Intermedin1–53 attenuates vascular smooth muscle cell calcification by inhibiting endoplasmic reticulum stress via cyclic adenosine monophosphate/protein kinase A pathway

2013 ◽  
Vol 238 (10) ◽  
pp. 1136-1146 ◽  
Author(s):  
Jin-Rui Chang ◽  
Xiao-Hui Duan ◽  
Bao-Hong Zhang ◽  
Xu Teng ◽  
Ye-Bo Zhou ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Endoplasmic Reticulum Stress ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Protein Kinase A ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Kinase A

scholarly journals Spatial targeting of type II protein kinase A to filopodia mediates the regulation of growth cone guidance by cAMP

2007 ◽  
Vol 176 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Jianzhong Han ◽  
Liang Han ◽  
Priyanka Tiwari ◽  
Zhexing Wen ◽  
James Q. Zheng
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Growth Cone ◽  
Regulatory Protein ◽  
Cyclic Adenosine Monophosphate ◽  
Spatial Localization ◽  
Adenosine Monophosphate ◽  
Type Ii ◽  
Regulation Of Growth ◽  
Kinase A

The second messenger cyclic adenosine monophosphate (cAMP) plays a pivotal role in axonal growth and guidance, but its downstream mechanisms remain elusive. In this study, we report that type II protein kinase A (PKA) is highly enriched in growth cone filopodia, and this spatial localization enables the coupling of cAMP signaling to its specific effectors to regulate guidance responses. Disrupting the localization of PKA to filopodia impairs cAMP-mediated growth cone attraction and prevents the switching of repulsive responses to attraction by elevated cAMP. Our data further show that PKA targets protein phosphatase-1 (PP1) through the phosphorylation of a regulatory protein inhibitor-1 (I-1) to promote growth cone attraction. Finally, we find that I-1 and PP1 mediate growth cone repulsion induced by myelin-associated glycoprotein. These findings demonstrate that the spatial localization of type II PKA to growth cone filopodia plays an important role in the regulation of growth cone motility and guidance by cAMP.

scholarly journals Membrane-Bound Protein Kinase A Inhibits Smooth Muscle Cell Proliferation In Vitro and In Vivo by Amplifying cAMP–Protein Kinase A Signals

2001 ◽  
Vol 88 (3) ◽  
pp. 319-324 ◽  
Author(s):  
Ciro Indolfi ◽  
Eugenio Stabile ◽  
Carmela Coppola ◽  
Adriana Gallo ◽  
Cinzia Perrino ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Smooth Muscle Cell ◽  
Protein Kinase A ◽  
Membrane Bound ◽  
Proliferation In Vitro ◽  
Kinase A

Antiproliferative effect of brief exposure to cholera toxin in vascular smooth muscle cells: role of cAMP and protein kinase A

2001 ◽  
Vol 79 (6) ◽  
pp. 471-480 ◽  
Author(s):  
Nathalie Thorin-Trescases ◽  
Sergei N Orlov ◽  
Sébastien Taurin ◽  
Nickolai O Dulin ◽  
Bruce G Allen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Protein Kinase A ◽  
Cholera Toxin ◽  
Antiproliferative Effect ◽  
Continuous Exposure ◽  
Α Subunit ◽  
Vsmc Proliferation ◽  
Kinase A

The effect of cholera toxin (CTX), an activator of the adenylate cyclase-coupled G protein αS subunit, was studied on cultured vascular smooth muscle cell (VSMC) proliferation. Continuous exposure (48 h) to CTX as well as 2-min pretreatment of VSMC with CTX led to the same level of cAMP production, inhibition of DNA synthesis, and arrest in the G1 phase without induction of necrosis or apoptosis in VSMC. Protein kinase A (PKA) activity in CTX-pretreated cells was transiently elevated by 3-fold after 3 h of incubation, whereas after 48 h it was reduced by 2-fold compared with baseline values without modulation of the expression of its catalytic α subunit. The PKA inhibitors H89 and KT 5720 did not protect VSMC from the antiproliferative effect of CTX. Two-dimensional electrophoresis was used to analyze the influence of CTX on protein phosphorylation. After 3 h of incubation of CTX-pretreated cells, we observed both newly-phosphorylated and dephosphorylated proteins (77 and 50 protein species, respectively). After 24 h of incubation, the number of phosphorylated proteins in CTX-treated cells was decreased to 39, whereas the number of dephosphorylated proteins was increased to 106. In conclusion, brief exposure to CTX leads to full-scale activation of cAMP signaling and evokes VSMC arrest in the G1 phase.Key words: vascular smooth muscle, proliferation, cholera toxin, cAMP, protein kinase A.

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