion of Z-type alpha 1-antitrypsin, whereas inhibition of de novo glycosylation by tunicamycin blocked the secretion of Z-type alpha 1-antitrypsin completely.

Alkaloids↗
PubMed1991

[Action of neurotensin on duodenal alkaline secretion in rats. Comparison with pancreatic and gastric secretion].

Neurotensin is released from endocrine N cells of the ileum after meals, and might take part in the regulation of bicarbonate secretion by the pancreas and duodenum. The aim of this study was to define the effect of neurotensin on duodenal bicarbonate secretion, in comparison with its effect on gastric and pancreatic secretions. Neurotensin produced a dose-related increase of duodenal bicarbonate secretion with an ED50 of 60 pmol/kg.h. The maximal effect (about 2 times the basal level) was observed with 600 pmol/kg.h. Equimolar doses (600 pmol/kg.h) of xenopsin, neuromedin N, neurotensin 8-13 produced the same effect as neurotensin 1-13. Neurotensin fragments 1-11 and 9-13 (600 pmol/kg.h) had no significant effect on duodenal bicarbonate secretion. Indomethacin, atropine, naloxone, or the CCK antagonist L364,718 had no effect on neurotensin-stimulated bicarbonate secretion. Hexamethonium and vagotomy reduced the neurotensin effect by about 50 percent (P less than 0.05). Neurotensin produced a dose-related increase of pancreatic bicarbonate secretion with an ED50 of 150 pmol/kg.h, a decrease of gastric acid secretion with an ED50 of 2,400 pmol/kg.h, and a decrease of gastric pepsin secretion with an ED50 of 2,760 pmol/kg.h. This study shows that neurotensin stimulates duodenal bicarbonate secretion in doses which may be physiological. This biological activity depends on the presence of the C-terminal 8-13 fragment. The mechanism is complex, and depends, for approximately half, on vagal fibers (sensitive or motor), nicotinic synapses, and a non cholinergic effector. The other half of the effect, still unexplained, could be a direct effect on mucosal cells. Pancreatic and duodenal bicarbonate secretions were more sensitive to neurotensin than gastric secretion (acid and pepsin).

Animals↗
PubMed1996

Low rates of apoB secretion from HepG2 cells result from reduced delivery of newly synthesized triglyceride to a "secretion-coupled" pool.

The present study was aimed at defining the roles of intracellular triglyceride pools in apolipoprotein B secretion from HepG2 cells. Oleic acid (0.2 mmol/L) in the medium stimulated both triglyceride synthesis and apolipoprotein B secretion. Stimulation of apolipoprotein B secretion was lost about 30-40 min after oleic acid was removed from the medium, despite the finding that most newly synthesized triglyceride was still present in the cells. This suggested that only a small fraction of newly synthesized triglyceride was transferred to a pool available for assembly of nascent apoB into lipoproteins. Using cell fractionation, we analyzed two triglyceride pools in HepG2 cells: a microsomal pool and a cytoplasmic pool. Oleic acid-induced increases in the microsomal pool were small and short-lived due to secretion; this pool, therefore, is a "secretion-coupled" pool. The large majority of newly synthesized triglyceride was in a cytosolic pool that was not associated with secretion of apoB. Dibutyryl cAMP treatment was associated with a 3-fold increase in the mobilization of the triglyceride droplets. Apolipoprotein B secretion, however, was not increased, suggesting that the amount of triglyceride that entered the "secretion-coupled" pool after hydrolysis and re-esterification of cytoplasmic triglyceride was inadequate to stimulate apolipoprotein B secretion. In summary, the majority of newly synthesized triglyceride, whether derived from exogenous or endogenous fatty acids, is rapidly shifted to a cytoplasmic pool that does not play a regulatory role in apolipoprotein B secretion. The presence of a very small "secretion-coupled" pool of triglyceride in HepG2 cells likely explains the high rates of degradation of nascent apolipoprotein B, and the low rates of secretion of lipid-poor lipoproteins.

Apolipoproteins B↗
PubMed1995

Pulsatile insulin secretion accounts for 70% of total insulin secretion during fasting.

The purpose of the present study was to determine the contributions of discrete insulin secretory bursts vs. basal insulin release to total insulin secretion in vivo. Quantification of the partitioning of pulsatile and basal insulin secretion is complicated by physiological delivery of these pulses into the portal vein and the absence of validated methods of measuring the rates of pulsatile and basal insulin secretion in vivo. We therefore 1) developed a canine model with chronically implanted portal vein catheters, 2) validated an established deconvolution technique as well as a novel direct catheterization technique (Clustcath) for measurement of pulsatile and nonpulsatile insulin secretion rates in this model, and 3) applied these methods to study insulin secretion in the overnight-fasted dog in vivo to determine the contribution of pulsatile vs. basal insulin secretion to total rates of endogenous insulin secretion. Rates of total, pulsatile, and nonpulsatile endogenous insulin secretion measured by Cluscath closely parallel those measured by deconvolution analysis (54 +/- 15 vs. 51 +/- 11, 38 +/- 12 vs. 36 +/- 11, and 16 +/- 4 vs. 14 +/- 4 pmol/min, respectively). Clustcath and deconvolution indicated that the majority of insulin was secreted as pulses (70 +/- 6 and 66 +/- 7%, respectively). These data infer that any process that selectively decreases the pulsatile component of insulin secretion (e.g., diabetes mellitus) will likely have a major impact on total insulin secretion.

Animals↗
PubMed1983

Separation of cholera enterotoxin-induced mucus secretion from electrolyte secretion in rabbit ileum by acetazolamide, colchicine, cycloheximide, cytochalasin B and indomethacin.

In vivo rabbit ileal loops were prepared and inoculated with purified cholera enterotoxin (CT). After a lag period of about 1 h there was persistent stimulation of water and electrolyte secretion and a transient stimulation of mucus secretion into the luminal fluid. Repeated intraluminal inoculation of prostaglandin E1 (PGE1) caused a pattern of water, electrolyte and mucus secretion which was qualitatively the same as that following CT, except that no lag period was observed. Doses of the protein synthesis inhibitor, cycloheximide, the microtubule disrupter, colchicine, and the microfilament disrupter, cytochalasin B, were found that inhibited CT-induced mucus secretion but not water and electrolyte secretion. The carbonic anhydrase inhibitor, acetazolamide, inhibited CT-induced water and electrolyte secretion without inhibiting the mucus secreted over a 5-hour test period. Thus a variety of agents can be used to demonstrate a separation of intestinal water and electrolyte secretion from mucus secretion. The prostaglandin synthesis inhibitor, indomethacin, also inhibited CT-induced water, electrolyte and mucus secretion, but no dose of this agent was found that completely separated the water and electrolyte from the mucus secretion.

Acetazolamide↗
PubMed1994

Duodenal mucosal bicarbonate secretion in pigs is accompanied by compensatory changes in pancreatic and biliary HCO3- secretion.

BACKGROUND: The purpose of the study was to examine the effect of stimulation and inhibition of duodenal mucosal bicarbonate secretion on pancreatic and hepatic bicarbonate secretion in response to acid. METHODS: The effect of inhibition (indomethacin) or stimulation (misoprostol) of duodenal mucosal bicarbonate secretion on pancreatic and biliary bicarbonate secretion in response to intraduodenal infusion of HCl or intravenous infusion of secretin was studied in anaesthetized pigs. RESULTS: The hepatic and pancreatic response to exogenous secretin was not significantly altered by stimulation/inhibition of duodenal bicarbonate secretion. However, pancreatic and biliary bicarbonate secretion in response to duodenal acidification was significantly augmented by inhibition of duodenal mucosal bicarbonate secretion; conversely, it was reduced by stimulation of duodenal bicarbonate secretion. The increase in plasma secretin levels in response to duodenal acidification was reduced by stimulation and augmented by inhibition of duodenal mucosal bicarbonate secretion. CONCLUSIONS: Duodenal mucosal bicarbonate secretion can serve as a modulator of both pancreatic and biliary bicarbonate secretion in response to luminal acidification, possibly through regulation of the release of secretin.

Acid-Base Equilibrium↗
PubMed1984

Lipoprotein synthesis and secretion by cultured rat hepatocytes. Parallel inhibition of secretion of VLDL, HDL and albumin by monensin.

The biosynthesis and secretion of very-low-density lipoproteins (VLDL) and high-density lipoproteins (HDL) by cultured normal rat hepatocytes was investigated with particular emphasis on its modification by monensin. This acidic ionophore coordinately inhibited the rates of secretion of the several VLDL apolipoproteins and the VLDL lipids, suggesting an effect late in the process of biosynthesis and secretion, probably at the stage of exiting from the Golgi apparatus. The secretion of immunoreactive albumin into the medium was comparably inhibited, implying that the pathway and mechanisms involved in albumin secretion may be closely similar to those for VLDL synthesis and secretion. Secretion of phospholipids and of apolipoproteins E and A-I in the HDL fraction increased progressively with time over 18 h in control incubations but was strongly inhibited by monensin. During extended incubation with monensin at high concentrations (10 microM), there was a net release to the medium of a number of hepatocyte proteins, including some that comigrated with apolipoprotein A-I and apolipoprotein C, making it appear that monensin increased the secretion of these apolipoproteins. However, using labeled amino acids, it was shown by autoradiography and by immunoprecipitation that secretion of newly-synthesized, radioactive apolipoprotein A-I and apolipoprotein C was actually inhibited by monensin. These results are compatible with the conclusion that HDL synthesis and secretion may occur by mechanisms closely related to those for synthesis and secretion of albumin and VLDL.

Amino Acids↗
PubMed2006

Identification of a rat bone marrow-derived dendritic cell population which secretes both IL-10 and IL-12: evidence against a reciprocal relationship between IL-10 and IL-12 secretion.

The qualitative nature of immune responses induced by dendritic cells (DCs) is influenced by the balance of pro-inflammatory (e.g. IL-12) and anti-inflammatory (e.g. IL-10) cytokines that they secrete. Evidence to date suggests that IL-12 and IL-10 secretion is reciprocally regulated and that IL-10 inhibits IL-12 secretion. This study identifies a population of resting, immature rat bone marrow-derived DCs (BMDCs) which secretes IL-10, the IL-12(p70) heterodimer and the free IL-12(p40) subunit, the latter in vast excess of IL-12(p70). Counter-intuitively, activation with LPS induces the secretion of high and equivalent levels of IL-10 and IL-12(p40), but only quantitatively small increases in IL-12(p70). Neutralization of IL-10 increased the secretion of IL-12(p40) by resting BMDCs, but decreased IL-12(p40) secretion by LPS-activated BMDCs. Pre-incubation of resting BMDCs for 24h with neutralizing antibody to IL-10 reduced the subsequent secretion of IL-10 in allogeneic cultures of Lewis CD3(+) T cells with resting and LPS-activated Wistar BMDCs, and enhanced IL-12(p40) secretion in allogeneic cultures with LPS-activated BMDCs. IL-10 neutralization had no effect on the levels of IL-12(p70), IFN-gamma or IL-4 in allogeneic cultures. In summary, this study has identified a population of rat BMDCs that secretes low levels of bioactive IL-12(p70), but high levels of IL-10 and IL-12(p40). These findings argue against the concept that there is a reciprocal relationship between IL-10 and IL-12 secretion. They might also have implications for understanding the role of DCs in post-activation qualitative skewing of immune responses.

Animals↗