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Biomedical subjects

L Kjellen

Publications and source records attributed to L Kjellen.

5 recordsLinked to original sources
PubMed2006

Heparan sulphate requirement in platelet-derived growth factor B-mediated pericyte recruitment.

HS (heparan sulphate) plays a key role in angiogenesis, by interacting with growth factors required in the process. It has been proposed that HS controls the diffusion, and thus the availability, of platelet-derived growth factor B that is needed for pericyte recruitment around newly formed capillaries. The present paper summarizes our studies on the importance of HS structure in this regulatory process.

Animals↗
PubMed2000

Defective heparan sulfate biosynthesis and neonatal lethality in mice lacking N-deacetylase/N-sulfotransferase-1.

Heparan sulfate is a sulfated polysaccharide present on most cell surfaces and in the extracellular matrix. In vivo functions of heparan sulfate can be studied in mouse strains lacking enzymes involved in the biosynthesis of heparan sulfate. Glucosaminyl N-deacetylase/N-sulfotransferase (NDST) catalyzes the first modifying step in the biosynthesis of the polysaccharide. This bifunctional enzyme occurs in several isoforms. We here report that targeted gene disruption of NDST-1 in the mouse results in a structural alteration of heparan sulfate in most basement membranes as revealed by immunohistochemical staining of fetal tissue sections using antibodies raised against heparan sulfate. Biochemical analysis of heparan sulfate purified from fibroblast cultures, lung, and liver of NDST-1-deficient embryos demonstrated a dramatic reduction in N-sulfate content. Most NDST-1-deficient embryos survive until birth; however, they turn out to be cyanotic and die neonatally in a condition resembling respiratory distress syndrome. In addition, a minor proportion of NDST-1-deficient embryos die during the embryonic period. The cause of the embryonic lethality is still obscure, but incompletely penetrant defects of the skull and the eyes have been observed.

Amidohydrolases↗
PubMed1989

On the origin of antibodies to immunoglobulin genetic markers in rheumatoid arthritis. An outline of a novel concept of the nature of rheumatoid arthritis--transduction in man.

Anti-Gm's in rheumatoid arthritis patients detect products of the Mendelian genes G1ma, G1mx, G3mb, G3mc, G3mg, G3mst. Commonly, these anti-Gm's are specific for other individuals immunoglobulin allotypes. Reasons are given for the contention that such anti-Gm's in patients with rheumatoid arthritis are indicative of the expression of nonnominal allotypes, the genes for which have been transferred from one individual to another by means of a B cell virus. This process - akin to transduction and occurring after the tolerance induction period - may lead to a chimaeric state of the B cell compartment in rheumatoid arthritis patients. Special features of Ig gene regulation in normal B cell progression are allelic exclusion and the excision-expulsion-rejoining of DNA segments. Perturbation of B cell regulation by external genomes may be favoured by allelic exclusion. The DNA excision-rejoining processes may have consequences for concomitant (viral) nucleic acid assembly, particularly for viruses sharing nucleotide sequences with the Ig switch regions.

Antibodies, Anti-Idiotypic↗
PubMed1985

Kinetics of di-(2-ethylhexyl) phthalate in immature and mature rats and effect on testis.

The testicular response of di-(2-ethylhexyl) phthalate (DEHP), as well as the kinetics of DEHP and its primary metabolite mono-(2-ethylhexyl) phthalate (MEHP), were studied in immature and mature rats. After 14 daily oral doses of 1.0 g DEHP/kg body weight to 25, 40 and 60-day-old rats, testicular damage was observed in the youngest age group only. DEHP was not found to any significant extent in the peripheral plasma after an oral dose of 1.0 g DEHP/kg body weight. High plasma levels of MEHP were found, with maximal plasma concentrations ranging from 48 to 152 micrograms/ml. The in vitro plasma protein binding of MEHP was extensive, approximately 98%, in all age groups and no age-related difference in the elimination half-life was observed. The amount of DEHP-derived material excreted in urine was twice as high in 25 as in 60-day-old rats. The mean area under the plasma concentration-time curve of MEHP was also significantly larger in 25 than in 40 and 60-day-old rats. These observations suggest that the extent of absorption, and hence total exposure to MEHP and its metabolites, is higher in young than in more mature rats after oral administration of DEHP. It seems probable that this finding is relevant to the age-related difference in the toxic effects on the testis.

Aging↗