Ultrastructural changes in the plasma membrane and sarcoplasmic reticulum of myocardial cells during hibernation

Cryobiology ◽  
1970 ◽  
Vol 7 (1) ◽  
pp. 14-18 ◽  
Author(s):  
T.H. Rosenquist
Keyword(s):  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Ultrastructural Changes ◽  
Myocardial Cells

Ultrastructural Changes Produced in Cultured, Adriamycin-Treated Myocardial Cells,

1976 ◽  
Vol 62 (5) ◽  
pp. 537-543 ◽  
Author(s):  
Anna Necco ◽  
Teresa Dasdia ◽  
Silvia Cozzi ◽  
Marco Ferraguti
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Gap Junctions ◽  
Ultrastructural Changes ◽  
Heart Cells ◽  
Myocardial Cells

The ultrastructural evaluation of the early alterations adriamycin-induced on cultured mice heart cells is reported. The major effects are hypertrophy of the sarcoplasmic reticulum and a market increase of the number and total extension of the gap junctions. These findings are discussed in the light of the information available in the literature.

scholarly journals Spontaneous calcium release in tissue from the failing canine heart

2009 ◽  
Vol 297 (4) ◽  
pp. H1235-H1242 ◽  
Author(s):  
Gregory S. Hoeker ◽  
Rodolphe P. Katra ◽  
Lance D. Wilson ◽  
Bradley N. Plummer ◽  
Kenneth R. Laurita
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Tissue Level ◽  
Calcium Handling ◽  
Canine Heart ◽  
Myocardial Cells ◽  
Spontaneous Release ◽  
Adrenergic Stimulation ◽  
Electrical Instability ◽  
Delayed Afterdepolarization

Abnormalities in calcium handling have been implicated as a significant source of electrical instability in heart failure (HF). While these abnormalities have been investigated extensively in isolated myocytes, how they manifest at the tissue level and trigger arrhythmias is not clear. We hypothesize that in HF, triggered activity (TA) is due to spontaneous calcium release from the sarcoplasmic reticulum that occurs in an aggregate of myocardial cells (an SRC) and that peak SCR amplitude is what determines whether TA will occur. Calcium and voltage optical mapping was performed in ventricular wedge preparations from canines with and without tachycardia-induced HF. In HF, steady-state calcium transients have reduced amplitude [135 vs. 170 ratiometric units (RU), P < 0.05] and increased duration (252 vs. 229 s, P < 0.05) compared with those of normal. Under control conditions and during β-adrenergic stimulation, TA was more frequent in HF (53% and 93%, respectively) compared with normal (0% and 55%, respectively, P < 0.025). The mechanism of arrhythmias was SCRs, leading to delayed afterdepolarization-mediated triggered beats. Interestingly, the rate of SCR rise was greater for events that triggered a beat (0.41 RU/ms) compared with those that did not (0.18 RU/ms, P < 0.001). In contrast, there was no difference in SCR amplitude between the two groups. In conclusion, TA in HF tissue is associated with abnormal calcium regulation and mediated by the spontaneous release of calcium from the sarcoplasmic reticulum in aggregates of myocardial cells (i.e., an SCR), but importantly, it is the rate of SCR rise rather than amplitude that was associated with TA.

Abstract 274: Spatiotemporal Regulation of β Adrenergic Signaling In Heart failure

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Yang K Xiang ◽  
Federica Barbagallo ◽  
Bing Xu ◽  
Qin Fu
Keyword(s):  
Heart Failure ◽  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Myocytes ◽  
Cardiac Disease ◽  
Spatiotemporal Regulation ◽  
Disease Therapy ◽  
Functional Implications ◽  
Underlying Mechanisms

Our long-term goal is to understand mechanisms that govern spatiotemporal regulation of cAMP/PKA signaling in cardiac myocytes under physiological and pathophysiological conditions, and their implication in cardiac disease therapy. Here we use a series of biosensors to measure cAMP/PKA activity under βAR subtype regulation. In failing cardiac myocytes, the cAMP and PKA activity are shifted from the plasma membrane to the intracellular sarcoplasmic reticulum and the myofilaments. Meanwhile, β2AR displays an increased role in signaling to the myofilaments in failing myocytes when compared to the control myocytes. Moreover, we show that an increased βAR association with phosphodiesterases promotes the alteration in spatiotemporal propagation of cAMP/PKA signaling in failing myocytes. These observations and the underlying mechanisms and functional implications will be discussed.

Ultrastructural Changes in the Surface Layers of the Newt's Egg in Relation to the Mechanism of Its Cleavage

1970 ◽  
Vol 6 (1) ◽  
pp. 207-227 ◽  
Author(s):  
G. G. SELMAN ◽  
M. M. PERRY
Keyword(s):  
Plasma Membrane ◽  
Leading Edge ◽  
Ultrastructural Changes ◽  
Cortical Layers ◽  
Active Growth ◽  
Structural Modifications ◽  
Cell Cleavage ◽  
Surface Irregularities ◽  
Dense Band ◽  
10 Nm Filaments

The surface and cortical layers of an uncleaved newt egg have a characteristic ultrastructure which remains unaltered during cleavage; ultrastructural changes are confined to the region of the furrow. At the onset of cleavage there is a dipping inwards of the rough heavily pigmented animal surface to form a groove. Along the bottom of the groove the surface irregularities are reduced and a dense band (0.1 µm thick and 16 µm wide) is formed immediately below the plasma membrane. Within this band there are parallel filaments, 8-10 nm in diameter, oriented in the direction of the future furrow. No structural modifications were observed below the cortical layers of the leading part of the furrow apart from accumulations of granules and the mid-bodies of the spindle remnant. It is proposed that the dipping-in of the groove is due to contraction within the filamentous band, rather than contraction in a sheet of subcortical gel as proposed previously. The filamentous band persists below the furrow during the later stages of cleavage. The new unpigmented surface first forms as a strip across the animal surface and begins to grow at the bottom of the groove. Over most of its area, it is much smoother than the pigmented surface and has less material on the outside of the plasma membrane. There are microvilli along the bottom of the groove. The join between the new unpigmented and the old pigmented surface is abrupt. As the new unpigmented surface grows in extent, a narrow furrow forms below the lowest part of the groove and progresses towards the vegetal surface. For most of its length the furrow is between 10-nm and 0.5 µm wide, but at its leading edge it is 2 µ wide with microvilli on its surface and 10-nm filaments below the plasma membrane. It is concluded that the progressive formation of the furrow is due to active growth of new unpigmented cell surface. At late cleavage a ridge 10 µm high forms at the join between the new and old surface. After cleavage the ridges approach and meet to form the intercellular junction by which daughter blastomeres are held together along the animal surface. The mechanism of cell cleavage in the newt egg and in other forms is discussed in the light of the present observations.

scholarly journals Ultrastructural Changes in Bovine Lingual Epithelium Infected with Vesicular Stomatitis Virus

1975 ◽  
Vol 12 (5-6) ◽  
pp. 362-377 ◽  
Author(s):  
S. J. Proctor ◽  
K. C. Sherman
Keyword(s):  
Plasma Membrane ◽  
Vesicular Stomatitis Virus ◽  
Ultrastructural Changes ◽  
Intercellular Spaces ◽  
Lingual Epithelium ◽  
Vesicular Stomatitis

Vesicular stomatitis virus was inoculated into the dorsal lingual epithelium of three cows. The reaction that developed in 72 h was characterized by severe acute diffuse glossitis with intercellular edema and necrosis of keratinocytes. Virions budded from the plasma membrane and were in the intercellular spaces. Reduplication of desmosomes was a prominent alteration, and normal desmosomes were within the cytoplasm. Intracytoplasmic desmosomes appeared to be formed by endocytosis after breaks occurred in the plasma membrane of one cell; endocytosis of loops of plasma membrane containing desmosomes; and formation of desmosomes on invagination of the plasma membrane.

scholarly journals Anchorage of secretion-competent dense granules on the plasma membrane of bovine platelets in the absence of secretory stimulation.

1990 ◽  
Vol 111 (1) ◽  
pp. 79-86 ◽  
Author(s):  
T Morimoto ◽  
S Ogihara ◽  
H Takisawa
Keyword(s):  
Plasma Membrane ◽  
Average Distance ◽  
Ultrastructural Changes ◽  
Thin Sections ◽  
Regulated Exocytosis ◽  
Permeabilized Cells ◽  
Dense Granules ◽  
Amorphous Structures ◽  
Stimulation Of

The ultrastructural changes in electropermeabilized bovine platelets that accompany the Ca2(+)-induced secretion of serotonin were investigated in ultra-thin sections of chemically fixed cells. Such preparations permitted us to study both the localization of and the structures associated with serotonin-containing dense granules. Localization of dense granules within cells was examined by measuring the shortest distances between the granular membranes and the plasma membrane. About 40% of total granules were located close to the plasma membrane at an average distance of 10.8 +/- 1.6 nm. 71% of the total number of granules were localized at a similar average distance of 12.5 +/- 2.7 nm in intact platelets. The percentage of granules apposed to the plasma membrane corresponded closely to the percentage of total serotonin that was maximally secreted after stimulation of the permeabilized (38 +/- 4.9%) and the intact platelets (72 +/- 3.6%). Furthermore, the percentage of granules anchored to the membrane, but not of those in other regions of permeabilized cells, decreased markedly when cells were stimulated for 30 s by extracellularly added Ca2+. The decrease in the numbers of granules in the vicinity of the plasma membrane corresponded to approximately 22% of the total number of dense granules that were used for measurements of the distances between the two membranes and corresponded roughly to the overall decrease (15%) in the average number of the granules per cell. Most dense granules were found to be associated with meshwork structures of microfilaments. Upon secretory stimulation, nonfilamentous, amorphous structures found between the plasma membrane and the apposed granules formed a bridge-like structure that connected both membranes without any obvious accompanying changes in the microfilament structures. These results suggest that the dense granules that are susceptible to secretory stimulation are anchored to the plasma membrane before stimulation, and that the formation of the bridge-like structure may participate in the Ca2(+)-regulated exocytosis.

Sign in / Sign up

Export Citation Format

Share Document