The Binding of Plasma Proteins to Human Placental Cell Membranes

1977 ◽  
Vol 52 (4) ◽  
pp. 383-394
Author(s):  
A. H. Balfour ◽  
E. A. Jones
Keyword(s):  
Plasma Proteins ◽  
Cell Membranes ◽  
Erythrocyte Membranes ◽  
Heavy Chains ◽  
Order Of Magnitude ◽  
Microvillus Membrane ◽  
Specific Receptors ◽  
Placental Membranes ◽  
Syncytial Trophoblast ◽  
Specific Membrane

1. To investigate the relative degree to which human IgG and other plasma proteins bind to cell membranes of the full-term human placenta, suspensions of membranes mixed with radio-iodinated proteins were incubated at pH 6·5 and subjected to Sepharose 2B column chromatography. The amount of labelled protein associated with membrane protein in membrane-containing fractions of the eluate was then determined. 2. Binding of IgG and each of the four subclasses of IgG was appreciable. Binding of IgG was markedly reduced if membranes were incubated at pH 8·0 rather than 6·5. Binding of labelled IgG was inhibited by excess of unlabelled IgG but not by excess of unlabelled albumin. Placental membranes bound much more IgG than did erythrocyte membranes. 3. Binding of insulin was relatively greater than that of IgG, whereas binding of IgE, IgM, IgA, albumin, transferrin and polyvinylpyrrolidone was much less than that of IgG and each of its subclasses. 4. The relative binding of IgG and fragments of the IgG molecule was, in decreasing order of magnitude: light chains, IgG, Fc, heavy chains and F(ab′)2. 5. The results are consistent with Brambell's hypothesis for the mechanism of the transmission of passive immunity from mother to young. In particular the data are consistent with the existence of a limited number of IgG specific receptors on the microvillus membrane of the syncytial trophoblast. Such receptors could protect IgG molecules from degradation during their transplacental transport. The submolecular region of the IgG molecule involved in specific membrane binding appears to be common to all four subclasses and to include the Fc region.

scholarly journals Endothelial Dysfunction in Diabetes Is Aggravated by Glycated Lipoproteins; Novel Molecular Therapies

Biomedicines ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 18
Author(s):  
Laura Toma ◽  
Camelia Sorina Stancu ◽  
Anca Volumnia Sima
Keyword(s):  
Plasma Proteins ◽  
Diabetes Complications ◽  
Vascular Complications ◽  
High Density Lipoproteins ◽  
Diabetic Patients ◽  
Inflammatory Stress ◽  
Glycation End Products ◽  
Molecular Therapies ◽  
Specific Receptors

Diabetes and its vascular complications affect an increasing number of people. This disease of epidemic proportion nowadays involves abnormalities of large and small blood vessels, all commencing with alterations of the endothelial cell (EC) functions. Cardiovascular diseases are a major cause of death and disability among diabetic patients. In diabetes, EC dysfunction (ECD) is induced by the pathological increase of glucose and by the appearance of advanced glycation end products (AGE) attached to the plasma proteins, including lipoproteins. AGE proteins interact with their specific receptors on EC plasma membrane promoting activation of signaling pathways, resulting in decreased nitric oxide bioavailability, increased intracellular oxidative and inflammatory stress, causing dysfunction and finally apoptosis of EC. Irreversibly glycated lipoproteins (AGE-Lp) were proven to have an important role in accelerating atherosclerosis in diabetes. The aim of the present review is to present up-to-date information connecting hyperglycemia, ECD and two classes of glycated Lp, glycated low-density lipoproteins and glycated high-density lipoproteins, which contribute to the aggravation of diabetes complications. We will highlight the role of dyslipidemia, oxidative and inflammatory stress and epigenetic risk factors, along with the specific mechanisms connecting them, as well as the new promising therapies to alleviate ECD in diabetes.

Impermeability of rabbit erythrocytes to prostaglandins

1975 ◽  
Vol 229 (6) ◽  
pp. 1580-1584 ◽  
Author(s):  
LZ Bito ◽  
RA Baroody
Keyword(s):  
Fatty Acids ◽  
Cell Membranes ◽  
Erythrocyte Membranes ◽  
Rabbit Erythrocyte ◽  
The Mean ◽  
Intracellular Volume ◽  
Distribution Spaces ◽  
Apparent Distribution ◽  
Initial Uptake

Washed rabbit erythrocytes were suspended in Tris-electrolyte buffer containing [3H]prostaglandin (PG) E1, F1alpha, F2alpha, or A1 and one 14C-labeled compound such as sucrose. After up to 24 h of incubation, aliquots of centrifuged, packed cells and supernatant were oxidized and the 3H and 14C samples were counted. The mean sucrose space of the packed cell was 7.4%. After 1 min the E1, F1alpha, and F2alpha spaces were 16, 15.4, and 10.0%, respectively, and showed no increase even after 24 h of incubation at either 23 or 5 degrees C. At 23 degrees C the initial (0.5 min) PGA1 and thiourea spaces were 94 and 75%, respectively, whence the PGA1, but not the thiourea, space declined, reaching 30% at 4 h. The large initial uptake of PGA1 was eliminated at 5 degrees C, while it was accentuated at pH 6.8 or at a PGA1, concentration of 10(-3) M. 14C-Labeled arachidonic, octanoic, and other non-PG fatty acids gave apparent distribution spaces of 140-300%. These results show that PG's can partition into rabbit erythrocyte membranes, but the intracellular volume of the erythrocytes is not freely accessible to these autacoids. The implications of the finding that some cell membranes are impermeable to prostaglandins are discussed.

Colocalization of GAPDH and band 3 (AE1) proteins in rat erythrocytes and kidney intercalated cell membranes

1992 ◽  
Vol 262 (5) ◽  
pp. F892-F896 ◽  
Author(s):  
L. Ercolani ◽  
D. Brown ◽  
A. Stuart-Tilley ◽  
S. L. Alper
Keyword(s):  
Plasma Membrane ◽  
Cell Membranes ◽  
Basolateral Membrane ◽  
Integral Membrane Protein ◽  
Band 3 ◽  
Erythrocyte Membranes ◽  
Rat Erythrocytes ◽  
Kidney Medulla ◽  
Multifunctional Protein ◽  
Alternatively Spliced

Glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.2.12) (GAPDH) is a multifunctional protein that associates with the cytoplasmic face of intact human erythrocyte membranes. This association has been postulated to be critically dependent on the interaction of GAPDH with the highly acidic NH2-terminal domain of the principal integral membrane protein of the erythrocyte plasma membrane, the band 3 anion exchanger (AE1). This domain is not conserved in murine erythrocyte AE1 and is fully deleted in the alternatively spliced AE1 isoform that is expressed in the kidney. The lack of conservation of this domain has been proposed to explain the reported absence of GAPDH association with rodent erythrocyte membranes. To determine whether GAPDH could be associated with AE1 proteins in rodent cell membranes, specific rabbit antibodies to peptide sequences of rat GAPDH and mouse AE1 were used to immunolocalize these proteins in sequential semithin sections of rat erythrocytes and kidney medulla. In rat erythrocytes, GAPDH immunoreactivity was predominantly membrane associated and colocalized with AE1. In the kidney medulla, GAPDH was concentrated in the basolateral membrane of type A intercalated cells, where it colocalized with the alternatively spliced kidney form of AE1. GAPDH immunoreactivity was not detected in the plasma membrane of any other cell type in the kidney, indicating its predominant association with AE1-rich membranes. If this membrane interaction occurs via AE1 binding, then GAPDH must have binding sites in addition to those previously described for such binding in human AE1.

scholarly journals Identification of the glucose transporter in mammalian cell membranes with a125I-forskolin photoaffinity label

1988 ◽  
Vol 255 (3) ◽  
pp. 983-990 ◽  
Author(s):  
B E Wadzinski ◽  
M F Shanahan ◽  
R B Clark ◽  
A E Ruoho
Keyword(s):  
Smooth Muscle ◽  
Molecular Mass ◽  
Mammalian Cell ◽  
Cell Membranes ◽  
Plasma Membranes ◽  
Glucose Transporter ◽  
Apparent Molecular Mass ◽  
Synaptic Membranes ◽  
Placental Membranes ◽  
Adipocyte Plasma Membranes

The glucose transporter has been identified in a variety of mammalian cell membranes using a photoactivatable carrier-free radioiodinated derivative of forskolin, 3-[125I]iodo-4-azidophenethylamido-7-O-succinyldeacetylforskoli n ([125I]IAPS-forskolin) at 1-3 nM. The membranes that were photolabelled with [125I]IAPS-forskolin were human placental membranes, rat cortical and cerebellar synaptic membranes, rat cardiac sarcolemmal membranes, rat adipocyte plasma membranes, smooth-muscle membranes, and S49 wild-type (WT) lymphoma-cell membranes. The glucose transporter in plasma membranes prepared from the insulin-responsive rat cardiac sarcolemmal cells, rat adipocytes and smooth-muscle cells were determined to be approx. 45 kDa by SDS/polyacrylamide-gel electrophoresis (PAGE). Photolysis of human placental membranes, rat cortical and cerebellar synaptic membranes, and WT lymphoma membranes with [125I]-IAPS-forskolin, followed by SDS/PAGE, indicated specific derivatization of a broad band (43-55 kDa) in placental membranes and a narrower band (approx. 45 kDa) in synaptic membranes and WT lymphoma membranes. Digestion of the [125I]IAPS-forskolin-labelled placental and WT lymphoma membranes with endo-beta-galactosidase showed a reduction in the apparent molecular mass of the radiolabelled band to approx. 40 kDa. The membranes that were photolabelled with [125I]IAPS-forskolin and trypsin-treated produced a radiolabelled proteolytic fragment with an apparent molecular mass of 18 kDa. [125I]IAPS-forskolin is a highly effective probe for identifying low levels of glucose transporters in mammalian tissues.

VIP stimulation of β-naphthylamidase activity in guinea-pig thyroid sections

1985 ◽  
Vol 109 (4) ◽  
pp. 505-510 ◽  
Author(s):  
P. A. Ealey ◽  
N.J. Marshall ◽  
R. P. Ekins
Keyword(s):  
Dose Response ◽  
Response Curve ◽  
Receptor Site ◽  
Dose Response Curve ◽  
Tsh Receptor ◽  
Maximal Response ◽  
Cytochemical Bioassay ◽  
Order Of Magnitude ◽  
Specific Receptors ◽  
Stimulation Of

Abstract. Subsequent to the discovery of vasoactive intestinal peptide (VIP) in the thyroid gland, VIP has been shown to stimulate various thyroid functions. The site of interaction of VIP with the thyroid follicular cell is at present not known, and this study has used the ultrasensitive cytochemical bioassay (CBA) for thyroid stimulators to investigate this further. Exposure of thyroid sections for 3 min to VIP resulted in increased naphthylamidase activity, with half-maximal response observed at 3 × 10−13 m VIP. This response to such low doses of VIP is consistent with the CBA being ultrasensitive to other thyroid stimulators e.g. TSH, thyroid stimulating antibodies and forskolin. The response to VIP was abolished by rabbit anti-VIP antiserum. The dose-response curve to VIP was bell-shaped (as with the other stimulators), maximal stimulation occurring at 10−12 m VIP. In contrast, however, to other thyroid stimulators, namely TSH, LATS-B and 3 monoclonal stimulating antibodies, whose ascending limbs of the doseresponse curves extended over 3-4 orders of magnitude, the VIP curve rose rapidly from basal to maximal tissue stimulation from 10−13 to 10−12m VIP, i.e. one order of magnitude. This unusual dose-response curve to VIP was parallel to that produced by forskolin. 11E8, a monoclonal 'blocking' antibody which is a potent inhibitor of TSH stimulation, did not 'block' forskolin stimulation, consistent with the belief that forskolin acts at a post-receptor site. However, unlike forskolin, VIP was inhibited by monoclonal 11E8, which may imply a hitherto unexpected involvement of the TSH receptor in VIP stimulation of the thyroid or, alternatively, steric inhibition by 11E8 when bound to the TSH receptor of VIP interaction with adjacent VIP-specific receptors.

scholarly journals Short communications. Subunit A from cholera toxin is an activator of adenylate cyclase in pigeon erythrocytes

1975 ◽  
Vol 146 (1) ◽  
pp. 269-271 ◽  
Author(s):  
S Van Heyningen ◽  
C A King
Keyword(s):  
Adenylate Cyclase ◽  
Cholera Toxin ◽  
Cell Membranes ◽  
Erythrocyte Membranes ◽  
Subunit A ◽  
Subunit B

Intact cholera toxin and its purified subunit A both activate the adenylate cyclase of pigeon erythrocyte membranes, but subunit B does not. The activation by subunit A is unaffected by treatments that inhibit whole toxin by interfering with the binding of subunit B to cell membranes.

scholarly journals Types of vegetative reactions in healthy people at different level of Na+/Li+ countertransport in erythrocyte membranes

1998 ◽  
Vol XXX (1-2) ◽  
pp. 26-35
Author(s):  
D. R. Khasanova
Keyword(s):  
Functional Status ◽  
Cell Membranes ◽  
Healthy People ◽  
Erythrocyte Membranes ◽  
Genetically Determined

Types of vegetative responding were studied with evaluation of initial vegetative reactions and vegetative activity in healthy people, aged from 7-42, in association with one of the markers of genetically determined structural and functional status of cell membranes - velocity of Na+/Li+ countransport in erythrocyte membranes. It was found that level of intensity of vegetative effects with transition of adaptation reactions to orthostasis is most characterestic of high values of transmembrane monotransport velocity.

scholarly journals Indicators of adrenergic reactivity of erythrocyte membranes in patients with myocardial infarction and nonobstructive atherosclerosis of the coronary arteries after 1 year

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
D Vorobyeva ◽  
TYU Rebrova ◽  
SA Afanasyev ◽  
VV Ryabov
Keyword(s):  
Cell Membranes ◽  
Acute Myocarditis ◽  
The Body ◽  
Erythrocyte Membranes ◽  
Control Group ◽  
Index Hospitalization ◽  
Funding Sources ◽  
Artery Disease ◽  
Time Of Admission ◽  
And Control

Abstract Funding Acknowledgements Type of funding sources: None. Background We hypothesized that MINOCA patients have distinctive features of sympatho-adrenal system (SAS) activation in comparison with patients with stenosis atherosclerosis which can play a significant role in the development of ischemic events at the time of the index hospitalization and after 1 year. Aim To study the parameters of β-adrenoreception of cell membranes in patients with MINOCA compared with patients with AMI and single-vessel coronary artery disease after 1 year. Material and methods: The study is non-randomized open controlled. Adrenergic reactivity of the body was assessed by the method for assessing the β-adrenergic reactivity of erythrocyte membranes (β-ARM) for studying the parameters of adrenergic reception of cell membranes. This parameter (β-ARM) was studied upon admission, at days 2, 4 and 7 and 1 year after AMI. The normal level of β- ARM <20 rel.units. Results The study included 40 patients with AMI (19 patients in the main group and 21 patients in the control group). Three patients (15.7%) with diagnosed acute myocarditis were excluded from the analysis. The median age in the main and control groups was 66 (54; 70) years and 59 (55; 65) years, respectively. These groups were different at the admission in such parameters: in smoking frequency (31,3% vs 52.3%), history of angina pectoris (62,5% vs 28,5%), time of admission to the hospital (390 min. vs 180 min.) and thrombolytic therapy at the prehospital phase (3% vs 11%), p < 0,05.  The median β-ARM in MINOCA patients upon admission was 41.7 (29.0; 61.5) rel. units, 1 day - 48.6 (38.5; 57.3) rel. units, 4 days - 49, 4 (39.0; 63.3) rel. units, 7 days - 53.5 (35.2; 67.7) rel. units, after 1 year - 35.7 (25.5; 42.6) rel. units. In the control group, the median β-ARM upon admission was 52.5 (25.4; 64.5) rel. units, 1 day –51.6 (28.3; 56.9) rel. units, 4 days - 48, 5 (34.9; 61.2) rel. units, 7 days - 45.1 (32.2; 68.9) rel. units, after 1 year - 20.8 (14.8; 29.3). In MINOCA patients β-ARM indices in the early postinfarction period statistically higher than the 1 year:  at  1, 2, 4 days, p <0.05, on day 7 no differences were found (p = 0.34). A dynamic comparison of β-ARM indicators in the control group at the time of the index hospitalization and through 1 year revealed differences  at all days early postinfarction period, p <0.05. In the control group, the β-ARM indicator reached normal values by 1-year follow-up period. In MINOCA patients, β-ARM indices after 1 year were statistically higher than in the control group, p = 0.008. Conclusions: The β - ARM indices in MINOCA patients after 1 year from the ischemic event are higher than in the control group. In dynamics, the β - ARM indices statistically decreased in the control group, but did’n change in MINOCA patients. Despite the use of a beta-blocker in MINOCA patients, increased SAS activity persists; therefore, β-APM values did’n change significantly after 1 year.

scholarly journals Genes and Dietary Fatty Acids in Regulation of Fatty Acid Composition of Plasma and Erythrocyte Membranes

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1785 ◽  
Author(s):  
Maria Lankinen ◽  
Matti Uusitupa ◽  
Ursula Schwab
Keyword(s):  
Fatty Acids ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Cell Membranes ◽  
Dietary Fatty Acids ◽  
Erythrocyte Membranes ◽  
Extensive Literature ◽  
Chromosome 11 ◽  
Fatty Acid Compositions

The fatty acid compositions of plasma lipids and cell membranes of certain tissues are modified by dietary fatty acid composition. Furthermore, many other factors (age, sex, ethnicity, health status, genes, and gene × diet interactions) affect the fatty acid composition of cell membranes or plasma lipid compartments. Therefore, it is of great importance to understand the complexity of mechanisms that may modify fatty acid compositions of plasma or tissues. We carried out an extensive literature survey of gene × diet interaction in the regulation of fatty acid compositions. Most of the related studies have been observational studies, but there are also a few intervention trials that tend to confirm that true interactions exist. Most of the studies deal with the desaturase enzyme cluster (FADS1, FADS2) in chromosome 11 and elongase enzymes. We expect that new genetic variants are being found that are linked with the genetic regulation of plasma or tissue fatty acid composition. This information is of great help to understanding the contribution of dietary fatty acids and their endogenic metabolism to the development of some chronic diseases.

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