Elevation of Protein Kinase C in Thyrocytes Isolated from a Lewis Rat Model of Autoimmune Thyroiditis Prevents Assembly of Immunodetectable Connexin43 Gap Junctions and Reduces Intercellular Communication

Thyroid ◽  
1997 ◽  
Vol 7 (6) ◽  
pp. 913-921 ◽  
Author(s):  
L.M. GREEN ◽  
J.P. LAZARUS ◽  
X. SONG ◽  
R.B. STAGG ◽  
M. LaBUE ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Gap Junctions ◽  
Rat Model ◽  
Intercellular Communication ◽  
Autoimmune Thyroiditis ◽  
Lewis Rat ◽  
Kinase C ◽  
Connexin43 Gap Junctions

Protein kinase C-dependent regulation of connexin43 gap junctions and hemichannels

2015 ◽  
Vol 43 (3) ◽  
pp. 519-523 ◽  
Author(s):  
Jette Skov Alstrom ◽  
Line Waring Stroemlund ◽  
Morten Schak Nielsen ◽  
Nanna MacAulay
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Gap Junctions ◽  
Fluorescent Dyes ◽  
Current Knowledge ◽  
Physiological Role ◽  
Kinase C ◽  
C Terminus ◽  
Gap Junctional ◽  
Connexin43 Gap Junctions

Connexin43 (Cx43) generates intercellular gap junction channels involved in, among others, cardiac and brain function. Gap junctions are formed by the docking of two hemichannels from neighbouring cells. Undocked Cx43 hemichannels can upon different stimuli open towards the extracellular matrix and allow transport of molecules such as fluorescent dyes and ATP. A range of phosphorylated amino acids have been detected in the C-terminus of Cx43 and their physiological role has been intensively studied both in the gap junctional form of Cx43 and in its hemichannel configuration. We present the current knowledge of protein kinase C (PKC)-dependent regulation of Cx43 and discuss the divergent results.

scholarly journals Rho Kinase and Protein Kinase C Pathways are Responsible for Enhanced Carbachol Contraction in Permeabilized Detrusor in a Rat Model of Cystitis

2018 ◽  
Vol 123 (5) ◽  
pp. 567-576
Author(s):  
Merve Denizalti ◽  
Nezahat Tugba Durlu-Kandilci ◽  
Gul Simsek ◽  
Turgut Emrah Bozkurt ◽  
Inci Sahin-Erdemli
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Rat Model ◽  
Rho Kinase ◽  
Kinase C

scholarly journals Pharmacologic inhibition of Protein Kinase C α and Protein Kinase C β halts renal function decline indirectly, by blunting hyperphagia, and directly reduces adiposity in the ZSF1 rat model of type 2 diabetes

2020 ◽  
Author(s):  
Ju Wang ◽  
Agustin Casimiro-Garcia ◽  
Bryce G. Johnson ◽  
Jennifer Duffen ◽  
Michael Cain ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Renal Function ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Rat Model ◽  
Therapeutic Potential ◽  
Metabolic Derangement ◽  
Renal Function Decline ◽  
Kinase C

AbstractType 2 diabetes (T2D) and its complications can have debilitating, sometimes fatal consequences. Despite advances that address some of the metabolic aspects of T2D, for many patients these approaches do not sufficiently control the disease. As a result, an emerging therapeutic strategy is to target the pathobiological mechanisms downstream of T2D metabolic derangement that can result in organ damage, morbidity, and mortality in afflicted individuals. One such proposed mechanism involves the Protein Kinase C (PKC) family members PKCα and PKCβ, which have been linked to diabetes-induced tissue damage to organs including the kidneys. To evaluate the therapeutic potential of dual inhibition of PKCα and PKCβ in the context of T2D, we have evaluated a potent and orally bioavailable inhibitor, herein referred to as Cmpd 1, in the ZSF1 rat model of leptin-receptor deficiency, obesity-driven T2D. Therapeutic dosing of Cmpd 1 virtually halted renal function decline but did so indirectly by blunting the hyperphagia response of these animals. Beyond this clear but indirect effect, Cmpd 1 had direct and prominent effects on body weight and in liver and inguinal white adipose tissue (iWAT) when administered to ZSF1 obese rats.

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