Marker enzymes, phospholipids and acyl group composition of a somal plasma membrane fraction isolated from rat cerebral cortex: a comparison with microsomes and synaptic plasma membranes

Gy, Sun; Huang, Huijie; Ja, Kelleher; Eb, Stubbs; Ay, Sun

doi:10.1016/0197-0186(88)90150-7

Cited by 75 publications

(40 citation statements)

References 16 publications

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“…Crude plasma membranes were isolated from HEK293 cells transiently transfected with rHuPCaR4.0 (10) or the mutant receptor by differential speed centrifugation as described by Sun et al (29). Confluent cultured cells in 100-mm culture plates were rinsed twice with PBS and treated with 0.02% EDTA in PBS at 37 Њ C for 5 min.…”

Section: Methodsmentioning

confidence: 99%

Markedly reduced activity of mutant calcium-sensing receptor with an inserted Alu element from a kindred with familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism.

Bai¹,

Janicic²,

Trivedi³

et al. 1997

J. Clin. Invest.

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Missense mutations have been identified in the coding region of the extracellular calcium-sensing receptor (CASR) gene and cause human autosomal dominant hypo-and hypercalcemic disorders. The functional effects of several of these mutations have been characterized in either Xenopus laevis oocytes or in human embryonic kidney (HEK293) cells. All of the mutations that have been examined to date, however, cause single putative amino acid substitutions. In this report, we studied a mutant CASR with an Alu-repetitive element inserted at codon 876, which was identified in affected members of families with the hypercalcemic disorders, familial hypocalciuric hypercalcemia (

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Section: Methodsmentioning

confidence: 99%

Markedly reduced activity of mutant calcium-sensing receptor with an inserted Alu element from a kindred with familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism.

Bai¹,

Janicic²,

Trivedi³

et al. 1997

J. Clin. Invest.

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“…That intracellular membranes are affected in platelets from AD patients had been shown earlierby Zubenko et al (1987a), and was confirmed by Hajimohammadreza et al (1990), who found proliferation of a system of trabeculated cisternae bounded by the smooth endoplasmic reticulum (SER) in platelets from AD patients as compared to controls after electron microscopic analysis. For the determination of such a proliferation of intracellular membranes in platelets, we measured NADH cytochrome-C reductase, which is a marker enzyme for the smooth endoplasmic reticulum (Sun et al, 1988), and the protein/phospholipid ratio in platelet homogenates, which is expected to decrease when there is proliferation of intracellular membranes without an increase in the cytoplasm. These markers for the possible increase in the amount of intracellular membranes did not differ in homogenates of platelets from AD patients and controls.…”

Section: Discussionmentioning

confidence: 99%

“…Because disease-specific abnormalities in the brain can be reflected in platelets, and because platelets have a complete phosphoinositide metabolism with both P1 4-kinase and PT 3-kinase, we compared PT kinase activity in platelets from AD patients with that of platelets from age-matched controls. We also measured NADH cytochrome-C reductase as a marker for the endoplasmic reticulum (Sun et a!., 1988).…”

Section: Introductionmentioning

confidence: 99%

Platelet phosphatidylinositol kinase activity is not altered in Alzheimer disease

Bothmer

Markerink

Coppens

et al. 1993

Molecular and Chemical Neuropathology

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We previously reported a specific decline in phosphatidylinositol (PI) kinase activity in the neocortex of patients with Alzheimer disease (AD) as compared to controls, whereas phosphatidylinositol phosphate (PIP) kinase activity appeared not to be affected (Jolles et al., 1992). In search of a possible systemic effect of AD, in the present study we investigated phosphoinositide kinase activity in platelets from patients with AD and from control subjects. The study was based on the notion that disease-specific abnormalities in the brain could be reflected in blood platelets. PI kinase activity was studied in platelet homogenates and in a salt-solubilized protein fraction of platelets, because of the difference in subcellular localization of the different types of PI kinases. In addition, NADH cytochrome-C reductase was measured in platelet homogenates as a marker for the endoplasmic reticulum, to detect a possible proliferation of the endoplasmic reticulum. AD patients and normal elderly controls showed no difference in PI kinase activity in either enzyme fraction. Furthermore, NADH cytochrome-C reductase activity and the protein/phospholipid ratio per 10(6) platelets were the same for AD patients and controls. This was taken as an indication that platelets in AD patients do not show proliferation of intracellular membranes.

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“…Human tissue (peripheral nerve) was obtained fresh at autopsy or frozen from the University of Miami Brain and Tissue Bank for Developmental Disorders (contract #NOI-HD-8-3284) and immediately homogenized (10% by vol) in ice-cold 10 mM Tris buffer (pH 7.3) containing: sucrose 250 mM, EDTA 1 mM, EGTA 2 mM that was supplemented with a commercial cocktail of protease inhibitors (Roche, Indianapolis, IN, USA). Myelin was purified from rat peripheral nerve as previously described (Sun et al 1988). Primary cultures of rat dorsal root ganglia neurons or rat Schwann cells were prepared according to Neuberger and De Vries (1993).…”

Section: Immunoblottingmentioning

confidence: 99%

Antibodies to L‐periaxin in sera of patients with peripheral neuropathy produce experimental sensory nerve conduction deficits

Lawlor¹,

Richards

Vries

et al. 2002

Journal of Neurochemistry

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L-Periaxin is a PDZ-domain protein localized to the plasma membrane of myelinating Schwann cells and plays a key role in the stabilization of mature myelin in peripheral nerves. Mutations in L-periaxin have recently been described in some patients with demyelinating peripheral neuropathy, suggesting that disruption of L-periaxin function may result in nerve injury. In this study, we report the presence of autoantibodies to L-periaxin in sera from two of 12 patients with diabetes mellitus (type 2)-associated neuropathy and three of 17 patients with IgG monoclonal gammopathy of undetermined significance (MGUS) neuropathy, an autoimmune peripheral nerve disorder. By comparison, anti-L-periaxin antibodies were not present in sera from nine patients with IgM MGUS neuropathy or in sera from 10 healthy control subjects. The effect of anti-L-periaxin serum antibody on peripheral nerve function was tested in vivo by intraneural injection. Sera containing anti-L-periaxin antibody, but not sera from age-matched control subjects, injected into the endoneurium of rat sciatic nerve significantly (p < 0.005, n ¼ 3) attenuated sensory-evoked compound muscle action potential (CMAP) amplitudes in the absence of temporal dispersion. In contrast, motor-evoked CMAP amplitudes and latencies were not affected by intraneural injection of sera containing anti-L-periaxin antibody. Light and electron microscopy of anti-L-periaxin serum-injected nerves showed morphologic evidence of demyelination and axon enlargement. Depleting sera of anti-L-periaxin antibodies neutralized the serum-mediated effects on nerve function and nerve morphology. Together, these data support anti-L-periaxin antibody as the pathologic agent in these serum samples. We suggest that anti-L-periaxin antibodies, when present in sera of patients with IgG MGUS-or diabetesassociated peripheral neuropathy, may elicit sensory nerve conduction deficits. Keywords: antibody, diabetes, MGUS, neuropathy, periaxin. Peripheral neuropathies are a heterogeneous group of nerve disorders often characterized by a mixture of sensory and motor disturbances (Adams et al. 1997). Although the etiology of the peripheral neuropathy is often obscure, some patients exhibit strong familial histories consistent with an autosomal dominance, autosomal recessive, or X-linked pattern of inheritance. In other patients, the peripheral neuropathy is acquired such as in monoclonal gammopathy of undetermined significance (MGUS) neuropathy (Kyle 1992) or is secondary to a metabolic disturbance such as diabetes mellitus.Serum autoantibodies have been implicated as potential pathogenic agents in several autoimmune-mediated peripheral nerve disorders (Ho et al. 1998;Quarles and Weiss 1999). In addition, a role of autoimmunity in peripheral nerve disorders associated with metabolic disturbances, such as diabetic neuropathy, has been entertained (Said et al. 1994;Krendel et al. 1995). However, the antigenic specificities Abbreviations used: CMAP, compound muscle action potential; D/P, distal (ankle) to...

show abstract

Marker enzymes, phospholipids and acyl group composition of a somal plasma membrane fraction isolated from rat cerebral cortex: a comparison with microsomes and synaptic plasma membranes

Cited by 75 publications

References 16 publications

Markedly reduced activity of mutant calcium-sensing receptor with an inserted Alu element from a kindred with familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism.

Markedly reduced activity of mutant calcium-sensing receptor with an inserted Alu element from a kindred with familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism.

Platelet phosphatidylinositol kinase activity is not altered in Alzheimer disease

Antibodies to L‐periaxin in sera of patients with peripheral neuropathy produce experimental sensory nerve conduction deficits

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