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L Brezina

Publications and source records attributed to L Brezina.

10 recordsLinked to original sources
PubMed1990

Structural requirements for neural cell adhesion molecule-heparin interaction.

Two biological domains have been identified in the amino terminal region of the neural cell adhesion molecule (NCAM): a homophilic-binding domain, responsible for NCAM-NCAM interactions, and a heparin-binding domain (HBD). It is not known whether these two domains exist as distinct structural entities in the NCAM molecule. To approach this question, we have further defined the relationship between NCAM-heparin binding and cell adhesion. A putative HBD consisting of two clusters of basic amino acid residues located close to each other in the linear amino acid sequence of NCAM has previously been identified. Synthetic peptides corresponding to this domain were shown to bind both heparin and retinal cells. Here we report the construction of NCAM cDNAs with targeted mutations in the HBD. Mouse fibroblast cells transfected with the mutant cDNAs express NCAM polypeptides with altered HBD (NCAM-102 and NCAM-104) or deleted HBD (HBD-) at levels similar to those of wild-type NCAM. Mutant NCAM polypeptides purified from transfected cell lines have substantially reduced binding to heparin and fail to promote chick retinal cell attachment. Furthermore, whereas a synthetic peptide that contains both basic amino acid clusters inhibits retinal-cell adhesion to NCAM-coated dishes, synthetic peptides in which either one of the two basic regions is altered to contain only neutral amino acids do not inhibit this adhesion. These results confirm that this region of the NCAM polypeptide does indeed mediate not only the large majority of NCAM's affinity for heparin but also a significant portion of the cell-adhesion-mediating capability of NCAM.

Amino Acid Sequence↗
PubMed1987

Nerve fibers surrounding intracranial and extracranial vessels from human and other species contain dynorphin-like immunoreactivity.

Dynorphin B(20-32) was visualized by immunohistochemistry in guinea-pig and rat perivascular nerve fibers and was measured by radioimmunoassay within the walls of feline, canine, bovine and human cephalic and systemic arteries and veins. Canine vessels contained the highest levels. When human blood vessels or trigeminal ganglia were subjected to reverse-phase high-performance liquid chromatography, dynorphin immunoreactivity exhibited a retention time identical to that of synthetic dynorphin B. No differences in dynorphin-like immunoreactivity were measurable between feline systemic arteries and veins, or between cephalic and systemic vessels. The highest amounts were present in leptomeninges devoid of large pial arteries. Relatively high levels were also measured in feline and human trigeminal ganglia and feline superior cervical and sphenopalatine ganglia, three sources of projecting perivascular axons. Levels did not diminish, however, in ipsilateral feline cephalic vessels following either unilateral trigeminal or superior cervical ganglionectomies. Hence, dynorphin-containing fibers may project from parasympathetic cell bodies or perhaps from intrinsic brain sources. Previously published reports indicate that the kappa agonist dynorphin does not modify vessel tone when added in vitro but does inhibit release of neurotransmitters from afferent and sympathetic axons via prejunctional receptors. These observations suggest a pharmacological role for dynorphin on sensory and autonomic functions of the vasculature.

Aged↗
PubMed1981

Tracheal submucosal gland serous cells stimulated in vitro with adrenergic and cholinergic agonists. A morphometric study.

A morphometric analysis was made of alterations in serous cell structure induced by adrenergic and cholinergic agonists. Ferret tracheal rings were exposed for 30 min in vitro to one of the following agonists: phenylephrine, terbutaline, or methacholine (all at 10(-5) M). Controls were incubated similarly in medium containing no drugs or medium containing both the agonist and an excess of the appropriate antagonist (phentolamine, propranolol or atropine, all at 10(-4) M). Electron microscopic observation and stereological analysis of the incubated samples revealed that the volume density of serous cell granules in controls (0.30 +/- 0.02, mean +/- SE, n = 4) was significantly reduced by phenylephrine (0.19 +/- 0.03, n = 4) and methacholine (0.17 +/- 0.01, n = 4), but not by terbutaline (0.27 +/- 0.04, n = 4). The presence of antagonists in the medium prevented the observed changes (phenylephrine/phentolamine: 0.29 +/- 0.03, n = 3 and methacholine/atropine: 0.33 +/- 0.06, n = 3). In addition, the volume density of intracellular vacuoles in controls (0.02 +/- 0.05, n = 4) was increased in response to methacholine stimulation (0.12 +/- 0.05, n = 4), but not in response to the other agonists. This effect was blocked by atropine (0.01 +/- 0.00, n = 3). We conclude that serous-cell granules are discharged by both alpha-adrenergic and cholinergic, but not beta-adrenergic stimulation. In addition, cholinergic stimulation evokes the formation of intracellular vacuoles, a possible indication of active ion and water transport.

Animals↗