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At least 109 records · Page 6Linked to original sources
PubMed2002

[Type III secretion system in Se9R can recognize and secret harpin in Erwinia amylovora].

Bacterial pathogens of both animals and plants use type III secretion machines to secret virulence proteins. The signal that leads to tye type III secretion is encoded as stem loop structure in the messenger RNA. Harpin, produced by Erwinia anylovora is secreted via type III secretion. Erwinia carotovora Se9R and Erwinia amylovora belong to the same genus and they use type III secretion machines to secret virulence proteins. We used PCR to amplify hrpN from pCPP430 which harbors hrpN gene cluster, and cloned it to pGEM-T vector to get pWGF1, which was then chemically transformed into DH5 alpha (pCPP430hrpN-) and electrotransformed into Se9R. DH5 alpha (pCPP430hrpN-/pWGF1) induced hypersensitive response on tomato leaf and Se9R(pWGF1) showed significantly reduced virulence than Se9R on Chinese cabbage leaf. Western-blotting analysis of the CFEP of Se9R(pWGF1) showed production of harpin protein. These results suggest the type III secretion machine in Se9R can recognize secretion singal in the gene of harpin in Erwinia amylovora and secret it as a biologically native form.

Bacterial Outer Membrane Proteins↗
PubMed1992

Corticotropin-releasing factor, but not arginine vasopressin, stimulates concentration-dependent increases in ACTH secretion from a single corticotrope. Implications for intracellular signals in stimulus-secretion coupling.

The two fundamental parameters of corticotropin (ACTH) secretion are the number of secreting corticotropes and the amount of ACTH secreted by each cell. We have measured these parameters in rat corticotropes in response to increasing concentrations of corticotropin-releasing factor (CRF) or arginine vasopressin (AVP). Increasing concentrations of AVP stimulated more corticotropes to secrete, while the amount of ACTH each cell secreted remained relatively fixed (nongraded secretory response). Conversely, increasing concentrations of CRF stimulated more ACTH secretion per cell (graded secretory response), while the number of secretory cells remained relatively constant. When viewed from the perspective of a single corticotrope, it was clear that CRF and AVP induced completely distinct specific responses. We have previously shown, and provide further evidence here, that secretory responses to CRF or AVP occur in the same cell. It is therefore apparent that a single corticotrope is able to generate either a graded, or a nongraded secretory response. We have also considered the potential intracellular changes that must direct graded or nongraded secretion. It is generally accepted that CRF stimulates activation of adenylate cyclase, whereas AVP activates phosphoinositidase in pituitary corticotropes. Our findings, and others surveyed here, suggest that the activation of adenylate cyclase results in graded secretion, while the activation of phosphoinositidase induces the nongraded secretion. Graded or nongraded secretion may therefore be linked to specific second messengers. It is hypothesized that the inositol 1,4,5-trisphosphate-mediated release of an intracellular Ca2+ store constitutes a mechanism whereby phosphoinositidase-coupled hormones set in motion the nongraded secretory response. These findings suggest novel functions for individual second messengers.

Adrenalectomy↗
PubMed1992

Feedback control of pancreatic secretion in rats. Role of gastric acid secretion.

Pancreatic secretion in rats is regulated by feedback inhibition of cholecystokinin (CCK) release by proteases in the gut lumen, but little is known about the role of gastric acid in this regulation. This study, carried out on conscious rats with large gastric fistulas (GF) and pancreatic fistulas, shows that diversion of pancreatic juice results in the progressive stimulation of pancreatic secretion only in rats with the GF closed. When the GF was kept open, the diversion resulted in only small increment in pancreatic secretion and this was accompanied by progressive increase in gastric acid outputs. Similar amounts of HCl instilled into the duodenum in rats with the GF open fully reproduced the increase in pancreatic secretion observed after the diversion of pancreatic juice. Pretreatment with omeprazole (15 mumol/kg) to suppress gastric acid secretion or with L-364,718 (5 mumol/kg) to antagonize CCK receptors in the diverted state, resulted in the decline in pancreatic secretion similar to that observed after opening the GF. CCK given s.c. (20-320 pmol/kg) failed to cause any significant rise in the post-diversion pancreatic secretion in rats with the GF closed, but stimulated this secretion dose-dependently when the GF was open. Camostate (6-200 mg/kg) in rats with pancreatic juice returned to the duodenum caused dose-dependent increase in pancreatic secretion, but after opening the GF or after omeprazole this increase was reduced by about 75%. This study provides evidence that gastric acid plays a crucial role in the pancreatic response to diversion of pancreatic juice or inhibition of luminal proteases, and that factors that eliminate gastric acid secretion reduce this response.

Animals↗
PubMed1982

Potassium ion concentration alters glucagon secretion independently of insulin secretion in the isolated rat pancreas.

In the arginine-stimulated perfused rat pancreas, elevated concentrations of potassium ion inhibited glucagon secretion while stimulating the secretion of insulin. Decreased potassium ion produced the reverse effect. The observed inverse correlation between changes in insulin and glucagon secretion (r = -0.64; p less than 0.001) was suggestive of local interactions between islet hormones, and prompted us to determine whether potassium-induced changes in glucagon secretion were dependent upon concurrent changes in insulin release. We found that when insulin secretion was greatly suppressed, either through acute induction of diabetes with streptozotocin or by utilization of a glucose-free perfusate, no qualitative differences in glucagon responsiveness to altered potassium ion were evident, although the amplitude of these glucagon changed was enhanced. Similarly, when exogenous insulin (20,000 mU/l) was added to the perfusate in order to render potassium-induced changes in endogenous insulin secretion insignificant, glucagon responsiveness to altered potassium ion was maintained. Exogenous insulin alone had no effect on arginine-stimulated glucagon secretion. We conclude that any indirect effects of potassium ion on arginine-stimulated glucagon secretion are not mediated by insulin, but could be related to changes in somatostatin secretion.

Animals↗
PubMed1979

Adrenergic modulation of pancreatic A, B, and D cells alpha-Adrenergic suppression and beta-adrenergic stimulation of somatostatin secretion, alpha-adrenergic stimulation of glucagon secretion in the perfused dog pancreas.

The effects of adrenergic substances on pancreatic insular secretions were studied in a completely isolated canine pancreas with exclusion of the duodenum from the perfusion circuit. To ensure adequate blockade, blockers were infused before agonists. A dose range of beta-receptor blockade was tested, and putative alpha-adrenergic effects were confirmed by combined alpha- and beta-adrenergic receptor blockade.beta-Adrenergic agonism (2 ng/ml isoproterenol) induced a mean integrated increase of 79+/-20% in somatostatin secretion, whereas glucagon and insulin secretion were increased by 185+/-45 and 495+/-146%, respectively. The stimulations of D, A, and B cells were abolished by propranolol.alpha-Adrenergic agonism (10 ng/ml epinephrine) after beta-adrenergic blockade) moderately decreased somatostatin (-37+/-7%) secretion, moderately increased glucagon (91+/-19%), and markedly decreased insulin (-85+/-3%) release. Similar effects on D-, A-, and B-cell secretion were induced with 2 ng/ml epinephrine or 10 ng/ml norepinephrine after beta-adrenergic blockade. The alpha-adrenergic effects on the D and A cell were abolished by either phentolamine or by phenoxybenzamine. This study showed that there are indeed alpha-adrenergic receptors on A cells and that the secretion of glucagon, a "stress" hormone, was stimulated either by alpha- or beta-adrenergic receptor agonism. D-cell secretion, like that of the B cell, was inhibited by alpha-adrenergic agonism and was stimulated by beta-adrenergic agonism. However, beta-adrenergic-induced changes in D-cell secretion were smaller in magnitude than those of B-cell secretion.

Adrenergic alpha-Agonists↗
PubMed1988

Effects of aging on insulin synthesis and secretion. Differential effects on preproinsulin messenger RNA levels, proinsulin biosynthesis, and secretion of newly made and preformed insulin in the rat.

Aging in men and rodents is associated with a marked decline in glucose stimulated insulin secretion by pancreatic beta cells (B cells). Secreted insulin is the end result of a series of steps along the biosynthetic protein-secretion pathway, including insulin gene transcription, processing of transcripts to preproinsulin mRNA, translation of mRNA, segregation and processing of newly made proinsulin in secretory vesicles, proinsulin to insulin conversion, transport of vesicles to the plasma membrane, and exocytosis. We have examined the influence of age at three stages along this pathway: preproinsulin mRNA levels, proinsulin synthesis, and secretion of newly made and preformed insulin, using Fischer rats, a widely studied rodent model of aging. Pancreatic weights and total insulin contents, islet sizes, and mean insulin content per islet were the same in young adult (4-5 mo) and senescent (21-22 mo) animals. There was no effect of age on preproinsulin mRNA levels in whole pancreata of fed animals, or in isolated islets cultured for 16 h in 5.5 mM glucose. Proinsulin biosynthesis and the secretion of newly made insulin were compared in isolated islets preincubated in 5.5 mM glucose. After a pulse label at 16.7 mM glucose, proinsulin synthesis, assayed by immunoprecipitation, was decreased 16% in 7 mo islets and 39% in 21-22 mo islets, compared with 4-5 mo islets, though total protein synthesis was not reduced. When chased at 2.8 mM glucose, 4-5 month and 21-22 mo islets showed no difference in release of preformed or newly made insulin. When chased at 16.7 mM glucose, there was a significant decrease in the secretion of newly made insulin in the old islets compared with the young islets. There was preferential release of newly made insulin over preformed insulin in both young and old islets. However, since secretion of preformed insulin was decreased much more than secretion of newly made insulin in senescent islets, these displayed a two- to threefold increase in the proportion of newly made insulin relative to total immunoreactive insulin released compared with young adult islets. The differential effects of aging on these steps in the insulin synthesis-secretion pathway may be due to varying impairments in signals transducing the glucose stimulus into the wide range of B cell responses to glucose.

Aging↗
PubMed2006

Gamma-aminobutyric acid secreted from islet beta-cells modulates exocrine secretion in rat pancreas.

AIM: To investigate the role of endogenous gamma-amino-butyric acid (GABA) in pancreatic exocrine secretion. METHODS: The isolated, vascularly perfused rat pancreas was employed in this study to eliminate the possible influences of extrinsic nerves and hormones. Cholecystokinin (CCK; 10 pmol/L) was intra-arterially given to stimulate exocrine secretion of the pancreas. RESULTS: Glutamine, a major precursor of GABA, which was given intra-arterially at concentrations of 1, 4 and 10 mmol/L, dose-dependently elevated the CCK-stimulated secretions of fluid and amylase in the normal pancreas. Bicuculline (10 micromol/L), a GABA(A) receptor antagonist, blocked the enhancing effect of glutamine (4 mmol/L) on the CCK-stimulated exocrine secretions. Glutamine, at concentrations of 1, 4 and 10 mmol/L, dose-dependently increased the GABA concentration in portal effluent of the normal pancreas. The effects of glutamine on the CCK-stimulated exocrine secretion as well as the GABA secretion were markedly reduced in the streptozotocin-treated pancreas. CONCLUSION: GABA could be secreted from beta-cells into the islet-acinar portal system after administration of glutainine, and could enhance the CCK-stimulated exocrine secretion through GABA(A) receptors. Thus, GABA in islet beta-cells is a hormone modulating pancreatic exocrine secretion.

Animals↗
PubMed2000

Balance of two secretion pathways of nerve growth factor in PC12 cells changes during the progression of their differentiation, with a decrease in constitutive secretion in more differentiated cells.

Proteins are secreted from animal cells by either a constitutive or a regulated pathway. When cDNA of nerve growth factor (NGF) was introduced into PC12 cells, these cells produced and secreted active NGF, where NGF was secreted not only in constitutive but also in activity-dependent regulated way according to the results of pulse-chase and ELISA studies. The regulated secretion was caused by depolarization, cyclic AMP analogue, or beta-adrenergic agonist but not by glutamate or carbachol. Because these transfected cells differentiated into a morphology indistinguishable from that incubated with NGF protein, we next compared the secretion pathways of NGF from PC12 cells at different stages of the differentiation. NGF was secreted in both constitutive and regulated way at 2 and 7 days after the transfection of NGF-cDNA, but the constitutive secretion of NGF from the more differentiated cells of Day 7 was decreased and mature NGF tended to accumulate in the cells. These results indicate that the neurotrophin secretion mechanism is intimately regulated in the course of the differentiation of PC12 cells. Such a change in the protein secretion pathway might have an profound role in the development of neurons.

Animals↗
PubMed1992

Dissociation of CCK-8-induced fluid secretion from protein secretion by ion-transport blockers in rat pancreas.

The effects of ion-transport blockers on CCK-8-induced protein output and concomitant fluid secretion were compared in isolated, perfused normal and hypertrophied rat pancreata. In the normal pancreas, perfusion with ouabain (1 mM), amiloride (1 mM), furosemide (1 mM), or SITS (0.1 mM) caused corresponding inhibition of both fluid and protein secretion that was induced by 100 pM CCK-8. Hypertrophy of the pancreas was produced by oral administration of a synthetic protease inhibitor (FOY-305) once a day for 3 wk. In the hypertrophied pancreas, perfusion with ouabain (0.1 or 1 mM) or amiloride (0.1 mM or 1 mM) decreased CCK-8-induced fluid secretion without changing CCK-8-induced protein output. Perfusion with furosemide (1 mM) inhibited both fluid and protein secretion induced by CCK-8, but the amount of inhibition of fluid secretion was much greater than that of protein secretion. Perfusion with SITS (0.1 mM) significantly decreased CCK-8-induced fluid secretion but not protein secretion. These results indicate that in contrast to a normal rat pancreas, the coupling of fluid and protein secretion induced by CCK-8 can be disrupted by experimental procedures that induce hypertrophy in the rat pancreas.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1990

CD4 cells from patients with autoimmune thyroid disease secrete interferon gamma after stimulation by thyroid microsomal antigen; CD8 cells suppress this secretion.

The production of interferon gamma (IFN gamma) by peripheral blood mononuclear cells (PBMC) from normal persons and patients with autoimmune thyroid disease (AITD) has been studied in vitro either spontaneously or after stimulation with thyroid microsomal antigen (TMc) or liver microsomal antigen (LMc). The numbers of IFN gamma secreting cells were measured by a spot-ELISA technique. AITD PBMC spontaneously contained significantly more IFN gamma secreting cells than did normal control PBMC. Moreover, TMc antigen caused a significantly greater number of IFN gamma secreting cells in AITD PBMC than did LMc antigen, whereas there was no significant difference between the two antigens in the normal control PBMC preparations. Thus TMc antigen caused a stimulation of the number of IFN gamma secreting cells only in the AITD PBMC and not in the normal PBMC. CD4 plus B cells or CD4 cells alone (with monocytes in both instances) contained more IFN gamma secreting cells under unstimulated conditions than did CD8 cells in both groups. AITD CD4 plus B cells (or CD4 cells) contained more IFN gamma secreting cells than did normal cells, but there was no significant difference between both groups in terms of the number of CD8 IFN gamma secreting cells. Normal CD4 plus B cells (or CD4 cells) responded to TMc antigen significantly more than did total normal PBMC at 10 and 1,000 ng/ml TMc. This was not the case when patients' CD4 plus B cells (or CD4 cells) were compared with patients' total PBMC, in which there were no significant differences. This suggests that CD8 suppressor activity was inadequate in AITD and thus the deletion of CD8 cells did not result in an increase in IFN gamma secreting cells. When TMc antigen was added to AITD CD8 cells, there was a significant diminution of IFN gamma secreting cell numbers at 10 and 1,000 ng/ml TMc. Moreover, adding autologous CD8 cells to CD4 plus B cells resulted in a significant suppression of IFN gamma production at 100 and 1,000 ng/ml TMc in both groups. AITD CD8 cells appeared to be somewhat less effective than normal CD8 cells, but this did not reach significance. It is thus concluded that AITD CD4 cells respond specifically to TMc antigen. CD4 production of IFN gamma appears to be suppressed by CD8 cells activated with antigen and the CD8 cells appear to be involved in the regulation of IFN gamma production by the CD4 cells.

Adult↗
PubMed1982

A comparison of the effects of pirenzepine and atropine on gastric acid secretion, salivary secretion and pupil diameter in the rat.

The ability of pirenzepine and atropine, given i.v., to inhibit gastric acid and salivary secretion and increase pupil diameter has been assessed in the rat. Pirenzepine had a similar potency against acid secretion, ED 50 0.71 (0.41 to 1.1) mg.kg-1, and salivary secretion, ED 50 (0.43 to .59) mg.kg-1, whilst its potency was less in the eye, ED 50 1.8 (1.6 to 2.1) mg.kg-1. Atropine however, was more potent in reducing salivary secretion, ED 50 0.012 (0.010 to 0.016) mg.kg-1 and increasing pupil diameter, ED 50 0.028 (0.025 to 0.031) mg.kg-1 than in inhibiting gastric acid secretion, ED 50 0.056 (0.037 to 0.083) mg.kg-1. Therefore, that quantity of pirenzepine which inhibits gastric acid secretion by 50% will have only a slight effect on the eye and will inhibit salivary secretion by a similar magnitude. In contrast, the amount of atropine required to inhibit acid secretion by 50% will significantly increase pupil diameter and abolish salivary secretion.

Animals↗
PubMed1991

The importance of gastric secretion in the feedback control of interdigestive and postprandial pancreatic secretion in rats.

Previous studies demonstrated that pancreatic enzyme secretion in rats is stimulated by the diversion of pancreatic juice from the duodenum or by the inhibition of pancreatic proteinases in the intestinal lumen but little attention has been paid to the role of gastric secretion in this stimulation. This study, carried out on conscious rats with large gastric (GF) and pancreatic fistulas, confirms that diversion of pancreatic juice in rats with the GF closed results in the progressive stimulation of pancreatic secretion reaching the maximum similar to that induced by exogenous CCK. When the GF was kept open, the diversion resulted in only small increment in pancreatic secretion and this was accompanied by progressive increase in gastric acid outputs. Similar amounts of HCl (25-400 mumol/h) instilled intraduodenally (i.d.) in rats with the GF open fully reproduced the increase in pancreatic secretion observed after the diversion of pancreatic juice and this effect was completely abolished by the pretreatment with L-364,718, a specific CCK receptor antagonist. Pretreatment with omeprazole to suppress completely gastric acid secretion in the diverted state resulted in a decline in pancreatic secretion similar to that observed after opening the GF. Camostate given in graded doses (6-200 mg/kg) either i.d. or s.c. in rats with pancreatic juice returned to the duodenum caused a dose-dependent increase in pancreatic secretion, but after opening the GF or after omeprazole this increase was reduced by about 50% while after L-364,718 it was abolished. This study provides evidence that gastric secretion plays an important role in the pancreatic response to diversion of pancreatic juice or inhibition of luminal proteinases (but not to feeding) and the elimination of gastric acid reduces this response.

Animals↗
PubMed1997

Platelet activation with combination of ionophore A23187 and a direct protein kinase C activator induces normal secretion in patients with impaired receptor mediated secretion and abnormal signal transduction.

Defects in signal transduction mechanisms may underlie the impaired aggregation and secretion in patients with congenital platelet function defects (CPD). Both protein kinase C (PKC) induced pleckstrin phosphorylation and cytoplasmic Ca2+ mobilization play a major role in secretion. We postulated that combined platelet activation with a cell permeable direct PKC activator 1,2-dioctanoyl-sn-glycerol (DiC8) and ionophore A23187, which possibly bypass the steps involved in the intracellular synthesis of two major mediators (inositol trisphosphate, diacylglycerol), may induce normal dense granule secretion in patients with impaired receptor mediated secretion. We studied eight CPD patients with abnormal aggregation and secretion in response to several different surface receptor-mediated agonists despite the presence of normal dense granule contents. Receptor mediated Ca2+ mobilization and/or pleckstrin phosphorylation were abnormal in seven patients. Platelet activation with a combination of ADP (8 microM) with DiC8 (200 microM) or A23187 (10 microM) improved secretion in four patients. However, platelet activation with a combination of 200 microM DiC8 with 10 microM A23187, or 100 microM DiC8 with 5 microM A23187 induced normal secretion in platelet-rich plasma in all patients. These studies suggest that in such patients with CPD the ultimate process of exocytosis or secretion per se is intact and impaired secretion results from abnormalities in early signal transduction events, possibly upstream of diacylglycerol formation and calcium mobilization. Detailed studies are needed to delineate the specific abnormalities in these heterogenous patients with signal transduction defects.

Adolescent↗
PubMed2000

Participation of Na,K-ATPase in FGF-2 secretion: rescue of ouabain-inhibitable FGF-2 secretion by ouabain-resistant Na,K-ATPase alpha subunits.

We have examined the relationship between Na,K-ATPase and FGF-2 secretion in transfected primate cells. FGF-2 lacks a classic hydrophobic export signal, and the mechanisms mediating its secretion are unknown. To monitor secretion, a FLAG epitope tag was inserted into the carboxyl terminus of the 18 kDa form of human FGF-2, and the construct was transfected into either human HEK 293 or monkey CV-1 cells. Exported FGF-2 was detected in the culture medium using the FLAG-specific monoclonal antibody M2. FGF-2 secretion from HEK 293 or CV-1 cells was linear over time and sensitive to inhibition by the cardiac glycoside ouabain, a specific inhibitor of the Na,K-ATPase. In contrast, the secretion of FGF-8 (an FGF family member that contains a hydrophobic secretory signal) was not inhibited by treatment of HEK 293 or CV-1 cells with ouabain. FGF-2 secretion was also assayed in CV-1 cells expressing the naturally ouabain-resistant rodent Na,K-ATPase alpha1 subunit. In cells expressing the rodent alpha1 subunit, FGF-2 secretion was unaffected by high levels of ouabain, indicating that the rodent alpha1 subunit was capable of rescuing ouabain-inhibitable FGF-2 export. Expression of ouabain-resistant mutants of the rodent alpha2 and alpha3 subunits, or the naturally ouabain-resistant rodent alpha4 subunit, also supported FGF-2 secretion in ouabain-treated cells. Taken together, our studies are consistent with the idea that the Na,K-ATPase plays a prominent role in regulating FGF-2 secretion, although none of the alpha subunit isoforms exhibited specificity with regard to FGF-2 export.

Animals↗
PubMed1999

pH-dependent secretion of SseB, a product of the SPI-2 type III secretion system of Salmonella typhimurium.

The type III secretion system of Salmonella pathogenicity island 2 (SPI-2) is required for bacterial replication inside macrophages. SseB has been considered a putative target of the secretion system on the basis of its similarity with EspA, a protein secreted by the type III secretion system of enteropathogenic Escherichia coli (EPEC). EspA forms a filamentous structure on the bacterial cell surface and is involved in translocation of proteins into the eukaryotic cytosol. In this paper, we show that SseB is a secreted protein that associates with the surface of the bacterial cell and might, therefore, also be required for delivery of SPI-2 effector proteins to the eukaryotic cell cytosol. SseB begins to accumulate inside the bacterial cell when the culture enters early stationary phase. However, SseB is only secreted if the bacteria are grown at low pH or if the pH is shifted after growth from 7.0 to below pH 5.0. The secretion occurs within minutes of acidification and is totally dependent on a functional SPI-2 type III secretion system. As the pH of the Salmonella-containing vacuole inside host cells has been shown to acidify to between pH 4.0 and 5.0, and as SPI-2 gene expression occurs inside host cells, low pH might be a physiological stimulus for SPI-2-mediated secretion in vivo.

Agglutination Tests↗
PubMed1989

Effect of calcitonin and 1,25(OH)2-vitamin D3 on the FSH, LH and testosterone secretion at rest and LHRH stimulated secretion.

The calcium signal plays an important role in the control of the secretory process of some adenohypophyseal hormones which responds to the administration of calciotropic substances by a marked change. In the submitted work the effect of calcitonin and 1,25(OH)2-vitamin D3 (1,25(OH)2D3) on FSH, LH and testosterone secretion was investigated. A single dose of 50 U synthetic salmon calcitonin did not influence the FSH, LH and testosterone secretion at rest nor stimulated secretion. 1,25(OH)2D3 administered for four days in amounts of 3 micrograms/day did not affect the LH and testosterone secretion but increased slightly the secretory response of FSH to LHRH, significantly during the 80th minute following administration of the secretagogue (P less than 0.01). The indication of bi-phasic FSH secretion was eliminated by 1,25(OH)2D3. The significant decline of PTH levels following administration of 1,25(OH)2D3 is evidence of a biologically effective level of 1,25(OH)2D3 attained by the administered dose of hormone. As compared with the marked effect of calcitonin and 1,25(OH)2D3 on thyrotropic hormone secretion, it may be concluded that the gonadotropic system is considerably less sensitive to a change of calcium homeostasis induced by calcitonin or 1,25(OH)2D3. Nevertheless a slight increase of the FSH secretion and a change of the dynamics of its secretion suggest a modulating role of 1,25(OH)2D3 in the control of FSH secretion.

Adult↗
PubMed1998

Apolipoprotein(a) synthesis and secretion from hepatoma cells is coupled to triglyceride synthesis and secretion.

Apolipoprotein(a) (apo(a)) is synthesized and secreted from liver cells and represents one of the two major protein components of the atherogenic lipoprotein, Lp(a). Little is known, however, of the factors that regulate the secretion of this protein. We have undertaken an analysis of the response to oleate supplementation in stable clones of HepG2 and McA-RH7777 cells expressing either a 6 K-IV or 17 K-IV isoform of apo(a). These cell lines were examined by pulse-chase analysis and each demonstrated an increase (range 2-6-fold) in apo(a) secretion following supplementation with 0.8 mM oleate. Microsomal membranes, prepared from HepG2 cells expressing a 6 K-IV apo(a) isoform, demonstrated that oleate supplementation increased the apparent protection of apo(a) from protease digestion, suggesting that alterations in the translocation efficiency of apo(a) may accompany the addition of oleate. Cells incubated with brefeldin A demonstrated increased recovery of the precursor form of apo(a) with oleate supplementation, suggesting that alterations in post-translational degradation may also contribute to the observed increase in apo(a) secretion following oleate addition. To further characterize the oleate-dependent increase in apo(a) secretion, cells were incubated with an inhibitor of the microsomal triglyceride transfer protein. These experiments demonstrated a dose-dependent decrease in apo(a) secretion from both cell lines. Furthermore, addition of either the microsomal triglyceride transfer protein inhibitor or triacsin C, an inhibitor of acyl-CoA synthase, completely abrogated the oleate-dependent increase in apo(a) secretion. Taken together, these data provide evidence that apo(a) secretion from hepatoma cells may be linked to elements of cellular triglyceride assembly and secretion.

Apolipoproteins↗