G Protein Alterations in Hypertension and Aging

Hypertension ◽  
1995 ◽  
Vol 26 (5) ◽  
pp. 725-732 ◽  
Author(s):  
R.D. Feldman ◽  
C.M. Tan ◽  
J. Chorazyczewski
Keyword(s):  
G Protein ◽  
Protein Alterations

Glucocorticoids regulate the amount of G proteins in rat aorta

1990 ◽  
Vol 5 (2) ◽  
pp. 185-188 ◽  
Author(s):  
R. M. Haigh ◽  
C. T. Jones ◽  
G. Milligan
Keyword(s):  
G Protein ◽  
G Proteins ◽  
Adrenergic Receptors ◽  
Molecular Mechanisms ◽  
Rat Aorta ◽  
Β Subunit ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Replacement Treatment ◽  
Protein Alterations

ABSTRACT Glucocorticoids are known to influence cardiovascular sensitivity to catecholamines but the molecular mechanisms are undefined. We recently showed that glucocorticoids control the coupling of adrenergic receptors to G protein. Alterations in the amount of G protein is one mechanism by which receptor-G protein coupling may be controlled. Therefore, we set out to measure the levels of G proteins in aorta from normal, adrenalectomized and dexamethasonetreated adrenalectomized rats. G proteins were measured in plasma membrane preparations by immunoblotting and horseradish peroxidase staining. After adrenalectomy there was a 53% (n = 5) decrease in the density of staining for Gi (ANOVA; P<0.05 compared to controls). Conversely, there was a 210% (n = 5) increase in the density of staining for Gs. The levels of Go and the β-subunit of G proteins were not changed by adrenalectomy. Dexamethasone-replacement treatment after adrenalectomy returned Gi and Gs close to control values. Go remained unaltered compared to controls but was 24% (n=3) less than the adrenalectomized values (ANOVA; P<0.05). The levels of β-subunit after dexamethasone replacement were significantly greater (ANOVA; P<0.05) than both the controls and adrenalectomized values. These results show that glucocorticoids can differentially regulate the amounts of G proteins in rat aorta as in other tissues. This may be an important mechanism by which steroids control receptor-G protein coupling and hence transmembrane signalling pathways in vascular smooth muscle.

Formation and Structure of Casein Micelles in Lactating Mammary Tissue

1970 ◽  
Vol 28 ◽  
pp. 150-151
Author(s):  
Robert J. Carroll ◽  
Marvin P. Thompson ◽  
Harold M. Farrell
Keyword(s):  
Size Distribution ◽  
G Protein ◽  
Milk Proteins ◽  
Mammary Tissue ◽  
Colloidal System ◽  
Casein Micelles ◽  
The Stability

Milk is an unusually stable colloidal system; the stability of this system is due primarily to the formation of micelles by the major milk proteins, the caseins. Numerous models for the structure of casein micelles have been proposed; these models have been formulated on the basis of in vitro studies. Synthetic casein micelles (i.e., those formed by mixing the purified αsl- and k-caseins with Ca2+ in appropriate ratios) are dissimilar to those from freshly-drawn milks in (i) size distribution, (ii) ratio of Ca/P, and (iii) solvation (g. water/g. protein). Evidently, in vivo organization of the caseins into the micellar form occurs in-a manner which is not identical to the in vitro mode of formation.

A compendium of G-protein–coupled receptors and cyclic nucleotide regulation of adipose tissue metabolism and energy expenditure

2020 ◽  
Vol 134 (5) ◽  
pp. 473-512 ◽  
Author(s):  
Ryan P. Ceddia ◽  
Sheila Collins
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Signaling Pathways ◽  
G Protein ◽  
Uncoupling Protein ◽  
Beige Adipocytes ◽  
Nucleotide Regulation ◽  
Ucp1 Expression ◽  
Thermogenic Adipocytes ◽  
G Protein Coupled

Abstract With the ever-increasing burden of obesity and Type 2 diabetes, it is generally acknowledged that there remains a need for developing new therapeutics. One potential mechanism to combat obesity is to raise energy expenditure via increasing the amount of uncoupled respiration from the mitochondria-rich brown and beige adipocytes. With the recent appreciation of thermogenic adipocytes in humans, much effort is being made to elucidate the signaling pathways that regulate the browning of adipose tissue. In this review, we focus on the ligand–receptor signaling pathways that influence the cyclic nucleotides, cAMP and cGMP, in adipocytes. We chose to focus on G-protein–coupled receptor (GPCR), guanylyl cyclase and phosphodiesterase regulation of adipocytes because they are the targets of a large proportion of all currently available therapeutics. Furthermore, there is a large overlap in their signaling pathways, as signaling events that raise cAMP or cGMP generally increase adipocyte lipolysis and cause changes that are commonly referred to as browning: increasing mitochondrial biogenesis, uncoupling protein 1 (UCP1) expression and respiration.

791: Endothelial Rehabilitation - The Impact of Chronic PDE5 Inhibitors on Erectile Function and Protein Alterations in Cavernous Tissue of Diabetic Rats

2007 ◽  
Vol 177 (4S) ◽  
pp. 264-265
Author(s):  
Ling De Young ◽  
KokBin Lim ◽  
Jeffery Carson ◽  
Trustin Domes ◽  
Mussa Al-Numi ◽  
...  
Keyword(s):  
Erectile Function ◽  
Diabetic Rats ◽  
Pde5 Inhibitors ◽  
Cavernous Tissue ◽  
Protein Alterations ◽  
The Impact
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