scholarly journals Mitochondria in the Nuclei of Rat Myocardial Cells

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 712 ◽  
Author(s):  
Chupalav M. Eldarov ◽  
Irina M. Vangely ◽  
Valeriya B. Vays ◽  
Eugene V. Sheval ◽  
Susanne Holtze ◽  
...  
Keyword(s):  
Direct Interaction ◽  
Mitochondrial Network ◽  
Myocardial Cells ◽  
Biological Phenomenon ◽  
Electron Microscopic ◽  
Heterocephalus Glaber ◽  
Interfibrillar Mitochondria ◽  
Normal Rat ◽  
Rat Cardiac Myocytes ◽  
Species Dependency

Electron microscopic study of cardiomyocytes taken from healthy Wistar and OXYS rats and naked mole rats (Heterocephalus glaber) revealed mitochondria in nuclei that lacked part of the nuclear envelope. The direct interaction of mitochondria with nucleoplasm is shown. The statistical analysis of the occurrence of mitochondria in cardiomyocyte nuclei showed that the percentage of nuclei with mitochondria was roughly around 1%, and did not show age and species dependency. Confocal microscopy of normal rat cardiac myocytes revealed a branched mitochondrial network in the vicinity of nuclei with an organization different than that of interfibrillar mitochondria. This mitochondrial network was energetically functional because it carried the membrane potential that responded by oscillatory mode after photodynamic challenge. We suggest that the presence of functional mitochondria in the nucleus is not only a consequence of certain pathologies but rather represents a normal biological phenomenon involved in mitochondrial/nuclear interactions.

Nuclear location of PLA2-I in proliferative cells

1998 ◽  
Vol 111 (7) ◽  
pp. 985-994 ◽  
Author(s):  
J.M. Fayard ◽  
C. Tessier ◽  
J.F. Pageaux ◽  
M. Lagarde ◽  
C. Laugier
Keyword(s):  
Binding Sites ◽  
Culture Medium ◽  
Aristolochic Acid ◽  
Direct Interaction ◽  
Nuclear Level ◽  
Proliferative Effect ◽  
Stromal Cell Line ◽  
Normal Rat ◽  
Nuclear Location ◽  
Insight Into

We have previously demonstrated that pancreatic PLA2 (PLA2-I) stimulates the proliferation of UIII cells, a stromal cell line derived from normal rat uterus. In order to gain further insight into the mechanism of action of PLA2-I, we have investigated the intracellular processing of PLA2-I. Either highly proliferative or growth arrested UIII cells were analyzed. Growth arrested cells were obtained from a contact inhibited monolayer or from aristolochic acid-treated cultures. Using cellular fractionation, western blotting, immunocytochemistry and confocal microscopy, we demonstrate that endogenous PLA2-I was mainly located in the nucleus in highly proliferative cells whereas its location was cytoplasmic in non proliferative cells. When non confluent UIII cells were incubated with nanomolar amounts of exogenous PLA2-I, the enzyme was internalized and, in the majority of cells, appeared within the nucleus. Both internalization and nuclear location of exogenous PLA2-I were suppressed by the addition of aristolochic acid to the culture medium. Binding experiments performed on purified nuclear preparations showed the presence of specific cooperative binding sites for PLA2-I. Collectively our data suggest that the proliferative effect exerted by pancreatic PLA2 in UIII cells is mediated by a direct interaction of the enzyme at the nuclear level. Putative mechanisms and targets are discussed.

scholarly journals Chronic amphotericin nephropathy: morphometric, electron microscopic, and functional studies.

1993 ◽  
Vol 4 (1) ◽  
pp. 69-80
Author(s):  
S N Heyman ◽  
I E Stillman ◽  
M Brezis ◽  
F H Epstein ◽  
K Spokes ◽  
...  
Keyword(s):  
Renal Failure ◽  
Epithelial Cell ◽  
Direct Interaction ◽  
Lymphocytic Infiltration ◽  
Normal Serum ◽  
Electron Microscopic ◽  
Functional Studies ◽  
Salt Depletion ◽  
Direct Toxicity ◽  
Normal Serum Creatinine

The two major hypotheses for the pathogenesis of amphotericin nephrotoxicity are direct interaction with epithelial cell membranes and vasoconstriction. Studies indicating the special vulnerability of the medullary ray and medulla to hypoxia led to a reexamination of amphotericin nephrotoxicity. Twenty-four rats were divided into four groups: amphotericin injection (5 mg/kg daily for 3 wk), amphotericin plus salt depletion, vehicle, and salt depletion and vehicle. The amphotericin group had polyuria (P < 0.01) but normal serum creatinine. In contrast, amphotericin plus salt depletion rats exhibited renal failure (creatinine of 1.49 +/- 0.05 versus amphotericin alone 0.98 +/- 0.01; P < 0.01). Semiquantitative histologic analysis of cortical and medullary injury correlated with functional impairment. Cortical changes in the amphotericin group were largely restricted to the medullary ray, where focal rupture and calcification of thick ascending limbs were noted. The S2/S3 tubules in the medullary rays showed focally diminished cell complexity with histiocytic/lymphocytic infiltration. However, calcification was also seen in the area of the macula densa. Morphometry revealed that the thick ascending limbs in the medulla were hypertrophied (1,420 +/- 63 versus 1,195 +/- 48 microns 2 for vehicle; P < 0.05). In contrast, in the amphotericin and salt depletion group, the changes in the medullary ray extended to the labyrinth and the thick ascending limbs in the inner stripe showed atrophic changes (772 +/- 23 microns 2; P < 0.01 versus vehicle). Thus, changes as a result of amphotericin toxicity take place both in areas known to be most vulnerable to hypoxia (medullary ray and medulla), and in areas rich in oxygen (adjacent to glomerulus). Salt depletion potentiates the cortical changes and converts medullary hypertrophy to atrophy. These findings support a dual pathogenesis for amphotericin nephropathy (direct toxicity and vasoconstriction).

scholarly journals Effect of adrenaline and corticosterone on uptake and distribution atherogenic and antiatherogenic lipoproteins in the myocardium

2004 ◽  
Vol 50 (5) ◽  
pp. 45-48
Author(s):  
L. E. Panin ◽  
V. F. Maksimov ◽  
A. R. Kolpakov ◽  
I. M. Korostyshevskaya
Keyword(s):  
Metabolic Pathways ◽  
High Density Lipoproteins ◽  
Capillary Endothelium ◽  
Myocardial Cells ◽  
Electron Microscopic ◽  
Slowing Down ◽  
Endothelial Surface ◽  
Contracting Heart ◽  
Capillary Walls

An electron microscopic study of a model of the rat contracting heart perfused by the Langendorf procedure has indicated the myo¬cardial effects of epinephrine, corticosterone, high density lipoproteins (HDL), and low density lipoproteins (LDL) and revealed a role of hormones in the uptake and intercellular distribution of colloidal gold-labeled lipoproteins. Epinephrine enhanced LDL dis¬solution onto the endothelial surface, by slowing down their myocardial penetration, but failed to affect the penetration and distribution of labeled HDL that did not leave the capillary walls. Corticosterone drastically increased receptor-mediated absorption of HDL by the capillary endothelium and ensured their penetration into the interstitial macrophages, but it did not affect the myocardial pene¬tration of labeled LDL. In all experiments, corticosterone caused the lowered content of glycogen in the myocardial cells, sarcoplasmic sequestration of its residues and their interstitial release. Epinephrine and corticosterone differently affect the myocardial penetration and distribution of atherogenic and antiatherogenic lipoproteins. Under stress, it ensures mobilization of different metabolic pathways for myocardial energy supply.

scholarly journals A Scanning Electron Microscopic Study of the Spleen

Blood ◽  
1974 ◽  
Vol 43 (5) ◽  
pp. 665-691 ◽  
Author(s):  
Leon Weiss
Keyword(s):  
Tissue Preparation ◽  
Electron Microscopic ◽  
Sinus Wall ◽  
Scanning Electron Microscopic Study ◽  
Central Artery ◽  
Normal Rat ◽  
Reticular Cells ◽  
Adventitial Cells ◽  
Migratory Cells ◽  
Scanning Electron

Abstract The reticulum and vascular sinuses of the normal rat spleen were studied by scanning electron microscopy. Observations were also made of erythrocytes, macrophages, platelets, and other migratory elements. Reticular cells of the periarterial lymphatic sheath, the marginal zone, and cordal spaces were large, bulky, irregular cells with broad processes that formed a spongework. When marked retraction of these cells was induced in the drying phase of tissue preparation, they showed the slender multiple fingerlike processes characteristic of the argyrophilic reticulum. The reticular cells at the periphery of the periarterial lymphatic sheath were flattened and formed cylinders about the central artery. They were, moreover, associated with unusually heavy extracellular fibers. Vascular sinuses were suspended in the reticulum by attachments of cordal reticular cells and of fibrillar reticulum to the adventitial surface. Adventitial cells of the sinus, moreover, branched into the cords. Endothelial cells typically lay side by side without gaps, except as migratory cells passed through the wall. Erythrocytes were commonly observed in passage across the sinus wall. In sinuses and cords, they were often swollen, irregular, and bore blebs and crenulations. Macrophages displayed rich surface folds and processes. Platelets were abundant and were adherent to the surface of reticular cells and the endothelium of sinuses. Such adherence appeared to be the manner in which the platelets were sequestered in the spleen.

scholarly journals ULTRASTRUCTURAL IMMUNOCYTOCHEMISTRY WITH UNLABELED ANTIBODIES AND THE PEROXIDASE-ANTIPEROXIDASE COMPLEX A TECHNIQUE MORE SENSITIVE THAN RADIOIMMUNOASSAY

1973 ◽  
Vol 21 (9) ◽  
pp. 825-833 ◽  
Author(s):  
GWEN C. MORIARTY ◽  
C. MICHAEL MORIARTY ◽  
LUDWIG A. STERNBERGER
Keyword(s):  
Staining Intensity ◽  
Poor Quality ◽  
Immunocytochemical Staining ◽  
Great Promise ◽  
Electron Microscopic ◽  
Immunocytochemical Technique ◽  
Titration Curves ◽  
Rat Pituitary ◽  
Normal Rat ◽  
Unlabeled Antibody

Titration curves were developed with antisera to 17-39ACTH (adrenocorticotropin) and 1-39ACTH with the techniques of radioimmunoassay and electron microscopic immunocytochemistry. For the latter method, the unlabeled antibody peroxidase-antiperoxidase complex immunocytochemical technique was used to stain normal rat pituitary intermediate lobes. By radioimmunoassay standards, the 17-39ACTH antiserum was of poor quality. Its titration curve exhibited a flat slope and it did not bind a significant amount of labeled antigen beyond a 1: 30 dilution. However, immunocytochemical staining was detected with this antiserum at dilutions as high as 1:1,500. The antiserum to 1-39ACTH was of better quality by radioimmunoassay standards. It bound 45% of the labeled antigen at a dilution of 1:5,000. Immunocytochemical staining intensity was nearly maximal at a 1:5,000 dilution and decreased progressively to a limiting value at 1:16,000. However, when incubation times in the antisera were increased from 3 min to match those of the radioimmunoassay (48 hr) maximal staining was achieved at dilutions as great as 1:512,000 where only trace amounts of the labeled antigen were bound in the radioimmunoassay. It was concluded that the unlabeled antibody peroxidase-antiperoxidase complex immunocytochemical technique was sensitive enough to detect antibodies in sera of low titer and/or avidity which are not detected by a radioimmunoassay. The technique holds great promise for a sensitive assay system.

Heavy Meromyosin Binding Studies of Myocardial Cells in Cardiac Lethal Mutant Salamanders (Ambystoma Meximanum

1975 ◽  
Vol 33 ◽  
pp. 540-541
Author(s):  
Larry F. Lemanski
Keyword(s):  
Heart Development ◽  
Recessive Gene ◽  
Genetic Mutation ◽  
Heart Beat ◽  
Myocardial Cells ◽  
Binding Studies ◽  
Electron Microscopic ◽  
Lethal Mutant ◽  
Microscopic Studies ◽  
Gross Examination

A naturally-occurring genetic mutation, designated c for “cardiac lethal”, was discovered in Ambystoma meximanum. The effect of homozygosity for recessive gene c is the absence of a heart beat, even though initially heart development appears normal. Mutant embryos are first distinguishable form their normal siblings at Harrison stage 34, when the normals develop contracting hearts. The mutant hearts at this stage, upon gross examination appear structurally normal but fail to beat. Nevertheless, the mutants survive through stage 41, which is about 20 days beyond the heart-beat stage and exhibit normal swimming movements indicating that gene c does not affect skeletal muscle. Electron microscopic studies of normal hearts at stage 34 reveal that the myocardial cells contain organized myofibrils; these myofibrils first form directly beneath the plasma membrane. By stage 41, the normal myocardial cells contain numerous well-organized myofibrils and thus have now become highly differentiated muscle cells.

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