scholarly journals Phospholipid composition and metabolism in mouse muscular dystrophy

1978 ◽  
Vol 176 (1) ◽  
pp. 15-22 ◽  
Author(s):  
Chea T. Kwok ◽  
Lawrence Austin

1. The composition and metabolism of phospholipids were studied in various tissues from both normal and dystrophic mice of the 129 ReJ strain. Phospholipids extracted from forebrain, spinal cord, sciatic nerve and plasma were fractionated by t.l.c. and measured. 2. Very significant alterations were found in the choline phospholipids from these tissues, except forebrain. Plasma phosphatidylcholine in the dystrophic mouse was increased by 38%. There was a 2-fold increase in lysophosphatidylcholine in the spinal cord of dystrophic mice. The sciatic nerve showed a marked decrease in sphingomyelin content, which is approximately half of that in the controls. 3. Five enzymes involved in phosphatidylcholine metabolism [namely cholinephosphotransferase (EC 2.7.8.2); phospholipases A (EC 3.1.1.4, EC 3.1.1.32); lysophospholipase (EC 3.1.1.5); lysophosphatidylcholine acyltransferase (EC 2.3.1.23); phospholipase C (EC 3.1.4.3)] were studied in tissue preparations from forebrain, spinal cord, sciatic nerves, gastrocnemius muscles and liver. 4. Activities of phospholipases A and C were significantly increased, about 5-fold and 60% respectively, in gastrocnemius muscle of dystrophic mice compared with controls. Phospholipases A also showed 50% higher activity in the sciatic nerves of dystrophic than of normal mice. Lysophosphatidylcholine acyltransferase activities were significantly increased in the sciatic nerves and spinal cord, by 50–100% over that of the controls. The forebrain and spinal cord from dystrophic mice, however, had only 60% of lysophospholipase activities of that of the normal control. Cholinephosphotransferase activity was unchanged in these tissues from both normal and dystrophic mice. 5. It is suggested that are number of features of mouse muscular dystrophy related to altered membrane structure and function can be rationalized in terms of changes in lipid composition and metabolism.

1995 ◽  
Vol 58 (4) ◽  
pp. 416-420 ◽  
Author(s):  
XINTIAN MING ◽  
MARK A. DAESCHEL

A nisin-resistant mutant of Listeria monocytogenes Scott A has been characterized by comparing its phospholipid composition with the nisin-sensitive parental strain. The total phospholipids of resistant cells were significantly (P < 0.001) decreased compared to the parental strain. The types of phospholipids isolated from nisin-resistant and sensitive cells were identical, but there was a significant decrease (P < 0.01) in the amount of three individual phospholipids. Nisin-resistant cells were found to bind less nisin and release less phospholipids than sensitive cells when treated with same concentrations of nisin. The cell surface of resistant cells was less hydrophobic compared to sensitive cells, which also may have contributed to the observed nisin resistance. The results suggest that fundamental changes occurred in the membrane structure and function of the resistant mutant as a response to nisin.


1988 ◽  
Vol 255 (4) ◽  
pp. H953-H959
Author(s):  
T. Sakamoto ◽  
S. Shimazaki ◽  
W. W. Monafo

[14C]butanol distribution was used to quantitate regional blood flow (SCBF) in the spinal cord (levels T3-5, T7-9, L1-2, L3-S) and in the sciatic nerves (NBF) of control pentobarbital sodium-anesthetized rats (group A), after 1 h of hemorrhagic hypotension (group B), after 15 min of stimulation of one sciatic nerve (group C-1), and after stimulation of one sciatic nerve plus hemorrhage, which maintained mean arterial pressure (MAP) at control (130 mmHg). Group A SCBF ranged from 52.3 +/- 3.5 (L3-S) to 67.4 +/- 2.7 (L1-2) ml.min-1.100 g-1. NBF was 8.0 +/- 0.9 ml.min-1.100 g-1. Group B SCBF was unchanged. NBF fell to 4.0 +/- 0.4 ml.min-1.100 g-1. Group C-1 SCBF was markedly elevated (range 122 +/- 23.1 to 150.1 +/- 18.7 ml.min-1.100 g-1). NBF was 33.5 +/- 4.1 ml.min-1.100 g-1 (stimulated side) and 14.7 +/- 1.4 ml.min-1.100 g-1 (nonstimulated). MAP was elevated (163 +/- 6 mmHg). In group C-2 (MAP was 130 +/- 4 mmHg), SCBF was still elevated at T3-5, L3-S, and marginally elevated at L1-2. NBF was 22.6 +/- 4.7 ml.min-1.100 g-1 (stimulated) but unchanged contralaterally. [14C]butanol distribution provides a sensitive reproducible measure of SCBF and NBF. Autoregulation of SCBF (but not of NBF) occurred in the range 60-160 mmHg MAP. Spinal cord stimulation via the sciatic nerve increased SCBF two- to threefold, but when hypertension was avoided by blood withdrawal, a modest (38%) increase in SCBF still occurred.


2019 ◽  
Author(s):  
Justin G. Boyer ◽  
Sarah Han ◽  
Vikram Prasad ◽  
Hadi Khalil ◽  
Ronald J. Vagnozzi ◽  
...  

AbstractSatellite cells are skeletal muscle resident stem cells that regenerate adult myofibers following an acute injury to muscle. Despite the assumption that the loss of satellite cells would be detrimental in a chronic regeneration-inducing muscle disease such as muscular dystrophy, this assumption has never been tested using mouse genetics. Here we generated a novel model of satellite cell ablation and crossed it with mouse models of muscular dystrophy to directly investigate how critical these cells are in maintaining muscle during a chronic degenerative disorder. Satellite cell deletion in 2-week-old young dystrophic mice provided noticeable improvements in histopathology and function, although at this early timepoint it was utimately detrimental because muscle size was not sufficient to permit survival. However, depletion of satellite cells beginning at 2 months of age in dystrophic mice provided similar histological and functional improvements but without compromising muscle size. The improved profile showed fewer damaged fibers, less myofiber central nucleation, increased sarcolemma integrity, decreased fibrosis and a dramatic size increase in the remaining myofibers. At the functional level, young adult dystrophic mice lacking satellite cells performed significantly better than those with satellite cells when exercised on a treadmill. Thus, loss of satellite cells during early adulthood in dystrophic mice produces an unexpected protective effect.


Author(s):  
S. K. Pena ◽  
C. B. Taylor ◽  
J. Hill ◽  
J. Safarik

Introduction: Oxidized cholesterol derivatives have been demonstrated in various cell cultures to be very potent inhibitors of 3-hvdroxy-3- methylglutaryl Coenzyme A reductase which is a principle regulator of cholesterol biosynthesis in the cell. The cholesterol content in the cells exposed to oxidized cholesterol was found to be markedly decreased. In aortic smooth muscle cells, the potency of this effect was closely related to the cytotoxicity of each derivative. Furthermore, due to the similarity of their molecular structure to that of cholesterol, these oxidized cholesterol derivatives might insert themselves into the cell membrane, alter membrane structure and function and eventually cause cell death. Arterial injury has been shown to be the initial event of atherosclerosis.


Author(s):  
Frank A. Rawlins

Several speculations exist as to the site of incorporation of preformed molecules into myelin. The possibility that an autoradiographic analysis of cholesterol-1,2-H3 incorporation at very short times after injection might shed some light in the solution of that problem led to the present experiment.Cholesterol-1,2-H3 was injected intraperitoneally into 24 tenday old mice. The animals were then sacrificed at 10,20,30,40,60,90,120 and 180 min after the injection and the sciatic nerves were processed for electron microscope autoradiography. To analyze the grain distribution in the autoradiograms of cross and longitudinal sections from each sciatic nerve myelin sheaths were subdivided into three compartments named: outer 1/3, middle 1/3 and inner 1/3 compartments.It was found that twenty min. after the injection of cholesterol -1.2-H3 (Figs. 1 and 2), 55% of the total number of grains (t.n.g) found in myelin were within the outer 1/3 compartment, 9% were within the middle 1/3 and 36% within the inner 1/3 compartment


1978 ◽  
Vol 39 (01) ◽  
pp. 177-185 ◽  
Author(s):  
Shuichi Hashimoto ◽  
Sachiko Shibata ◽  
Bonro Kobayashi

SummaryThe effect of Mitomycin C on aggregation, adenosine 3′, 5′-monophosphate (cyclic AMP) metabolism and reactions induced by thrombin was studied in rabbit platelets. Mitomycin C inhibited the platelet aggregation induced by adenosine diphosphate or thrombin. The level of radioactive cyclic AMP derived from 8-14C adenine or 8-14C adenosine increased after incubating intact platelets with Mitomycin G. Formation of radioactive adenosine triphosphate also increased though mitochondrial oxidation was not stimulated. Similar effect was observed also in rabbit liver. Mitomycin C failed to stimulate platelet adenyl cyclase but inhibited cyclic AMP phosphodiesterase in the absence of theophylline. In the platelets preincubated with Mitomycin C, thrombin-induced inhibition of adenyl cyclase, stimulation of membrane-bound cyclic AMP phosphodiesterase, and release of 250,000 dalton protein from platelet membranes were prevented. These results suggest that Mitomycin C will affect cellular membrane structure and function, and this extranuclear effect of Mitomycin C will lead to inhibition of aggregation in blood platelets.


2020 ◽  
Vol 14 (4) ◽  
pp. 263-269
Author(s):  
A. A. Starinets ◽  
E. L. Egorova ◽  
A. A. Tyrtyshnaia ◽  
I. V. Dyuisen ◽  
A. N. Baryshev ◽  
...  

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