scholarly journals Distribution of Nidogen in the Murine Eye and Ocular Phenotype of the Nidogen-1 Knockout Mouse

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Christian Albrecht May

Distribution and lack of nidogen-1, part of numerous basement membranes, were studied in the mouse eye. For that purpose, eyes of C57BL/6 and nidogen-1 knockout mice were stained immunohistochemically for nidogen-1, and intraocular pressure measurements and light- and electron microscopy were used to study the nidogen-1 knockout animals. In normal mice, nidogen-1 was present in many basement membranes, but showed irregularities underneath the corneal epithelium, in Bruch’s membrane and in the iris. Homozygous knockout of nidogen-1 in the mouse showed only mild pathological changes. In the anterior eye segment, small interruptions were noted in the nonpigmented ciliary epithelium without further consequences. In the posterior eye segment, interruptions of the inner limiting membrane led to small retinal ectopias and subsequent changes in the optic nerve. In summary, the knockout of nidogen-1 showed mild but significant morphological changes pointing to the importance of this protein which can in part, but not completely; be replaced by nidogen-2.

1993 ◽  
Vol 41 (7) ◽  
pp. 1053-1073 ◽  
Author(s):  
S K Aggarwal

The effects of cisplatin (CDDP), a potent anti-cancer agent, and its various analogues were analyzed for any biochemical changes involving Ca2+ and lysosomal and membrane-associated transport enzymes in rat kidney, liver, serum, urine, tissue homogenates, and isolated mitochondria. Correlation was made with any morphological changes observed by light and electron microscopy to gain an insight into the mechanism of action of various platinum coordination complexes. CDDP in its hydrolyzed state under conditions of low chloride ion concentrations causes uncoupling of oxidative phosphorylation, calcium efflux from the mitochondria, inhibits ATP synthesis, lowers membrane-associated calcium and various membrane transport enzymes, and induces an increase in the number of lysosomes. Enzymes such as alkaline phosphatase are stripped from the brush borders of the proximal tubule cells and are discharged in the urine. However, daily IV injections of calcium (1.1 ml of 1.3% CaCl2) supplementation protect the membrane-associated enzymes from cisplatin action. Carboplatin (CBDCA), an analogue of CDDP and the least nephrotoxic of all its analogues, shows little effect on the membrane-associated transport enzymes. Therefore, cisplatin and its various analogues seem to affect the membrane transport enzymes to varying degrees with related nephrotoxicity. Calcium supplementation seems to protect these enzymes and preserve kidney function.


1989 ◽  
Vol 35 (3) ◽  
pp. 388-398 ◽  
Author(s):  
Irene E. Ronning ◽  
Hilmer A. Frank

Putrefactive anaerobe 3679 (Clostridium sporogenes), a gram-positive bacterium, was examined by light and electron microscopy during normal growth and in a medium containing sorbate (50 mM, pH 6.5), hydrochloric acid (pH of medium adjusted from 7 to 5 with HCl), or nitrite (1 mM, pH 7). During the early exponential growth phase, untreated cells were filamentous and nonseptate, but became septate later and divided when the culture entered the stationary phase. Untreated short and filamentous cells had a double-layered cell wall. Sorbate-treated cells were usually filamentous and nonseptate, but with distorted shapes characterized by numerous bends and bulges. Septation, when present, resulted in minicells. The inner cell wall appeared to be thickened and the outer wall was absent in many areas. Acid-treated cells were similar to sorbate-treated cells but contained septa. Considerable cellular debris was present in the suspension. Nitrite-treated cells were also filamentous, bent, and bulged but the cell wall appeared normal. Considerable cellular debris was also present in suspensions of nitrite-treated cells. Changes in morphology are discussed in relation to possible mechanisms of cell growth regulation and the inhibitory action of sorbate, acid, and nitrite.Key words: putrefactive anaerobe 3679, sorbate, hydrochloric acid, nitrite.


2004 ◽  
Vol 287 (3) ◽  
pp. C655-C663 ◽  
Author(s):  
Pawel Fidzinski ◽  
Mercedes Salvador-Silva ◽  
Lars Choritz ◽  
John Geibel ◽  
Miguel Coca-Prados

The natriuretic peptides (NPs) atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) display hypotensive effects in the mammalian eye by lowering the intraocular pressure (IOP), a function that is mediated by the bilayer ocular ciliary epithelium (CE), in conjunction with the trabecular meshwork. ANP regulates Na+/H+ exchanger (NHE) activity, and inhibitors of NHE have been shown to lower IOP. We examined whether NPs influence the NHE activity of the CE, which is comprised of pigmented (PE) and nonpigmented (NPE) epithelial cells, by directly recording the rate of intracellular pH (pHi) recovery from its inner NPE cell layer. NPs inhibited, in a dose-dependent manner (1–100 nM), the rate of pHi recovery with the order of potency CNP > ANP > BNP, indicative that this inhibition is mediated by the presence of NPR type B receptors. 8-Bromo-cGMP (8-BrcGMP), a nonhydrolyzable analog of cGMP, mimicked NPs in inhibiting the rate of Na+-dependent pHi recovery. In contrast, ethylisopropyl amiloride (EIPA, 100 nM) or amiloride (10 μM) completely abolished the pHi recovery by NHE. 18α-Glycyrrhetinic acid (18α-GA), a gap junction blocker, attenuated the inhibitory effect of CNP on the rate of pHi recovery, suggesting that NHE activity in both cell layers of the CE is coregulated. This interpretation was supported, in part, by the coexpression of NHE-1 isoform mRNA in both NPE and PE cells. The mechanism by which the inhibitory effect of NPs on NHE-1 activity might influence the net solute movement or fluid transport by the bilayer CE remains to be determined.


1997 ◽  
Vol 273 (5) ◽  
pp. C1700-C1706 ◽  
Author(s):  
Qiang Wu ◽  
Nicholas A. Delamere

Aqueous humor secretion is in part linked to [Formula: see text]transport by nonpigmented ciliary epithelium (NPE) cells. During this process, the cells must maintain stable cytoplasmic pH (pHi). Because a recent report suggests that NPE cells have a plasma membrane-localized vacuolar H+-ATPase, the present study was conducted to examine whether vacuolar H+-ATPase contributes to pHi regulation in a rabbit NPE cell line. Western blot confirmed vacuolar H+-ATPase expression as judged by H+-ATPase 31-kDa immunoreactive polypeptide in both cultured NPE and native ciliary epithelium. pHi was measured using 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Exposing cultured NPE to K+-rich solution caused a pHi increase we interpret as depolarization-induced alkalinization. Alkalinization was also caused by ouabain or BaCl2. Bafilomycin A1 (0.1 μM; an inhibitor of vacuolar H+-ATPase) inhibited the pHi increase caused by high K+. The pHi increase was also inhibited by angiotensin II and the metabolic uncoupler carbonyl cyanide m-chlorophenylhydazone but not by ZnCl2, 4-acetamido-4′-isothiocyanostilbene-2,2′-disulfonic acid (SITS), 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS), omeprazole, low-Cl−medium, [Formula: see text]-free medium, or Na+-free medium. Bafilomycin A1 slowed the pHi increase after an NH4Cl (10 mM) prepulse. However, no detectable pHi change was observed in cells exposed to bafilomycin A1 under control conditions. These studies suggest that vacuolar H+-ATPase is activated by cytoplasmic acidification and by reduction of the proton electrochemical gradient across the plasma membrane. We speculate that the mechanism might contribute to maintenance of acid-base balance in NPE.


2016 ◽  
Vol 36 (suppl 1) ◽  
pp. 89-94 ◽  
Author(s):  
Luciana S. Simões ◽  
Rose E.G. Rici ◽  
Phelipe O. Favaron ◽  
Taís Harumi de Castro Sasahara ◽  
Rodrigo S.N. Barreto ◽  
...  

Abstract: al for both, the establishment of appropriate management systems, and for the use of new species as animal models. In this study, we used light and electron microscopy to characterize the sexual development stages of the guinea pig (Cavia porcellus) in specimens of 30, 45 and 90 days of age. We observed the differentiation of spermatocytes only through transmission electron microscopy in the leptotene, zygotene and pachytene phases of meiosis, in 30-day-old animals. During puberty, there was differentiation of the germinative epithelium and formation of the acrosome. Spermatozoa, however, were not detected. Thus, we could infer that puberty happens after 45 days of age. Sexual maturity was evident in 90-day-old specimens. Our results showed that changes in the testicular germinative epithelium during the postnatal sexual development in guinea pig led to morphological changes, including the ones related to the development of Leydig and Sertoli cells, which are directly related to puberty. In this work, we provide new morphological subsidies for a better understanding of reproductive parameters of this species, enabling its use as an animal model in the field of the reproductive biology.


2001 ◽  
Vol 239 (11) ◽  
pp. 876-881 ◽  
Author(s):  
Hiroko Terasaki ◽  
Tetsuro Nagasaka ◽  
Masashi Arai ◽  
Tomoko Harada ◽  
Yozo Miyake

2008 ◽  
Vol 128 (9) ◽  
pp. 2259-2267 ◽  
Author(s):  
Sharada Mokkapati ◽  
Anke Baranowsky ◽  
Nicolae Mirancea ◽  
Neil Smyth ◽  
Dirk Breitkreutz ◽  
...  
Keyword(s):  

2007 ◽  
Vol 61 (4) ◽  
pp. 460-466 ◽  
Author(s):  
M Pronicki ◽  
E Matyja ◽  
D Piekutowska-Abramczuk ◽  
T Szymańska-Dębińska ◽  
A Karkucińska-Więckowska ◽  
...  

Aims:Leigh syndrome (LS) is characterised by almost identical brain changes despite considerable causal heterogeneity. SURF1 gene mutations are among the most frequent causes of LS. Although deficiency of cytochrome c oxidase (COX) is a typical feature of the muscle in SURF1-deficient LS, other abnormalities have been rarely described. The aim of the present work is to assess the skeletal muscle morphology coexisting with SURF1 mutations from our own research and in the literature.Methods:Muscle samples from 21 patients who fulfilled the criteria of LS and SURF1 mutations (14 homozygotes and 7 heterozygotes of c.841delCT) were examined by light and electron microscopy.Results:Diffuse decreased activity or total deficit of COX was revealed histochemically in all examined muscles. No ragged red fibres (RRFs) were seen. Lipid accumulation and fibre size variability were found in 14 and 9 specimens, respectively. Ultrastructural assessment showed several mitochondrial abnormalities, lipid deposits, myofibrillar disorganisation and other minor changes. In five cases no ultrastructural changes were found. Apart from slight correlation between lipid accumulation shown by histochemical and ultrastructural techniques, no other correlations were revealed between parameters investigated, especially between severity of morphological changes and the patient’s age at the biopsy.Conclusion:Histological and histochemical features of muscle of genetically homogenous SURF1-deficient LS were reproducible in detection of COX deficit. Minor muscle changes were not commonly present. Also, ultrastructural abnormalities were not a consistent feature. It should be emphasised that SURF1-deficient muscle assessed in the light and electron microscopy panel may be interpreted as normal if COX staining is not employed.


2002 ◽  
Vol 50 (12) ◽  
pp. 1625-1632 ◽  
Author(s):  
Fang-Xu Jiang ◽  
Gaetano Naselli ◽  
Leonard C. Harrison

Tissue function is regulated by the extracellular microenvironment including cell basement membranes, in which laminins are a major component. Previously, we found that laminin-1 promotes differentiation and survival of pancreatic islet cells. Here we characterize the expression pattern of laminins and their integrin receptors in adult pancreas. Although they are expressed in the basement membrane of acinar cells and duct epithelium, no laminin chains examined were detected extracellularly in the pancreatic islets. In contrast to laminin β1- and γ1-chains, the α1-chain, unique to laminin-1, was not detected. Laminin-10 (α5β1γ1) was expressed in acinar tissue, whereas laminins-2 (α2β1γ1) and -10 were expressed in the blood vessels. The laminin connector molecule, nidogen-1, had a distribution similar to that of laminin β1 and γ1, whereas fibulin-1 and -2, which compete with nidogen-1, were mostly confined to blood vessels. Integrin subunits α6 and α3 were detected in acinar cells and duct epithelial cells, but α6 was absent in islet cells. Integrin α6β4 was detected only in duct cells, α6β1 in both acinar and ductal cells, and α3β1 in acinar, duct, and islet cells. These findings are a basis for further investigation of the role of extracellular matrix molecules and their receptors in pancreas function.


Sign in / Sign up

Export Citation Format

Share Document