scholarly journals AMP-activated Protein Kinase (AMPK) Signaling in Endothelial Cells Is Essential for Angiogenesis in Response to Hypoxic Stress

2003 ◽  
Vol 278 (33) ◽  
pp. 31000-31006 ◽  
Author(s):  
Daisuke Nagata ◽  
Masaki Mogi ◽  
Kenneth Walsh
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
Hypoxic Stress ◽  
Ampk Signaling ◽  
Amp Activated Protein Kinase

scholarly journals Activation of AMP-Activated Protein Kinase by Adenine Alleviates TNF-Alpha-Induced Inflammation in Human Umbilical Vein Endothelial Cells

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0142283 ◽  
Author(s):  
Yi-Fang Cheng ◽  
Guang-Huar Young ◽  
Jiun-Tsai Lin ◽  
Hyun-Hwa Jang ◽  
Chin-Chen Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
Umbilical Vein ◽  
Tnf Alpha ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Amp Activated Protein Kinase

scholarly journals Adiponectin Stimulates Angiogenesis by Promoting Cross-talk between AMP-activated Protein Kinase and Akt Signaling in Endothelial Cells

2003 ◽  
Vol 279 (2) ◽  
pp. 1304-1309 ◽  
Author(s):  
Noriyuki Ouchi ◽  
Hideki Kobayashi ◽  
Shinji Kihara ◽  
Masahiro Kumada ◽  
Kaori Sato ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
Cross Talk ◽  
Akt Signaling ◽  
Amp Activated Protein Kinase

scholarly journals Myeloid deletion and therapeutic activation of AMP-activated protein kinase (AMPK) do not alter atherosclerosis in male or female mice

2020 ◽  
Author(s):  
Nicholas D. LeBlond ◽  
Peyman Ghorbani ◽  
Conor O’Dwyer ◽  
Nia Ambursley ◽  
Julia R. C. Nunes ◽  
...  
Keyword(s):  
Protein Kinase ◽  
First Generation ◽  
Western Diet ◽  
Daily Injection ◽  
Catalytic Subunits ◽  
Male And Female ◽  
Ampk Signaling ◽  
Female Mice ◽  
Amp Activated Protein Kinase ◽  
Progression Of Atherosclerosis

AbstractObjectiveThe dysregulation of myeloid-derived cell metabolism can drive atherosclerosis. AMP-activated protein kinase (AMPK) controls various aspects of macrophage dynamics and lipid homeostasis, which are important during atherogenesis.Approach and ResultsWe aimed to clarify the role of myeloid-specific AMPK signaling by using LysM-Cre to drive the deletion of both the α1 and α2 catalytic subunits (MacKO), in male and female mice made acutely atherosclerotic by PCSK9-AAV and Western diet-feeding. After 6 weeks of Western diet feeding, half received daily injection of either the AMPK activator, A-769662 or a vehicle control for a further 6 weeks. After 12 weeks, myeloid cell populations were not different between genotype or sex. Similarly, aortic sinus plaque size, lipid staining and necrotic area were not different in male and female MacKO mice compared to their littermate floxed controls. Moreover, therapeutic intervention with A-769662 had no effect. There were no differences in the amount of circulating total cholesterol or triglyceride, and only minor differences in the levels of inflammatory cytokines between groups. Finally, CD68+ area or markers of autophagy showed no effect of either lacking AMPK signaling or systemic AMPK activation.ConclusionsOur data suggest that while defined roles for each catalytic AMPK subunit have been identified, global deletion of myeloid AMPK signaling does not significantly impact atherosclerosis. Moreover, we show that intervention with the first-generation AMPK activator, A-769662, was not able to stem the progression of atherosclerosis.Highlights- The deletion of both catalytic subunits of AMPK in myeloid cells has no significant effect on the progression of atherosclerosis in either male or female mice- Therapeutic delivery of a first-generation AMPK activator (A-769662) for the last 6 weeks of 12-week study had no beneficial effect in either male or female mice- Studying total AMPK deletion may mask specific effects of each isoform and highlights the need for targeted disruption of AMPK phosphorylation sites via knock-in mutations, rather than the traditional “sledgehammer” knockout approach

AMP-activated protein kinase (AMPK) signaling in GnRH neurons links energy status and reproduction

Metabolism ◽  
2021 ◽  
Vol 115 ◽  
pp. 154460
Author(s):  
D. Franssen ◽  
A. Barroso ◽  
F. Ruiz-Pino ◽  
M.J. Vázquez ◽  
D. García-Galiano ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Energy Status ◽  
Ampk Signaling ◽  
Gnrh Neurons ◽  
Amp Activated Protein Kinase

scholarly journals P2-316: Disturbance in AMP-activated protein kinase (AMPK) signaling pathway in Alzheimer's disease

2010 ◽  
Vol 6 ◽  
pp. S406-S406
Author(s):  
Hyoung-Gon Lee ◽  
Hyun-Pil Lee ◽  
Wataru Kudo ◽  
Xiongwei Zhu ◽  
George Perry ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Kinase ◽  
Signaling Pathway ◽  
Ampk Signaling ◽  
Amp Activated Protein Kinase

scholarly journals AMP-activated protein kinase pathway and bone metabolism

2011 ◽  
Vol 212 (3) ◽  
pp. 277-290 ◽  
Author(s):  
J Jeyabalan ◽  
M Shah ◽  
B Viollet ◽  
C Chenu
Keyword(s):  
Protein Kinase ◽  
Energy Homeostasis ◽  
Bone Cells ◽  
Peripheral Tissues ◽  
Ampk Signaling ◽  
Obesity And Diabetes ◽  
Regulate Food Intake ◽  
Ampk Activity ◽  
Amp Activated Protein Kinase

There is increasing evidence that osteoporosis, similarly to obesity and diabetes, could be another disorder of energy metabolism. AMP-activated protein kinase (AMPK) has emerged over the last decade as a key sensing mechanism in the regulation of cellular energy homeostasis and is an essential mediator of the central and peripheral effects of many hormones on the metabolism of appetite, fat and glucose. Novel work demonstrates that the AMPK signaling pathway also plays a role in bone physiology. Activation of AMPK promotes bone formationin vitroand the deletion of α or β subunit of AMPK decreases bone mass in mice. Furthermore, AMPK activity in bone cells is regulated by the same hormones that regulate food intake and energy expenditure through AMPK activation in the brain and peripheral tissues. AMPK is also activated by antidiabetic drugs such as metformin and thiazolidinediones (TZDs), which also impact on skeletal metabolism. Interestingly, TZDs have detrimental skeletal side effects, causing bone loss and increasing the risk of fractures, although the role of AMPK mediation is still unclear. These data are presented in this review that also discusses the potential roles of AMPK in bone as well as the possibility for AMPK to be a future therapeutic target for intervention in osteoporosis.

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