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Results for “Cell Communication”

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At least 325 records · Page 18Linked to original sources
PubMed1991

Cell-cell communication in the testis.

In addition to the well-established endocrine regulation of testicular functions by gonadotropins, many data accumulated in the last few years indicate that a local control is required for a normal production of androgens and spermatogenesis. In the present paper we review the cell-cell interactions between somatic and germ cells in the testis and their role on the function of each cell type. Also, we will present evidences indicating that some of these interactions are mediated by several growth factors produced and acting within the testis. Moreover, very often the production of these factors are under control of gonadotropins, and in turn the growth factors regulate the sensitivity of testicular cells to these hormones.

Animals↗
PubMed1986

Blockage of cell-to-cell communication within pancreatic acini is associated with increased basal release of amylase.

To assess whether junctional coupling is involved in the secretory activity of pancreatic acinar cells, dispersed rat acini were incubated for 30 min in the presence of either heptanol (3.5 mM) or octanol (1.0 mM). Exposure to either alkanol caused a marked uncoupling of the acinar cells which, in control acini, were extensively coupled. Uncoupling was associated with an increased basal release of amylase that was at least twice that of controls. By contrast, carbamylcholine (10(-5) M)-induced maximal amylase secretion, cytosolic pH, and free Ca2+, as well as the structure of gap junctions joining the acinar cells, were unaffected. Both uncoupling and the alteration of basal secretion were already observed after only 5 min of exposure to heptanol, they both persisted throughout the 30-min exposure to the alkanols, and were reversible after removal of either heptanol or octanol. Since neither of the two uncouplers appeared to alter unspecifically the secretory machinery and the nonjunctional membrane of acinar cells, the data are consistent with the view that junctional coupling participates in the control of the basal secretion of acinar cells.

Alcohols↗
PubMedDate not supplied

Do changes in the cell membrane structure induce the generation of lipid peroxidation products which serve as first signalling molecules in cell to cell communication?

Evidence is presented that mammalian and plant cells respond equally to any event which changes their cell membrane structure. Proliferation, wounding or aging induces generation of lipidhydroperoxides from cell wall phospholipids. These are transformed to signalling compounds, some of these induce apoptosis. If the exerted impact exceeds a certain level, the original enzymic reaction switches to a non-enzymic one which produces peroxylradicals. The latter are not liberated enzymically. Peroxylradicals generate a second set of signalling compounds, but cause also severe damage: they epoxidize double bonds, and oxidize proteins, sugars and nucleic acids. Such reactions occur in all inflammatory diseases. Lipidhydoperoxides and their degradation products are incorporated in fat. Apparently, these compounds are transferred partly to LDL. Such LDL is still recognized by the cell LDL receptor. Toxic lipid peroxidation products are therefore introduced into cells and might be able to damage cells from inside long before the typical signs of atherosclerosis and other chronic diseases become visible.

Animals↗
PubMed2004

Kidney-bone, bone-kidney, and cell-cell communications in renal osteodystrophy.

The relationship between bone and the kidney in renal osteodystrophy is a complex interplay of kidney to bone connections, bone to kidney connections, and cell to cell connections. In addition, such interactions have a profound effect on the vasculature. In this review, we discuss the role of the bone morphogenetic proteins (BMPs) in the skeleton, kidney, and vasculature. In addition, we propose that deficiencies of these BMPs seen in chronic kidney disease (CKD) result in decreased bone remodeling and a compensatory secondary hyperparathyroidism (high turnover state). Treatment of the hyperparathyroidism blocks this compensatory arm and thus decreased bone remodeling occurs (low turnover). We review animal models of CKD in which treatment with BMP-7 resulted in normalization of both high and low turnover states. Finally, we discuss vascular calcification as it relates to bone metabolism. We discuss the roles of BMP-7 and 2 other bone regulatory proteins, osteoprotegerin (OPG) and alpha2-HS glycoprotein (AHSG, human fetuin), in the human vasculature and their implications for vascular calcification.

Bone Morphogenetic Proteins↗
PubMed1993

Effects of submicromolar concentrations of dopamine on photoreceptor to horizontal cell communication.

Dopamine has been postulated to act as an intraretinal messenger for light adaptation by biasing retinal circuits to favor cone over rod inputs to second- and third-order neurons. As an experimental test, we studied the effects of dopamine and related ligands on rod to horizontal cell synaptic transfer. Rods and horizontal cells (HC) were recorded from simultaneously. Red and green light-emitting diodes were modulated sinusoidally in counterphase at 1 Hz and their relative intensities adjusted to elicit a rod null. Dark-adapted HC's also showed a null, but exposure to 0.5-1.0 microM dopamine, which corresponds to the endogenous levels, elicited a large imbalance in the HC response while the rod null was maintained. Similar effects were achieved with either a D1 dopamine agonist, SKF 38393 (20 microM) or a D2 dopamine agonist, quinpirole HCl (1 microM). Correspondingly, the frequency range over which the HC responded to red flickering lights increased very substantially. Exposure to a D2, but not a D1 dopamine agonist increased rod flicker, but not as dramatically as in the HC. These data indicate that the synaptic gains of rod and cone transmission to a second order retinal neuron are modifiable by endogenous levels of dopamine. Secondly, the bandpass of rod flicker is altered by dopamine, acting through a D2 dopamine receptor.

Animals↗
PubMed1996

Impaired regulation of cell communication by beta-adrenergic receptor activation in the failing heart.

We investigated the influence of beta-adrenergic receptor activation on the control of gap junctional conductance (gj) in the heart of cardiomyopathic hamsters (11 months old). We measured gj in isolated ventricular cell pairs using two voltage-clamp circuits. Administration of isoproterenol (10(-6) mol/L) to the bath had no effect on gj in myopathic cell pairs but increased gj by 45 +/- 3% (+/- SE) in normal hamsters. Moreover, forskolin (10(-7) mol/L), an activator of adenyl cyclase, did not change gj in myopathic cells but enhanced gj by 23 +/- 2.8% in controls. Similar results were obtained with isobutylmethylxanthine (10(-6) mol/L), a phosphodiesterase inhibitor. Dibutyryl-cAMP (10(-6) mol/L), however, increased gj of cardiomyopathic cell pairs by 58 +/- 2.1% within 2 minutes and enhanced gj in controls by 50 +/- 3.6%. The effect of dibutyryl-cAMP on gj of myopathic cells was suppressed by intracellular dialysis of an inhibitor of protein kinase A. These observations indicate that the regulation of gj by the beta-adrenergic receptor-G protein-adenyl cyclase signaling system is greatly impaired in the failing heart but the ability of cAMP to increase gj is still preserved.

1-Methyl-3-isobutylxanthine↗