5′-AMP-Activated Protein Kinase Attenuates Adriamycin-Induced Oxidative Podocyte Injury through Thioredoxin-Mediated Suppression of the Apoptosis Signal-Regulating Kinase 1–P38 Signaling Pathway

2013 ◽  
Vol 85 (3) ◽  
pp. 460-471 ◽  
Author(s):  
Kun Gao ◽  
Yuan Chi ◽  
Wei Sun ◽  
Masayuki Takeda ◽  
Jian Yao
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Podocyte Injury ◽  
Amp Activated Protein Kinase

AMPK: A Key Sensor of Fuel and Energy Status in Skeletal Muscle

Physiology ◽  
2006 ◽  
Vol 21 (1) ◽  
pp. 48-60 ◽  
Author(s):  
D. Grahame Hardie ◽  
Kei Sakamoto
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Signaling Pathway ◽  
Recent Work ◽  
Metabolic Changes ◽  
Energy Status ◽  
Upstream Kinase ◽  
Amp Activated Protein Kinase

Contraction induces marked metabolic changes in muscle, and the AMP-activated protein kinase (AMPK) is a good candidate to explain these effects. Recent work using a muscle-specific knockout of the upstream kinase, LKB1, has confirmed that the LKB1→AMPK cascade is the signaling pathway responsible for many of these effects.

Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through a CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells

2016 ◽  
Vol 130 (17) ◽  
pp. 1523-1533 ◽  
Author(s):  
Chun-Yin Huang ◽  
An-Chen Chang ◽  
Hsien-Te Chen ◽  
Shih-Wei Wang ◽  
Yuan-Shun Lo ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Tube Formation ◽  
Human Chondrosarcoma ◽  
Dependent Protein ◽  
And Migration ◽  
Factor C ◽  
Amp Activated Protein Kinase

Chondrosarcoma is the second most frequently occurring type of bone malignancy characterized by distant metastatic propensity. Vascular endothelial growth factor-C (VEGF-C) is the major lymphangiogenic factor, and makes crucial contributions to tumour lymphangiogenesis and lymphatic metastasis. Adiponectin is a protein hormone secreted predominantly by differentiated adipocytes. In recent years, adiponectin has also been indicated as facilitating tumorigenesis, angiogenesis and metastasis. However, the effect of adiponectin on VEGF-C regulation and lymphangiogenesis in chondrosarcoma has remained largely a mystery. In the present study, we have shown a clinical correlation between adiponectin and VEGF-C, as well as tumour stage, in human chondrosarcoma tissues. We further demonstrated that adiponectin promoted VEGF-C expression and secretion in human chondrosarcoma cells. The conditioned medium from adiponectin-treated cells significantly induced tube formation and migration of human lymphatic endothelial cells. In addition, adiponectin knock down inhibited lymphangiogenesis in vitro and in vivo. We also found that adiponectin-induced VEGF-C is mediated by the calmodulin-dependent protein kinase II (CaMKII), AMP-activated protein kinase (AMPK) and p38 signaling pathway. Furthermore, the expression of miR-27b was negatively regulated by adiponectin via the CaMKII, AMPK and p38 cascade. The present study is the first to describe the mechanism of adiponectin-promoted lymphangiogenesis by up-regulating VEGF-C expression in chondrosarcomas. Thus, adiponectin could serve as a therapeutic target in chondrosarcoma metastasis and lymphangiogenesis.

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

Puerarin Attenuates Osteoarthritis via Upregulating AMP-Activated Protein Kinase/Proliferator-Activated Receptor-γ Coactivator-1 Signaling Pathway in Osteoarthritis Rats

Pharmacology ◽  
2018 ◽  
Vol 102 (3-4) ◽  
pp. 117-125 ◽  
Author(s):  
Luyao Wang ◽  
Haojie Shan ◽  
Bin Wang ◽  
Nan Wang ◽  
Zubin Zhou ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Cartilage Damage ◽  
Joint Disease ◽  
Mitochondrial Dysfunctions ◽  
Compound C ◽  
Amp Activated Protein Kinase ◽  
And Cartilage

Background/Aims: Osteoarthritis is the most common degenerative joint disease and causes major pain and disability in adults. It has been reported that mitochondrial dysfunction in chondrocytes was associated with osteoarthritis. Puerarin has multiple effects including restoring mitochondrial function. In this study, the potential effects of puerarin on osteoarthritis and osteoarthritis associated mitochondrial dysfunctions were evaluated. Methods: Osteoarthritis rats were treated with puerarin and the severity of osteoarthritis and cartilage damages was evaluated. The mitochondrial biogenesis and functions were analyzed by measuring related proteins expression, mitochondrial DNA content, ATP production, and oxygen consumption. The dependence of AMP-activated protein kinase (AMPK) pathway on puerarin-regulated mitochondrial function was analyzed by applying AMPK inhibitor Compound C. Results: Puerarin treatment alleviated mechanical hyperalgesia and cartilage damage in osteoarthritis rats. Puerarin increased mitochondrial biogenesis and attenuated mitochondrial dysfunctions in osteoarthritis rats. AMPK inhibitor Compound C abolished puerarin’s effects. Conclusion: Puerarin attenuates osteoarthritis by upregulating the AMPK/proliferator-activated receptor-γ coactivator signaling pathway in osteoarthritis rats.

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