Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunofluorescent staining with anti-smooth or anti-striated muscle myosin was carried out for 30 minutes at room temperature (18-20 degrees C) on cultures of smooth muscle cells and fibroblasts from guinea-pig vas deferens, taenia coli and ureter, rabbit aorta and chicken gizzard and of cardiac muscle cells and fibroblasts from rat ventricle. With anti-smooth muscle myosin, smooth muscle cells showed an intense fluorescent staining in fine fibrils with an "interrupted" appearance running parallel to the longitudinal axis of the cell throughout the cytoplasm, and also in coarser, "non-interrupted" fibrils (termed here "attachment fibrils") concentrated at the surface of the cell adjacent to the glass coverslip. Fibroblasts in the same cultures showed similar, but much weaker, reactions. When anti-striated myosin was added to the smooth muscle cultures, staining of neither cell type was observed. In contrast, cardiac muscle cells in cultures of rat ventricle did not react anti-smooth muscle myosin, but gave bright fluorescent A-band staining with anti-striated myosin. Fibroblasts in the ventricle cultures were unreactive with anti-striated muscle myosin but gave the characteristic weak reaction with anti-smooth muscle myosin. Thus immunofluorescent stainig with anti-smooth muscle myosin is useful for distinguishing between isolated smooth muscle cells and fibroblasts in tissue culture.
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PMID:Comparison of the reaction of cultured smooth and cardiac muscle cells and fibroblasts to specific antibodies to myosin. 109 79

The sequential changes in maximum active stress, contractile proteins and collagen contents in the dilated ureter were determined in the rabbit ureters, which was partially obstructed for the intervals of 2 to 48 weeks. Maximum active stress and myosin content showed similar changes with the obstruction interval, i.e., both decreased first and then increased from week 2, and reached maximum at week 8, and after that, gradually decreased. Actin content did not show any significant changes. Collagen content showed almost the same changes as myosin content and maximum active stress by week 2. Then the collagen content increased rapidly from week 6 to week 10, and continued to increase gradually until 48 weeks after obstruction. A significant correlation was demonstrated between maximum active stress and myosin content while no significant correlation was found between maximum active stress and actin content. The maximum active stress decreased as the collagen content increased after week 8. Thus, there was a significant, negative correlation between them. Finally, the ratio of myosin content to collagen content (myosin/collagen) was related to maximum active stress. This ratio was more closely correlated with maximum active stress, indicating that myosin-collagen ratio is a good means of predicting contractility of the obstructed ureter.
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PMID:[Sequential changes in maximum active stress, contractile proteins and collagen contents in obstructed ureters]. 204 4

Crude extracts of taenia coli (guinea-pig), gizzard (chicken), stomach, colon, ureter, bladder, mesenteric vein, mesenteric artery, uterus and vas deferens (dog) were electrophoresed under conditions which do not denature myosin (pyrophosphate gels). Two isozymes (G1 and G2) were observed in all cases. Their mobilities are the same in all organs, but there are some variations in their relative proportions. They have an ATPase activity. Based on electrophoretic mobility the light chains (L20 and L17) seem to be the same for both isozymes whilst the heavy chains are different. Isozyme G2 contains one type of heavy chain of an apparent molecular mass of 230 kDa, whilst isozyme G1 contains two types of heavy chains: one of apparent molecular mass of 230 kDa, and the other of apparent molecular mass of 200 kDa.
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PMID:Detection and distribution of myosin isozymes in vertebrate smooth muscle. 299 31

Maximum active stress and contractile protein contents of the dilated ureter were determined using the chronically obstructed rabbit ureter. Active length-tension curve was demonstrated for tissue strips obtained from normal and dilated ureters. In the normal ureter, maximum active stress of the strips was 10.4 +/- 2.04 X 10(4) dyne/cm.2 while the myosin and actin contents in the tissue were 6.05 +/- 0.44 and 15.46 +/- 1.96 mg./gm. tissue, respectively. Maximum active stress of the obstructed ureter varied from 5.1 X 10(4) to 19.0 X 10(4) dyne/cm.2 The amount of contractile protein in the obstructed ureter varied from 0.57 to 8.07 mg./gm. tissue for myosin and from 8.16 to 22.9 mg./gm. tissue for actin. For various degrees of ureteral dilatation, the active stress and contractile protein content showed similar changes. A significant correlation was demonstrated between maximum active stress and contractile protein content. The myosin amount was more closely correlated with maximum active stress, indicating that the content of myosin is a means of predicting contractility of the obstructed, dilated ureter.
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PMID:Relationship between maximum active stress and contractile protein contents in the chronically obstructed ureter. 647 Dec 33

Using an SDS-polyacrylamide gel electrophoresis, the contractile protein content of the normal rabbit ureter was compared with that of the dilated ureter. The relative amounts of the actin and myosin were significantly decreased in the dilated ureter.
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PMID:The contents of contractile proteins in the normal and dilated ureter. 663 44

We have previously reported the relevance of muscle dysplasia to the nonreflux megaureter. On electron microscopy, muscle cells which are scattered in large amounts of connective tissue without any bundle formation are found to be deficient in myosin filaments, which, with actin filaments, are believed to be an essential contractile unit of smooth muscle. Investigations of these dysplastic features of the ureter were extended to various other congenital disorders of the ureter experienced in our institution from 1963 to 1981. Muscle dysplasia was found in 8 of 34 cases of nonreflux megaureter, in 1 of 22 cases of reflux megaureter, in 4 of 23 cases of ectopic ureter of single system, in 4 of 9 cases of ectopic ureter of duplex system, 0 of 4 cases of the ureter of ureterocele of single system and in 1 of 13 cases of the ureter of ureterocele of duplex system. When muscle dysplasia was extensive, involving the whole length of the dilated ureter, incidence of associated renal dysmorphism was high in that 12 of 17 ureteral units as such demonstrated either severe renal dysplasia (9) or hypoplasia (3). Similar muscle dysplasia was also found in most of the dome of ureterocele (in 5 of 6 and 12 of 13 ureteroceles of single and duplex systems respectively). Muscle dysplasia is discussed as to its genesis, relevance to various congenital ureteral disorders and clinical implications.
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PMID:Muscle dysplasia in megaureters. 669 78

Chlorpromazine (ClP) and trifluoperazine (TFP) depress electrical and mechanical activity of ureter smooth muscle cells. Contraction was depressed by less doses of the substances applied as compared with the processes responsible for generation of spike activity. ClP causes the displacement of the dose-effect curve for Ca2+ towards larger concentrations of the latter. Trifluoperazine displaces the dose-effect curve for contraction to the right and downwards. It is concluded that inhibition of contraction and depression of ClP and TFP spikes is due to the calmodulin blocking on which kinase activity of myosin light chains depends. It is supposed that processes responsible for activation of the membrane systems of Ca2+ transport in the process of spike generation are also calmodulin-dependent.
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PMID:[Study of electromechanical coupling in smooth muscle cells of the ureter using phenothiazines]. 672 4

To investigate the role of myosin light chain kinase (MLCK) in phasic contractions of intact smooth muscle, we have applied Wortmannin, an MLCK inhibitor, to strips of guinea-pig ureter. Simultaneous measurements of electrical activity, intracellular [Ca2+] ([Ca2+]i) and phasic force showed that Wortmannin (1-4 microM) abolishes force with little or no change in [Ca2+]i and electrical activity. High-K+-induced force production was also abolished by Wortmannin. The effects of Wortmannin were dose dependent - at lower concentrations (100 nM) Wortmannin reduced phasic contractility by 40-50%. It also significantly increased the delay between the Ca2+ peak and force production. These data show that, in phasic smooth muscle, inhibition of MLCK causes contraction to fail, despite normal electrical activity and Ca2+ transients. Our results also indicate that Wortmannin has no secondary effects and that other means of producing force, independent of myosin phosphorylation, are negligible in this tissue. The increased lag between the rise of Ca2+ and force production when MLCK is inhibited was surprising and suggests that post-phosphorylation steps may play a larger role in the delay than was previously considered.
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PMID:The effect of inhibition of myosin light chain kinase by Wortmannin on intracellular [Ca2+], electrical activity and force in phasic smooth muscle. 971 16

1. We investigated the relationship between the action potential, Ca2+ and phasic force in intact guinea-pig ureter, following physiological activation. 2. The action potential elicited a Ca2+ transient consisting of three components: a fast increment, associated with the first action potential spike, a slower increment, associated with subsequent spikes and the initial part of the plateau component, and a steady-state phase associated with the plateau. 3. Prolongation of the plateau, by agonists, prolonged the third component of the Ca2+ transient and increased force amplitude and duration. 4. The force-Ca2+ relationship during phasic contractions showed hysteresis; more force was produced as Ca2+ declined than when it rose. Paired pulse stimuli suggested that the delay between Ca2+ and force was not due to mechanical properties. Wortmannin, which has been shown to selectively inhibit force and myosin light chain (MLC) phosphorylation in the guinea-pig ureter, did not affect electrical activity or Ca2+ but significantly increased the delay, suggesting that myosin phosphorylation is a major contributor to it. 5. Prolongation of the duration of the [Ca2+]i transient, at unchanged amplitude, increased force. The rise of [Ca2+]i did not limit the rate of contraction. Slowing of the rate of [Ca2+]i rise abolished the hysteresis between Ca2+ and force. 6. Cooling reduced force, increased the delay and hysteresis between Ca2+ and force, but did not affect the rate of rise of Ca2+. The reduction in force could be compensated, by increasing the duration of the Ca2+ transient. 7. We suggest that in vivo, steady-state force-Ca2+ relationships are not applicable in phasic smooth muscles. Furthermore, agonists increase force mainly by prolonging the action potential, which increases the duration of the [Ca2+] signal.
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PMID:The relationship between the action potential, intracellular calcium and force in intact phasic, guinea-pig uretic smooth muscle. 1054 50

In search of guiding principles involved in the branching of epithelial tubes in the developing kidney, we analyzed branching of the ureteric bud (UB) in whole kidney culture as well as in isolated UB culture independent of mesenchyme but in the presence of mesenchymally derived soluble factors. Microinjection of the UB lumen (both in the isolated UB and in the whole kidney) with fluorescently labeled dextran sulfate demonstrated that branching occurred via smooth tubular epithelial outpouches with a lumen continuous with that of the original structure. Epithelial cells within these outpouches cells were wedge-shaped with actin, myosin-2 and ezrin localized to the luminal side, raising the possibility of a "purse-string" mechanism. Electron microscopy and decoration of heparan sulfates with biotinylated FGF2 revealed that the basolateral surface of the cells remained intact, without the type of cytoplasmic extensions (invadopodia) that are seen in three-dimensional MDCK, mIMCD, and UB cell culture models of branching tubulogenesis. Several growth factor receptors (i.e., FGFR1, FGFR2, c-Ret) and metalloproteases (i.e., MT1-MMP) were localized toward branching UB tips. A large survey of markers revealed the ER chaperone BiP to be highly expressed at UB tips, which, by electron microscopy, are enriched in rough endoplasmic reticulum and Golgi, supporting high activity in the synthesis of transmembrane and secretory proteins at UB tips. After early diffuse proliferation, proliferating and mitotic cells were mostly found within the branching ampullae, whereas apoptotic cells were mostly found in stalks. Gene array experiments, together with protein expression analysis by immunoblotting, revealed a differential spatiotemporal distribution of several proteins associated with epithelial maturation and polarization, including intercellular junctional proteins (e.g., ZO-1, claudin-3, E-cadherin) and the subapical cytoskeletal/microvillar protein ezrin. In addition, Ksp-cadherin was found at UB ampullary cells next to developing outpouches, suggesting a role in epithelial-mesenchymal interactions. These data from the isolated UB culture system support a model where UB branching occurs through outpouching possibly mediated by wedge-shaped cells created through an apical cytoskeletal purse-string mechanism. Additional potential mechanisms include (1) differential localization of growth factor receptors and metalloproteases at tips relative to stalks; (2) creation of a secretory epithelium, in part manifested by increased expression of the ER chaperone BiP, at tips relative to stalks; (3) after initial diffuse proliferation, coexistence of a balance of proliferation vs. apoptosis favoring tip growth with a very different balance in elongating stalks; and (4) differential maturation of the tight and adherens junctions as the structures develop. Because, without mesenchyme, both lateral and bifid branching occurs (including the ureter), the mesenchyme probably restricts lateral branching and provides guidance cues in vivo for directional branching and elongation as well as functioning to modulate tubular caliber and induce differentiation. Selective cadherin, claudin, and microvillar protein expression as the UB matures likely enables the formation of a tight, polarized differentiated epithelium. Although, in vivo, metanephric mesenchyme development occurs simultaneously with UB branching, these studies shed light on how (mesenchymally derived) soluble factors alone regulate spatial and temporal expression of morphogenetic molecules and processes (proliferation, apoptosis, etc.) postulated to be essential to the UB branching program as it forms an arborized structure with a continuous lumen.
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PMID:Spatiotemporal regulation of morphogenetic molecules during in vitro branching of the isolated ureteric bud: toward a model of branching through budding in the developing kidney. 1546 72


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