Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the effect of stress on lymphocyte proliferation, SD rats were restrained with four limbs tied on a frame in supine position at room temperature (20 degrees C) for 20 h, and control animals were not disturbed in home cage. The blood was then collected from the heart under light ether anesthesia. The peripheral blood lymphocytes were separated from heparinized whole blood by density gradient (d 1.077) centrifugation, or the serum was obtained after the blood coagulated at 4 degrees C for about 6h. It was found that the blood lymphocyte proliferation induced by Con A was significantly inhibited in the stressed group as compared with the control (P less than 0.01, n = 8, ANOVA). The result was in accordance with our earlier study in which the animals were stressed with electric shock. In the present study, it was also found that the serum of the stressed animals was capable of suppressing Con A-induced lymphocyte proliferation of normal mice (P less than 0.01, n = 8, ANOVA) to a significant extent. Thus the present experiment suggests that there is some substance with suppressive activity on lymphocyte proliferation in the serum of the stressed rats. The serum lost its suppressive activity when it was heated to 100 degrees C (3 min), treated with 60% methanol or incubated with trypsin (64 micrograms/ml), thus suggesting that the suppressive factor(s) most likely is a kind of protein.
 ...
PMID:[A study on serum suppressive factor(s) on lymphocyte proliferation in rats under restraint stress]. 203 67

High-density lipoprotein (HDL) may inhibit the binding and cellular uptake of low-density lipoprotein (LDL) as one means of regulating the delivery of exogenous cholesterol to nonhepatic tissues. This may play an important role in atherogenesis, by altering lipid metabolism in cells of the arterial wall. To verify and better characterize this effect, endothelial cells were harvested from bovine aorta and maintained in tissue culture. Following initial preincubation in lipid-deficient culture media, these cells were incubated for 2 hr at 4 degrees C in media containing 125I-LDL (10 micrograms protein/ml) and varying concentrations of either HDL (0-400 micrograms protein/ml) or comparable amounts of Apoprotein A (Apo A), the major protein component of HDL. Intracellular and trypsin-released counts were assayed separately, as a measurement of cellular uptake and membrane bound LDL, respectively. Results of this study indicated an inhibition of LDL binding and uptake by HDL (P less than 0.005, ANOVA). A similar inhibition was found with Apo A alone (P less than 0.005). When identical studies were performed using 125I-Apoprotein B, the protein component of LDL, and Apo A, the latter was found to inhibit the binding of Apo B to the same extent (P less than 0.0006). These results indicate that HDL does inhibit LDL binding and uptake by bovine aortic endothelial cells and that, because this effect is seen equally with only the protein component of these lipoprotein particles, it is most likely due to competitive binding at the receptor level rather than to stearic hindrance or an alteration of the cell membrane.
 ...
PMID:Competitive inhibition of LDL binding and uptake by HDL in aortic endothelial cells. 239 70

After acute pancreatitis was induced, the residual pancreatic tissue contents were evaluated in two series of rats fed with diets that differed in the lipidic composition: 1--high lipid and balanced protein diet; 2--balanced diet. Total protein, nucleic acids, trypsinogen, chymotrypsinogen were quantified in the pancreatic tissue; amylase activity was measured in the pancreatic tissue and serum under the following conditions: 1--in rats fed "ad libitum" (groups CB and CL); 2--in rats submitted to a fast of 30 hs (groups JB and JL) and 3--twenty-four hours after acute pancreatitis was induced (group B and L). The results obtained were statistically compared among groups with the same kind of diets, using ANOVA and the Tukey test. Student t-test was used to compare the same parameters among similar groups with different diets (p less than 0.05). In comparison with the groups under same regimen it was verified that the pancreatic enzymes content didn't change in fasting groups, but did in PA groups. It was also found that trypsin was increased in all groups, RNA/DNA decreased and total protein increased in AP group in rats fed with hyperlipidic diet. It is concluded that high lipid intake can aggravate pancreatic injury.
 ...
PMID:[A hyperlipidic diet and acute pancreatitis: experimental study in rats]. 248 19

Early-, mid- and late-passage cultures (population doubling levels 12, 35, and 51, respectively) of IMR-90 fibroblasts were exposed to 3H-thymidine for 48 h prior to fixation in situ for morphometric analysis in order to determine quantitatively what ultrastructural changes accompany the loss of proliferative capacity during aging in vitro. Analysis of autoradiographs, both at the light and electron microscopic levels, with an image analyzer followed by ANOVA statistical scrutiny demonstrated that a significant increase in relative cell area, an indicator of cell size, was characteristic of cells unable to incorporate 3H-TdR at both mid- and late-passage, but not at early-passage levels. Nuclear size also increased significantly with progressive passage level but was not related to proliferative capacity. No significant difference in the area fraction of nucleoli per unit area of nucleus or of mitochondria, Golgi, or lysosomes was seen in either subpopulation at any passage level. Dilated cisternae of rough endoplasmic reticulum in early-passage cells were seen if cells were harvested with trypsin and fixed either before or after centrifugation, but were not seen in labeled or unlabeled cells from any passage level when cultures were fixed in situ. We conclude that a significant increase in cell size is the only significant morphological change associated with the loss of proliferative capacity of IRM-90 fibroblasts. Furthermore, our data indicate that there is no accumulation of secondary lysosomes in human diploid fibroblasts during aging in vitro; we therefore cannot support any hypothesis of aging or proliferative decline that is based mechanistically upon this phenomenon.
 ...
PMID:Quantitative morphological analysis of proliferating and nonproliferating subpopulations of IMR-90 fibroblasts during aging in vitro. 712 56

The uptake and degradation of the alpha 2 macroglobulin-trypsin (alpha 2 m-trypsin) complex have been studied using isolated liver cells but not in the liver as a whole. We report the clearance of the complex by the isolated and exsanguinated liver of Wistar male rats, weighing 150- 280 g, and compare it with that of the free enzyme. The hepatic clearance of the alpha 2m-trypsin complex follows a pattern with a distribution phase followed by an elimination phase, which contrasts with that of trypsin where only the distribution phase is observed. The extraction of trypsin from the perfusate is Ca(2+)-independent (156 +/- 14 pmol/g liver in the presence of 2.5 mM Ca2+, N = 9, versus 140 +/- 8 pmol/g liver in its absence, N = 7) and is not affected by 100 mM NH4Cl (152 +/- 7 pmol/g liver, N = 6), 100 U/ml heparin (164 +/- 14 pmol/g liver, N = 5), 30 microliters/ml carbon particle suspension (150 +/- 13 pmol/g liver, N = 7) or an acute-phase situation induced by turpentine (125 +/- 10 pmol/g liver, N = 6) (P > 0.05, ANOVA). The hepatic clearance of the alpha 2m-trypsin complex is Ca(2+)-dependent (1.8 +/- 0.2 ml/min in the presence of Ca2+, N = 8, versus 0.6 +/- 0.03 ml/min in its absence, N = 4), affected by NH4Cl (< 0.1 ml/min, N = 7), heparin (1.1 +/- 0.2 ml/min, N = 6) and the acute-phase (0.6 +/- 0.1 ml/min, N = 6) but not by the carbon particle suspension (1.8 +/- 0.2 ml/min, N = 7). These results show that trypsin is not internalized by hepatocytes (no NH4Cl effect) or Kupffer cells (no carbon particle effect) and that the alpha 2m-trypsin complex is internalized in a Ca(2+)-dependent process by hepatocytes, but not by Kupffer cells, and is affected by an acute-phase reaction.
 ...
PMID:Clearance of the alpha 2 macroglobulin-trypsin complex and uptake of trypsin by perfused liver. 907 Mar 93

Psoriatic plaque contains an increased number of mast cells that are thought to play an important role in the initiation and maintenance of the disease through the release of mediators such as histamine, proteoglycans, proteinases and cytokines. To verify the possible participation of these cells in the chronic inflammatory cutaneous response in psoriasis, we performed a double-blind controlled study to investigate the presence and activation of tryptase-positive mast cells in the lesional skin of 19 patients affected by active psoriasis vulgaris minima compared with five healthy, age-matched subjects. Psoriatic patients were randomized into two groups (A and B). The first group was treated with cetirizine (10 mg/three times a day for 15 days) and the second one was treated with placebo. Both groups underwent clinical staging [psoriasis area and severity index (PASI) score] and immunohistochemical evaluation [alkaline phosphatase antialkaline phosphatase (APAAP) procedure] before and after treatment. In group A, the PASI score ranged from 3.8 (SE +/- 1.00) to 1.8 (SE +/- 0.68) and in group B, from 5.0 (SE +/- 0.98) to 3.4 (SE +/- 0.47). The mean number of tryptase-positive mast cells for field, mainly distributed in the perivascular and periadnexal sites, ranged from 40.8 (SE +/- 7.15) to 21.6 (SE +/- 3.04) in group A and from 25.1 (SE +/- 3.78) to 26.3 (SE +/- 3.59) in group B (ANOVA test f = 6.95; gl = 1.16; p = 0.02). In our psoriatic patients, cetirizine significantly reduced the expression of tryptase-positive mast cells and produced a clinical improvement in erythema, suggesting a multilevel immunopharmacologic modulation of this antihistamine in psoriasis.
 ...
PMID:Cetirizine reduces the number of tryptase-positive mast cells in psoriatic patients: a double-blind controlled study. 1151 56

In order to clarify the potential physiological function of royal jelly (RJ), we report here the gastrointestinal enzyme production of antihypertensive peptides from RJ. Intact RJ and its protein fraction did not retard the action of angiotensin I-converting enzyme (ACE) activity at all. However, development of ACE inhibition power of RJ was newly observed by pepsin hydrolysis (IC(50)=0.358 mg protein/mL), and the subsequent trypsin and chymotrypsin hydrolyses (IC(50)=0.099 mg protein/mL). Single oral administration of this gastrointestinal RJ hydrolysate (1 g/kg dose) in 10-week spontaneously hypertensive rat resulted in a significant reduction of systolic blood pressure of 22.7 plus minus 3.6 mmHg at 2 hr (P<0.05 vs. 0 hr by one-way ANOVA, n=7). Then, the RJ hydrolysate was fractionated with gel permeation chromatography to obtain the di- and tri-peptides (DTP) fraction. As a result of isolation from the DTP fraction by reversed phase-high performance liquid chromatography, eleven ACE inhibitory peptides were isolated from the DTP-RJ hydrolysate. Some of the ACE inhibitors were derived from the RJ-glycoprotein; eight peptides with the IC(50) value of <10 &mgr;M were identified from natural resources for the first time. Consequently, RJ protein was thought to be a good resource of ACE inhibitory peptides produced by the gastrointestinal enzyme hydrolyses.
 ...
PMID:Gastrointestinal enzyme production of bioactive peptides from royal jelly protein and their antihypertensive ability in SHR. 1183 23

The monoclonal theory of atherosclerosis postulates that a subpopulation of vascular smooth muscle cells (VSMCs) is selectively expanded in response to pathologic stimuli and accumulates in vascular intima. The purpose of this research was to clone VSMC, determine growth rates of the clones and their ability to release the mitogenic cytokine tumor necrosis factor-alpha (TNF-alpha). With approval of the institutional animal care and use committee, VSMCs were isolated and cultured from the thoracic aortas of three rats. To confirm that the cells in primary culture were of smooth muscle origin, they were immunostained with anti-alpha-smooth muscle-actin antibodies. Single cell-derived individual colonies with uniform appearance were surrounded by cloning rings, released with trypsin, and expanded. Growth rates of the clones were assessed by the mitochondrial dependent reduction of methyltetrazolium (MTT) to formazan after 24-hour stimulation with 10 per cent serum. Additionally, cloned cells were stimulated with 0.1, 1, 10, and 20 microg/mL lipopolysaccharide (LPS) for 24 hours, and TNF-alpha was determined in the culture medium. Data were analyzed by ANOVA. Two clones were isolated that could be divided into categories based on distinctly different morphology: 1) spindle-shaped (SP) or 2) epithelioid-shaped (EP) VSMCs. The SP clone had a growth rate that was 25 per cent higher than the EP clone (P < 0.05). Also, the SP clone had significantly higher release of TNF-alpha in response to LPS. For instance, TNF-alpha released in response to 0.1 microg/mL of LPS in the SP clone was 157 +/- 45 pg/mL versus 21 +/- 8.5 pg/mL in the EP clone (P < 0.05). Primary cultures of rat VSMCs are heterogeneous and consist of at least two morphologically distinct cell types. These clones are different in growth rate and cytokine production. It is possible that selective expansion of one of these clones contributes to formation of stenotic vascular lesions.
 ...
PMID:Two distinct phenotypes of rat vascular smooth muscle cells: growth rate and Production of tumor necrosis factor-alpha. 1608 16

Pericryptal fibroblasts (PFs), a class of myofibroblasts, have strongly been implicated in the regulation of villous structure because of their location close to crypts and their ability to secrete cytokines affecting intestinal epithelial cell proliferation and differentiation. Recently, mast cells (MCs) have also been involved in the homeostasis of villous architecture. As myofibroblasts arise in a wide variety of settings concurrently with a local increase in the number of tissue MCs, we calculated in this study the density of both PF and distinct pericryptal MC phenotypes in the mucosa of human duodenum showing normal, defective, or atrophic villous profiles. In addition, we evaluated the statistical association between PF-MC densities and each pattern of villous architecture. Finally, we correlated the density of PF with the density of pericryptal MC phenotypes. For this purpose, samples taken by endoscopy from 30 patients complaining of inflammatory bowel disorders were studied by immunohistochemistry. The densities of alpha-smooth muscle actin-positive PFs as well as tryptase-, chymase-, and c-kit-positive MCs were determined in the crypt lamina propria. Villous architecture was found to be significantly associated with the number of PFs and tryptase-, chymase-, c-kit-positive MCs in the lamina propria (ANOVA group effect P < 0.001). High density of both PFs and MCs was found in intestinal samples with normal villous morphology while lower densities were associated with defective or atrophic villous profiles (Tukey's test for multiple comparison P < 0.001). In addition, a significant correlation was found between PF density and the density of each pericryptal MC phenotype (vs. tryptase-positive MCs, r = 0.913; vs. chymase-positive MC, r = 0.905; vs. c-kit-positive MC, r = 0.927; P < 0.001 in all cases). This study provides morphological support for an important cooperation between PFs and MCs in maintaining normal villous architecture.
 ...
PMID:Number of pericryptal fibroblasts correlates with density of distinct mast cell phenotypes in the crypt lamina propria of human duodenum: implications for the homeostasis of villous architecture. 1665 53

The structural integrity of fibrillar type I collagen is critical for effective dentin bonding. Since most noncollagenous matrix components in dentin are closely associated with collagen, we hypothesized that they may also contribute to dentin bonding. To test this hypothesis, bovine dentin was acid-etched, treated with chondroitinase ABC (C-ABC), endo-beta-galactosidase (Endo-beta), or trypsin. Controls were prepared in the same manner but without the enzymes. All control and experimental specimens were then bonded with One-Step. Bond strength data were analyzed by one-way ANOVA and Fisher's PLSD test (p < 0.05). When dentin was treated with C-ABC or trypsin, bond strengths significantly decreased for the rewetted groups (p < 0.05). The treatment with Endo-beta showed no effects on bond strengths (p > 0.05). When the treated dentin surfaces were observed under SEM, the C-ABC and trypsin treated groups revealed significant loss of collagen fibril architecture. The results indicate that chondroitin sulfate glycosaminoglycans and trypsin-digestible noncollagenous proteins play roles in maintaining the open dimensions of the collagen fibril scaffold, which is essential for optimal dentin bonding.
 ...
PMID:Removal of noncollagenous components affects dentin bonding. 1668 Jun 89


1 2 Next >>