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:3.4.24.3 (collagenase)
18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mesangial cells serve many functions in the glomerulus, including regulation of glomerular ultrafiltration coefficient, matrix production, and eicosanoid generation. The glomerulus is a vascular bed, and the mesangial cell is continually exposed to rhythmic alterations in intraglomerular pressure. Since increased intraglomerular pressure has been implicated as a potential causative agent in the ultimate development of nephrosclerosis, we sought to determine the effect of continuous stretch-relaxation upon parameters of mesangial cell growth and function. Early passage (2-4) cultured rat mesangial cells were plated onto either rigid-bottom or flexible-bottom culture plates coated with type I collagen. After cell attachment, the cells on flexible supports were exposed to continuous stretch-relaxation for 72 to 96 hours at a rate of 100 cycles/minutes at an applied pressure of 7 to 8 KPa (53 to 61 mm Hg). Cellular morphology was altered by continuous stretch-relaxation, with the majority of mesangial cells presenting stellate or straplike morphology. Fluorescein isothiocyanate-labeled phalloidin staining indicated an increase in density of actin filaments running the long axis of the cell. Stretch-relaxation resulted in an approximately 50% increase in cell number. Prostaglandin production, assessed as irPGE2 production, was increased by stretching in mesangial cells from 28 +/- 1 to 49 +/- 4 pg/10(6) cells (N = 12; p less than 0.005). Mechanical stretch/relaxation increased the percentage of protein representing collagenous proteins from 47 +/- 6% to 70 +/- 4%, as assessed by collagenase susceptibility (p less than 0.025). Analysis of pepsin-resistant proteins synthesized indicated that stretch/relaxation resulted in increases in the relative amounts of types I and III collagens produced/cell. Additionally, stretch/relaxation selectively increased the relative amount of type I-homotrimers produced. Thus, when mesangial cells are exposed to cyclic stretch/relaxation, they exhibit significant alterations in morphology, growth, prostaglandin and collagen production.
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PMID:Continuous stretch-relaxation in culture alters rat mesangial cell morphology, growth characteristics, and metabolic activity. 157 48

Ursodeoxycholate (UDC) and tauroursodeoxycholate (TUDC) have been reported to be protective against liver injury induced by other bile salts. UDC also has been shown to be effective against refluxed bile-induced gastritis after gastric surgery. However the mechanism of the therapeutic effect of UDC on gastric mucosa has not been known. In the present study, cytoprotective actions of UDC and TUDC against chenodeoxycholate (CDC)-induced gastric injury were investigated using rabbit gastric cell cultures without systemic factors. Rabbit gastric mucosal cells were cultured after the isolation of rabbit gastric cells with collagenase and ethylenediaminetetraacetic acid. Cytotoxicity was quantified by measuring 51Cr release from prelabeled cells and MTT assay. Prostaglandin (PG) E2 was assayed by radioimmunoassay. Concentrations of CDC greater than 0.5 mM or UDC greater than 5 mM caused cellular damage and increased 51Cr release in a dose-dependent and time-dependent fashion, while TUDC up to 10 mM did not. TUDC, but not UDC, showed a significant decrease of CDC (1.5 mM)-induced 51Cr release dose dependently. The protective effect of TUDC against CDC-induced damage was confirmed by MTT assay. On phase-contrast microscopy, disruption of monolayers induced by CDC (1.5 mM) was clearly protected by TUDC (10 mM). Free radical scavengers (500 units/ml of superoxide dismutase, 300 units/ml of catalase, and 100 mM of dimethyl sulfoxide) or a calcium blocker (10(-7)-10(-5) M verapamil) did not show significant protection against CDC-induced damage. Deprivation of Ca2+ in the media did not affect CDC-induced damage. Thus free radicals or Ca2+ might not be involved in the cell toxicity of CDC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of tauroursodeoxycholate against chenodeoxycholate-induced damage to cultured rabbit gastric cells. 200 57

The role of enzymatic collagen degradation in prostaglandin-induced and physiological cervical ripening was studied in guinea pigs. The cervices were removed from (a) 8 non-pregnant guinea pigs, (b) 8 animals at day 45 of pregnancy, (c) 14 pregnant animals of comparable gestational age which had either an intracervical application of 0.2 ml 5% tylose or 10 micrograms sulprostone gel, and (d) 8 guinea pigs at day 63 to 65 of pregnancy. Collagenase activity was assayed in a highly specific and sensitive system using native collagen type I as substrate. Protease activity was measured by the method of Green and Shaw. Collagen fragments were identified by SDS-polyacrylamide electrophoresis (SDS-PAGE) of acetic-soluble fractions. Collagenase and protease activities were found in all extracts from the different groups. However, there were no differences in enzymatic activities between the non-pregnant, early-pregnant and late-pregnant cervical specimens. Prostaglandin pre-treatment of the cervix led to no significant increase in either collagenase or protease activity as compared to the control groups. The absence of typical collagen degradation products in the SDS-PAGE suggested that no significant collagen breakdown had taken place. In contrast to previously published literature, we conclude that enzymatic collagen degradation is unlikely to be a key factor in prostaglandin-induced and physiological cervical ripening.
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PMID:Enzymatic collagen degradation in the pregnant guinea pig cervix during physiological maturation of the cervix and after local application of prostaglandins. 255 49

Prostaglandin (PG) inhibits the hydroosmotic effect of vasopressin. We therefore reexamined the interaction of vasopressin (VP), cAMP, and prostaglandins in toad bladder epithelial cells. Vasopressin slightly, but reproducibly, stimulated PGE2 and thromboxane B2 (TXB2) synthesis in cells prepared by the use of collagenase. When cells were prepared in the presence of a readily reversible cyclooxygenase inhibitor, ibuprofen, subsequent PGE2 synthesis was enhanced sevenfold but that of TXB2 was not. Increasing cAMP by either phosphodiesterase inhibition or 8-bromo-cAMP significantly inhibited both basal and VP-stimulated PGE2 synthesis. This inhibition was overcome by addition of arachidonic acid. Future studies employing these agents will have to consider these effects. VP enhanced 32P labeling of phosphatidylinositol (PI) and phosphatidic acid. This effect was prevented by the phosphodiesterase inhibitor, which also decreased phosphatidylcholine labeling. The results indicate that the phosphodiesterase inhibitor for cAMP may decrease PG formation by interfering with phospholipase activation. Furthermore, VP, similar to its effect in the liver, also increases PI turnover in toad bladder. This may initiate PG synthesis and provide a link among VP, cAMP, and calcium. A double-reciprocal feedback is proposed, whereby VP stimulates PG synthesis in a cAMP-independent manner and also inhibits PG synthesis in a cAMP-dependent manner.
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PMID:Interactions of vasopressin, cAMP, and prostaglandins in toad urinary bladder. 257 84

Rat renal medullary tubular cells, prepared by collagenase dispersion and hypotonic lysis, were introduced in Teflon chambers for superfusion. Prostaglandin (PG) E2 and cyclic adenosine 5'-monophosphate (cAMP) production was measured in the effluent. Arginine vasopressin (AVP) but not 1-deamino-8-D-arginine vasopressin (dDAVP) (10(-10)-10(-6) M), induced a dose-dependent increase in PGE2 synthesis, whereas AVP and dDAVP produced a similar dose-dependent increase in cAMP synthesis. The Ca2+ ionophore A23187 (10(-6) M) stimulated PGE2 synthesis but not cAMP production. In contrast, forskolin (10(-5) M) stimulated cAMP synthesis without affecting PGE2 generation. The pressor antagonists dEt2AVP and d(CH2)5Tyr(Me)AVP (10(-5) M) completely inhibited the PGE2 response to 10(-8) M AVP, whereas d(CH2)5-D-LeuVAVP (10(-6) M), a mixed pressor-antidiuretic antagonist, inhibited incompletely. dEt2AVP did not significantly affect cAMP synthesis in response to 10(-8) M AVP, whereas d(CH2)5-D-LeuVAVP, and unexpectedly also d(CH2)5Tyr(Me)AVP, were inhibitory. dPTyr(Me)AVP (10(-7) M), a pressor antagonist, had an unexpectedly high cAMP-stimulating capacity. In Ca2+-free media containing EGTA, the PGE2 response to AVP and A23187 was inhibited. Nifedipine (10(-6) M) did not significantly inhibit the AVP-stimulated PGE2 production. Thus AVP-stimulated PGE2 synthesis is linked to a V1-receptor in renal medullary tubular cells and occurs independently to the activation of adenylate cyclase through a V2-receptor.
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PMID:Prostaglandin E2 and cyclic AMP response to vasopressin in renal medullary tubular cells. 301 60

Corpora lutea from cyclic ewes were dissociated by collagenase and trypsin/EGTA treatments, and enriched fractions of small and large luteal cells were prepared on gradients of Ficoll. These fractions were incubated separately or remixed before incubation. Colchicine, cytochalasin B and the calcium channel-blocker verapamil significantly reduced progesterone production by both small and large luteal cell fractions, while isoprenaline stimulated an increase in progesterone production by large luteal cell fractions only. When fractions of small and large luteal cells were remixed, no more and no less progesterone was produced than would have been predicted from equivalent fractions incubated separately. There was therefore no evidence of synergism between small and large luteal cells in the production of progesterone. Prostaglandin F-2 alpha, which can inhibit LH-stimulated progesterone production by ovine luteal tissue in vitro, had no effect on LH-stimulated progesterone production by small luteal cell fractions, but significantly inhibited that by enriched fractions of large luteal cells. Since large luteal cell fractions were contaminated with small luteal cells, which are probably responsible for the progesterone-secretory response of these fractions to LH, it was concluded that the inhibition of LH-stimulated progesterone production by small luteal cells is dependent on the presence of large luteal cells. Oxytocin added to large and small luteal cell fractions did not affect progesterone production by either fraction. It was therefore concluded that the inhibitory action of PGF-2 alpha on LH-stimulated progesterone production may require the interaction of large and small luteal cells, but that oxytocin is not likely to be an intermediary in this interaction.
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PMID:Do small and large luteal cells of the sheep interact in the production of progesterone? 386 69

Prostaglandin (PG) E and F output was studied in collagenase-dispersed amnion cells to determine the effect of extracellular Ca2+ upon PG synthesis. In the presence of 2.5 mM CaCl2, PGE and PGF output (picograms per 10(5) cells per 3 h) by cells obtained at term prior to labour following elective cesarean section (CS) was 183 +/- 39 and 127 +/- 23, respectively. This increased to 435 +/- 111 (p less than 0.025) and 241 +/- 49 (p = 0.056) from cells obtained after spontaneous labour and delivery at term (SL). Exclusion of CaCl2 from the medium (plus 0.1 mM EGTA) significantly reduced (p less than 0.025) PGE output in CS and SL cells (83 +/- 22 and 183 +/- 47, respectively) and PGF output in CS cells (70 +/- 17). PGE output in both CS and SL cells was unchanged when CaCl2 concentrations in the medium were decreased from 2.5 to 0.25 mM, but significantly attenuated (p less than 0.01) when extracellular CaCl2 was decreased from 0.25 to 0 mM. The voltage-sensitive Ca2+ channel blocker, D-600, decreased PGE output in the presence of (2.5 mM) CaCl2 to levels observed in the absence of CaCl2. Ionophore A23187 restored PGE output in the presence of D-600 and Ca2+. PGE output from CS amnion cells was stimulated by A23187 and elevated extracellular K+ (40 mM). In each case, exclusion of CaCl2 from the medium eliminated the response. These results suggest that PG output by human amnion is dependent, in part, upon the presence of extracellular Ca2+ and that Ca2+ may enter the cell via a potential-sensitive mechanism.
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PMID:Prostaglandin synthesis by human amnion is dependent upon extracellular calcium. 664 Apr 32

Prostaglandin (PG) has been reported to be an important protective and acid-suppressive factor in the gastric mucosa. Although the mechanisms of some antiulcer drugs are attributed to their stimulatory effects on endogenous prostaglandins, an understanding of these actions has not been established. In the present study we investigated the effects of antiulcer drugs on PGE2 using cultured gastric mucosal cells. Rabbit gastric mucosal cells were cultured after isolation with collagenase and ethylenediaminetetraacetic acid. PGE2 was measured by enzyme-linked immunoassay. Histamine H2-blockers (cimetidine, ranitidine, famotidine), omeprazole, and sucralfate did not modulate the media content of PGE2, whereas sofalcone dose- and time-dependently increased it. Sofalcone-induced increase of PGE2 was dose-dependently prevented by indomethacin. Sofalcone did not affect intracellular Ca2+ as assessed by the calcium-sensitive probe indo-1. Deprivation of Ca2+ in the media did not modulate the action of sofalcone. Sofalcone significantly suppressed 15-OH-PG dehydrogenase. These results suggest that among the various antiulcer drugs only sofalcone increases PGE2, which may be a factor in its therapeutic effect against peptic ulcer diseases.
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PMID:Antiulcer drugs and gastric prostaglandin E2: an in vitro study. 790 84

This study examined the influence of dietary essential fatty acids on the cooperativity of isolated adipocytes and stromal-vascular cells in the biosynthesis of prostaglandins. Sprague-Dawley rats were fed either a diet rich in essential fatty acids (20% corn oil) or a diet poor in essential fatty acids (20% tallow) for 4 wk. Preparations containing primarily adipose cells (adipocytes) or stromal-vascular cells (nonfat cells) were obtained from epididymal fat pads by collagenase digestion and repeatedly washed. Prostaglandin production was evaluated in basal and epinephrine-stimulated media after incubation with either adipocytes or adipocytes+nonfat cells. Prostaglandin E2 and prostacyclin production by adipocytes+nonfat cells was dose-dependent with epinephrine stimulation in cells from rats fed both diets. Both prostaglandin E2 and glycerol release in response to epinephrine (10-100 mumol/L) stimulation from adipocytes or from adipocytes+nonfat cells were significantly higher for cells from corn oil-fed rats than for cells from tallow-fed rats. Regardless of dietary treatment, epinephrine-stimulated prostaglandin E2 and prostacyclin release from adipocytes+nonfat cells was much greater than from adipocytes. These results suggest that a diet high in essential fatty acids precipitates a higher prostaglandin E2 secretion and that nonfat cells potentiate the secretion of prostaglandin E2 and prostacyclin by adipocytes regardless of diet.
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PMID:The cooperation of adipocytes and stromal cells in the secretion of prostaglandins by rat adipose tissue is not influenced by diet. 832 May 61

Although contractile interstitial cells (CIC) in the alveolar septum have been suggested to be involved in hypoxic pulmonary vasoconstriction (HPV), direct demonstration of cellular contraction under hypoxia has been lacking. To achieve this, we purified CIC from collagenase-dissociated bovine lung cells and examined the response of these cells to hypoxia. Prostaglandin (PG) F synthase served as a marker of CIC, and the isolated PGF synthase-positive cells were shown to preserve the ultrastructural features characteristic of CIC, most notably bundles of microfilaments. Isolated CIC seeded onto collagen gel disks became embedded and formed a lattice network with collagen fibrils. Exposure of these CIC-bearing gels to hypoxia (PO2 = 20-40 Torr) evoked a reversible reduction in gel volume, as assessed by measuring the surface area of the gel disks photographically. Thus CIC were shown to contract under hypoxia, providing the supportive evidence for the involvement of CIC in HPV.
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PMID:Hypoxic contraction of contractile interstitial cells isolated from bovine lung. 876 21


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