Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effect of disruption to the epithelium of intact porcine bronchi was examined by comparing the responsiveness to agonists applied to the adventitial and luminal surfaces. The development of smooth muscle tone was measured as an increase in pressure in an isovolumic bronchial segment of approximately 2 mm i.d. The reactivity and sensitivity to acetylcholine (ACh) introduced intraluminally was greatly attenuated when compared with adventitial addition. 2. Luminal exposure to K+ and vanadate (VO3-) had little effect compared with strong responses obtained by adventitial application. 3. Intraluminal exposure to trypsin, chymotrypsin and elastase (1 mg/mL) selectively augmented both the sensitivity and the reactivity to the luminal addition of ACh, K+ and carbachol. 4. Mechanical removal of the epithelium produced a 716-fold increase in sensitivity to ACh introduced luminally but had no effect on ACh applied adventitially. 5. The inhibitory effects of luminally introduced isoprenaline on electrical field stimulation responses were also significantly potentiated in segments stripped of epithelium. 6. The evidence presented here indicates that the responsiveness of in vitro airways segments is highly influenced by the epithelial layer, which acts most prominently as a barrier inhibiting the penetration of luminally introduced agonists.
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PMID:Epithelial disruption by proteases augments the responsiveness of porcine bronchial segments. 147 93

The intestinal sucrase-isomaltase precursor is cleaved at the brush border membrane by luminal proteases. Whether the lactase precursor also is cleaved by luminal proteases is uncertain. Lactase synthesis and processing was studied in 0- and 15-day-old rats after IP administration of [35S]methionine, and changes in precociously cortisone-induced sucrase-isomaltase were used as an internal control. Mucosal lactase and sucrase-isomaltase were separately immunoprecipitated and analyzed by autoradiography after electrophoresis. In both 0- and 15-day-old rats, mucosal lactase appeared as a 200K lactase precursor band at 30 minutes and as 200K and 225K lactase precursor bands at 60 minutes and was cleaved to form a 130K lactase band 120-240 minutes after labeling; sucrase-isomaltase similarly appeared as 210K and 220K bands at 30-60 minutes and was cleaved to form 140K I and 120K S subunits by 240 minutes in day 15 rats. To determine the role of luminal proteases, intestinal segments were isolated in situ and the luminal contents were flushed 30 minutes after labeling. Unflushed segments were used as controls. Only lactase precursor and sucrase-isomaltase precursor were present 240 minutes after labeling in flushed intestinal segments, but lactase precursor and sucrase-isomaltase precursor were cleaved in unflushed segments. Addition of trypsin or elastase into the lumen of flushed segments resulted in partial cleavage of lactase precursor but not of sucrase-isomaltase precursor. Luminal contents collected from the small intestine of day 15 rats 120 and 240 minutes after labeling showed 35S-labeled 130K and 80K polypeptides in lactase immunoprecipitates. It is concluded that intestinal lactase is synthesized as lactase precursor and transported to brush border membrane and cleaved by luminal proteases, and the amino end polypeptide cleaved from lactase precursor is released into the lumen.
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PMID:Posttranslational cleavage of rat intestinal lactase occurs at the luminal side of the brush border membrane. 190 27

Immunohistochemical demonstration of alpha-amylase has been made in sialoadenitis-involved tissue and salivary gland tumors, as well as in normal salivary glands. Immunoreactive alpha-amylase with trypsin pretreatment was confined to irregularly staining serous acinar cells in the parotid and submandibular glands, and to demilunes in sublingual glands. In obstructive adenitis, staining was irregular from high to negative in acini in early or intermediate stages. Dilated ductal segments contained cells positive for alpha-amylase in the early stage following obstruction. Pleomorphic adenomas were usually negative for alpha-amylase but in rare cases tumor epithelia stained variably positive; i.e., staining occurred throughout the cytoplasm or at the periphery or apical part of the tumor cells. Luminal cavities of tubular and duct-like structures contained alpha-amylase-positive material. Epithelia in Warthin's tumor were also negative in general; however, scattered single or grouped tumor cells containing alpha-amylase were found. Mucoepidermoid tumors were also negative, though slightly positive cells were found intermingled among the negative squamous and mucous tumor cells. Cystic lesions in mucoepidermoid tumor were sometimes positive in the wall cells together with material secreted into the lumen.
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PMID:Immunohistochemical localization of amylase in sialoadenitis and salivary gland tumors. 243 8

Mucosal enterokinase activity was established at intervals throughout the small intestine in guinea-pigs; maximum activity was present in the duodenum and proximal jejunum in new born as well as adult animals. Transposition of 5 cm lengths of small gut from the high enterokinase containing proximal region to the distal intestine and vice versa showed that mucosal enterokinase activity in the transposed segments was little changed after several weeks of healthy life. Isolation of proximal jejunal loops from luminal continuity resulted in the fall of mucosal enterokinase activity to minimal levels within 16 hours. Low levels of mucosal enterokinase activity were identified in loops of both proximal and distal jejunum 12 weeks after isolation. Luminal perfusion studies in vivo in proximal jejunal loops 24 hours after isolation showed that mucosal enterokinase activity could be restored to near normal levels within four to six hours by luminal sodium in the presence of active pancreatic endopeptidases, oligopeptides, L-amino acids, or D-glucose but not D-amino acids or D-fructose. Near normal mucosal enterokinase activity persisted in the loops for as long as luminal perfusion with 144 mM sodium and L-lysine or trypsin was maintained (24 hours). The time course of the restoration of mucosal enterokinase activity was compatible with an initial precursor activation as well as biosynthesis. The requirement for luminal sodium appeared to be absolute regardless of the co-substrate and supports the conclusion that mucosal enterokinase activity is dependent on mediated sodium transport. The ability of proximal intestinal enterocytes to respond to sodium flux with an increase in enterokinase activity is a property determined in intrauterine life: distal intestinal enterocytes may have functioning structural genes for enterokinase but appear to be unable to respond.
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PMID:Induction and maintenance of mucosal enterokinase activity in proximal small intestine by a genetically determined response to mediated sodium transport. 702 75

Luminal proteolytic activity (PA) of different colonic segments was ascertained in animals subjected to pancreatic duct ligation (PDL) and in control rats. The PDL rats revealed a significant PA reduction in the cecum, proximal colon (P < 0.01), and distal colon (P < 0.005). Proteolytic activity, trypsin, and chymotrypsin activity in control rats diminished progressively from the cecum to the distal colon. Conversely in PDL rats, we found maximal PA in distal colon. The conclusion is drawn that a significant proportion of colonic proteolytic activity can be attributed to pancreatic proteases with a maximal contribution at cecum level.
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PMID:Colonic proteolysis following pancreatic duct ligation in the rat. 780 12

In conscious rats, bile inhibits pancreatic secretion. The role of luminal taurocholate (TC), a major component of rat bile, in the regulation of pancreatic secretion was studied in conscious rats with external bile and pancreatic fistulae. On the fourth postoperative day, after the basal collection of bile and pancreatic juice (PJ) returned to the duodenum, graded doses of TC (0, 0.4, 4, 40 mM) containing 10 mM CaCl2 were infused into the duodenum instead of bile and PJ for 2 hr (1 ml/hr), with or without 1 mg/ml of porcine trypsin. Luminal trypsin activities were not affected by any dose of TC. The increases in pancreatic secretion in response to diversion of bile and PJ were progressively inhibited with increasing doses of infused TC from 0 mM to 4 mM both with and without trypsin infusion. The effects with 4 and 40 mM TC were not significantly different. Changes in plasma cholecystokinin concentrations roughly correlated with changes in protein output in rats without trypsin infusion. We concluded that TC directly inhibited pancreatic secretion independent of the luminal trypsin activity and that its inhibitory action was concentration dependent.
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PMID:Direct, concentration-dependent inhibition by taurocholate of pancreatic exocrine secretion and CCK release in conscious rats. 802 68

Oral pancreatic enzyme supplements, including those protected from gastric acidity by enteric coating, often achieve only partial correction of pancreatic steatorrhoea. To characterise the mechanisms involved in vivo, eight patients with steatorrhoea due to advanced pancreatic insufficiency and nine healthy controls were studied. Two sets of studies (small bowel intubation and five day faecal fat quantification) were randomly performed while patients were either on enteric coated pancreatin or equivalent placebo. A 260 cm long multilumen tube was used for double marker perfusion of two 20 cm segments located in the duodenum and in the ileum respectively. Luminal pH, flow, and trypsin and lipase activity outputs were measured at each segment for four hours postcibally. Placebo treated patients with pancreatic steatorrhoea had low enzyme outputs in the duodenal test segment and even lower outputs in the ileal segment. Pancreatin treatment significantly decreased steatorrhoea (p < 0.05) and increased luminal enzyme outputs (p < 0.05). The increase was much greater in the ileal than in the duodenal segment. Thus enteric coated pancreatin treatment abolished the normal gradient between postcibal duodenal and ileal lipase output. The results suggest that enteric coated pancreatin nearly corrects severe pancreatic steatorrhoea. The ingested lipase was utilised inefficiently, however, as luminal enzyme activity in the ileum was enhanced to a greater extent than in the duodenum, and consequently the absorptive potential of the small bowel was only partially utilised.
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PMID:Fate of oral enzymes in pancreatic insufficiency. 850 76

Incorporated in the luminal glycocalyx of vascular endothelia (EC) are negatively charged microdomains (anionic sites). These sites are considered functionally important (a) in their interaction with circulating blood constituents, and (b) as a determinant of vascular permeability. The molecular composition of these EC sites, described for a number of tissues, has demonstrated a heterogeneity dependent on their anatomical location. Luminal anionic sites have not been characterized for EC of optic nerve. Optic nerves were removed from Sprague-Dawley rats previously fixed by vascular perfusion. EC anionic sites were labelled with the probes cationic colloidal gold (CCG) and cationic ferritin (CF), using the pre- and post-embedding techniques, and examined by electron microscopy. The effects of enzyme digestion of ultrathin sections on subsequent CCG labelling were determined using a battery of enzymes in association with the post-embedding technique. CCG labelling was quantified following each enzyme treatment using image analysis software. The biotinylated lectin wheat germ agglutinin (WGA) with streptavidin gold was also used to localize specific monosaccharide residues. The luminal front of intraneural EC showed a uniform labelling with CCG and CF which was greater than on the abluminal surface. Extracellular matrix components and basal laminae were moderately labelled. Digestion of tissue sections with heparitinase and trypsin had no significant effect on subsequent CCG labelling. Proteinase K was less effective than papain but both produced a significant reduction. Neuraminidase almost completely eliminated labelling. CCG binding to the luminal plasma membrane of optic nerve EC can be significantly reduced with proteolytic and glycolytic enzymes. The results demonstrate that sialoglycoproteins principally constitute these luminal EC anionic sites. Biotinylated WGA-streptavidin gold, which detects both N-acetylneuraminic (sialic) acid and N-acetylglucosamine, gave a similar pattern of labelling to CCG alone on the luminal versus abluminal EC fronts. These findings suggest that WGA is binding predominantly to N-acetylneuraminic acid residues since CCG would not label the neutral (uncharged) N-acetylglucosamine.
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PMID:Optic nerve microvessels: a partial molecular definition of cell surface anionic sites. 854 80

Luminal bile-pancreatic juice (BPJ) is involved in the induction of pancreatic proteases in rats fed a high-protein diet. Recently, we have demonstrated that a BPJ-independent mechanism is responsible for enhancement of pancreatic secretion after feeding of a dietary protein in chronic BPJ-diverted rats. The aim of the present study was to explore the existence of a BPJ-independent mechanism during adaptation of the exocrine pancreas to dietary protein. Rats, whose BPJ was diverted into the ileum through a common bile-pancreatic duct catheter for 5 days (PBD rat), were fed a fat-free diet containing 25% or 60% casein for 3 days. Messenger RNA levels for pancreatic enzymes, cholecystokinin, and secretin in the jejunal mucosa were evaluated by northern blotting method. Pancreatic trypsin and chymotrypsin activities and mRNA levels of their zymogens were higher in PBD rats than in rats whose diverted BPJ was returned into the duodenum (PBD returned rat). In the PBD groups, pancreatic protease activities were further increased by 3-day feeding of a high-protein diet without changes in mRNA levels of these proteases. Cholecystokinin mRNA was increased after feeding of a high-protein diet in the PBD rats. These results indicate that pancreatic proteases are induced by feeding a high-protein diet by a mechanism independent of luminal BPJ, which is associated with an increase in intestinal cholecystokinin mRNA level.
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PMID:Bile-pancreatic juice-independent increases in pancreatic proteases and intestinal cholecystokinin by dietary protein in rats. 945 41

Recently, we isolated a trypsin-sensitive cholecystokinin-releasing peptide (CCK-RP) from porcine and rat intestinal mucosa. The amino acid sequence of this peptide was determined to be identical to that of the diazepam-binding inhibitor (DBI). To test the role of DBI in pancreatic secretion and responses to feeding, we used pancreaticobiliary and intestinal cannula to divert bile-pancreatic juice from anesthetized rats. Within 2 hours, this treatment caused a 2-fold increase in pancreatic protein output and a >10-fold increase in plasma CCK. Luminal DBI levels increased 4-fold. At 5 hours after diversion of bile-pancreatic juice, each of these measures returned to basal levels. Intraduodenal infusion of peptone evoked a 5-fold increase in the concentration of luminal DBI. In separate studies, we demonstrated that intraduodenal administration of antiserum to a DBI peptide specifically abolished pancreatic secretion and the increase in plasma CCK levels after diversion of bile-pancreatic juice. To demonstrate that DBI mediates the postprandial rise in plasma CCK levels, we showed that intraduodenal administration of 5% peptone induced dramatic increases in pancreatic secretion and plasma CCK, effects that could be blocked by intraduodenal administration of anti-DBI antiserum. Hence, DBI, a trypsin-sensitive CCK-RP secreted from the proximal small bowel, mediates the feedback regulation of pancreatic secretion and the postprandial release of CCK.
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PMID:Diazepam-binding inhibitor mediates feedback regulation of pancreatic secretion and postprandial release of cholecystokinin. 1067 61


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