Literature DB >> 1718439

Phenotypic heterogeneity in cultured skin fibroblasts from patients with disorders of peroxisome biogenesis belonging to the same complementation group.

E A Wiemer1, M Out, A Schelen, R J Wanders, R B Schutgens, H Van den Bosch, J M Tager.   

Abstract

We have studied fibroblast cell lines derived from a control subject (cell line 85AD5035F) and three patients clinically described as having the Zellweger syndrome (cell line W78/515), the infantile form of Refsum disease (cell line BOV84AD) and hyperpipecolic acidaemia (cell line GM3605), respectively. The mutant cell lines belonged to the same complementation group. The fibroblasts were cultured under identical conditions and were harvested at different time intervals after reaching confluence. Several peroxisomal parameters were determined. In agreement with previous reports, a lowered enzymic activity of acyl-CoA: dihydroxyacetonephosphate acyltransferase and a decrease in latent catalase clearly distinguished the patient cell lines from the control cell line. However, the cell lines exhibited a phenotypic heterogeneity. This was most strikingly encountered when cells were processed for indirect immunofluorescence microscopy and stained with anti-(catalase). The control cells exhibited a punctate fluorescence, which is indicative of the presence of catalase in peroxisomes. In the mutant cell line W78/515 a diffuse fluorescence was observed, indicative of the presence of catalase in the cytosol. In the other two mutant cell lines a punctate fluorescence was observed in some of the cells. Moreover, clear differences in the extent of proteolytic processing of acyl-CoA oxidase were detected. The mutant cell line BOV84AD displayed a control-like pattern with all molecular forms of acyl-CoA oxidase (72, 52 and 20 kDa) present, whereas in the W78/515 cell line only the 72 kDa component could be visualised. The GM3605 cell line was intermediate in this respect.

Entities:  

Mesh:

Substances:

Year:  1991        PMID: 1718439     DOI: 10.1016/0925-4439(91)90041-7

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


  7 in total

Review 1.  Diagnostic work-up of a peroxisomal patient.

Authors:  J G Leroy; M Espeel; J F Gadisseux; H Mandel; M Martinez; B T Poll-The; R J Wanders; F Roels
Journal:  J Inherit Metab Dis       Date:  1995       Impact factor: 4.982

2.  Disorders of peroxisome biogenesis due to mutations in PEX1: phenotypes and PEX1 protein levels.

Authors:  C Walter; J Gootjes; P A Mooijer; H Portsteffen; C Klein; H R Waterham; P G Barth; J T Epplen; W H Kunau; R J Wanders; G Dodt
Journal:  Am J Hum Genet       Date:  2001-06-01       Impact factor: 11.025

3.  Presence of cytoplasmic factors functional in peroxisomal protein import implicates organelle-associated defects in several human peroxisomal disorders.

Authors:  M Wendland; S Subramani
Journal:  J Clin Invest       Date:  1993-11       Impact factor: 14.808

4.  Morphometry of peroxisomes and immunolocalization of peroxisomal proteins in the liver of patients with generalised peroxisomal disorders.

Authors:  J L Hughes; D I Crane; E Robertson; A Poulos
Journal:  Virchows Arch A Pathol Anat Histopathol       Date:  1993

Review 5.  Liver pathology and immunocytochemistry in congenital peroxisomal diseases: a review.

Authors:  F Roels; M Espeel; D De Craemer
Journal:  J Inherit Metab Dis       Date:  1991       Impact factor: 4.982

6.  Resistance to erucic acid as a selectable marker for peroxisomal activity: isolation of revertants of an infantile Refsum disease cell line.

Authors:  E Bachir Bioukar; F Straehli; K H Ng; M O Rolland; T Hashimoto; J P Carreau; J Deschatrette
Journal:  J Inherit Metab Dis       Date:  1994       Impact factor: 4.982

7.  Differential protein import deficiencies in human peroxisome assembly disorders.

Authors:  A Motley; E Hettema; B Distel; H Tabak
Journal:  J Cell Biol       Date:  1994-05       Impact factor: 10.539

  7 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.