scholarly journals SP6616 as a new Kv2.1 channel inhibitor efficiently promotes β-cell survival involving both PKC/Erk1/2 and CaM/PI3K/Akt signaling pathways

2016 ◽  
Vol 7 (5) ◽  
pp. e2216-e2216 ◽  
Author(s):  
T T Zhou ◽  
L L Quan ◽  
L P Chen ◽  
T Du ◽  
K X Sun ◽  
...  
Keyword(s):  
Cell Survival ◽  
Signaling Pathways ◽  
Akt Signaling ◽  
Β Cell

scholarly journals Cyclin-Dependent Kinase 5 Promotes Pancreatic  -Cell Survival via Fak-Akt Signaling Pathways

Diabetes ◽  
2011 ◽  
Vol 60 (4) ◽  
pp. 1186-1197 ◽  
Author(s):  
M. Daval ◽  
T. Gurlo ◽  
S. Costes ◽  
C.-j. Huang ◽  
P. C. Butler
Keyword(s):  
Cell Survival ◽  
Signaling Pathways ◽  
Akt Signaling ◽  
Cyclin Dependent Kinase ◽  
Pancreatic Cell ◽  
Cyclin Dependent Kinase 5

scholarly journals Puerarin protects pancreatic β-cell survival via PI3K/Akt signaling pathway

2014 ◽  
Vol 53 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Zhipeng Li ◽  
Zhaoshui Shangguan ◽  
Yijie Liu ◽  
Jihua Wang ◽  
Xuejun Li ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cell Mass ◽  
Akt Signaling ◽  
Pancreatic Β Cell ◽  
Diabetic Mice ◽  
Akt Signaling Pathway ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Stimulated Insulin Secretion ◽  
And Function

Pancreatic β-cell loss because of apoptosis is the major cause of type 1 diabetes (T1D) and late stage T2D. Puerarin possesses anti-diabetic properties; whether it acts directly on pancreatic β-cell is not clear. This study was designed to investigate the effects of puerarin on pancreatic β-cell survival and function. Diabetes was induced in male C57BL/6 mice by a single peritoneal injection of streptozotocin (STZ). Pancreatic β-cell survival and function were assessed in diabetic mice by measuring β-cell apoptosis, β-cell mass, pancreatic insulin content, and glucose tolerance, and in cultured islets and clonial MIN6 β-cells by measuring β-cell viability and apoptosis and glucose-stimulated insulin secretion. We found that pre-treatment with puerarin decreased the incidence of STZ-induced diabetes. Puerarin increased pancreatic β-cell mass via β-cell apoptosis inhibition in diabetic mice, and increased serum insulin, whereas it decreased blood glucose levels and improved glucose tolerance. In cultured islets and MIN6 cells, puerarin protected β-cell from cobalt chloride (CoCl2)-induced apoptosis and restored the impaired capacity of glucose-stimulated insulin secretion. Puerarin protection of β-cell survival involved the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. In conclusion, puerarin protects pancreatic β-cell function and survival via direct effects on β-cells, and its protection of β-cell survival is mediated by the PI3K/Akt pathway. As a safe natural plant extraction, puerarin might serve as a preventive and/or therapeutic approach for diabetes.

scholarly journals Proinsulin C-Peptide Enhances Cell Survival and Protects against Simvastatin-Induced Myotoxicity in L6 Rat Myoblasts

2019 ◽  
Vol 20 (7) ◽  
pp. 1654
Author(s):  
Sumia Essid ◽  
Alan Bevington ◽  
Nigel Brunskill
Keyword(s):  
Skeletal Muscle ◽  
Cell Survival ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Akt Signaling ◽  
Skeletal Muscle Function ◽  
Repair Capacity ◽  
C Peptide ◽  
Myoblast Cell ◽  
Induced Apoptosis

The repair capacity of progenitor skeletal muscle satellite cells (SC) in Type 1 diabetes mellitus (T1DM) is decreased. This is associated with the loss of skeletal muscle function. In T1DM, the deficiency of C-peptide along with insulin is associated with an impairment of skeletal muscle functions such as growth, and repair, and is thought to be an important contributor to increased morbidity and mortality. Recently, cholesterol-lowering drugs (statins) have also been reported to increase the risk of skeletal muscle dysfunction. We hypothesised that C-peptide activates key signaling pathways in myoblasts, thus promoting cell survival and protecting against simvastatin-induced myotoxicity. This was tested by investigating the effects of C-peptide on the L6 rat myoblast cell line under serum-starved conditions. Results: C-peptide at concentrations as low as 0.03 nM exerted stimulatory effects on intracellular signaling pathways—MAP kinase (ERK1/2) and Akt. When apoptosis was induced by simvastatin, 3 nM C-peptide potently suppressed the apoptotic effect through a pertussis toxin-sensitive pathway. Simvastatin strongly impaired Akt signaling and stimulated the reactive oxygen species (ROS) production; suggesting that Akt signaling and oxidative stress are important factors in statin-induced apoptosis in L6 myoblasts. The findings indicate that C-peptide exerts an important protective effect against death signaling in myoblasts. Therefore, in T1DM, the deficiency of C-peptide may contribute to myopathy by rendering myoblast-like progenitor cells (involved in muscle regeneration) more susceptible to the toxic effects of insults such as simvastatin.

Biological role of AKT, and regulation of AKT signaling pathway by thymoquinone: perspectives in cancer therapeutics

2020 ◽  
Vol 20 ◽  
Author(s):  
Md. Junaid ◽  
Yeasmin Akter ◽  
Syeda Samira Afrose ◽  
Mousumi Tania ◽  
Md. Asaduzzaman Khan
Keyword(s):  
Clinical Trials ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Inhibitory Effect ◽  
Akt Signaling ◽  
Review Article ◽  
Therapeutic Drug ◽  
Akt Signaling Pathway ◽  
Anti Cancer

Background: AKT/PKB is an important enzyme with numerous biological functions, and its overexpression is related to the carcinogenesis. AKT stimulates different signaling pathways that are downstream of activated tyrosine kinases and phosphatidylinositol 3-kinase, hence functions as an important target for anti-cancer drugs. Objective: In this review article, we have interpreted the role of AKT signaling pathways in cancer and natural inhibitory effect of Thymoquinone (TQ) in AKT and its possible mechanism. Method: We have collected the updated information and data on AKT, their role in cancer and inhibitory effect of TQ in AKT signaling pathway from google scholar, PubMed, Web of Science, Elsevier, Scopus and many more. Results: There are many drugs already developed, which can target AKT, but very few among them have passed clinical trials. TQ is a natural compound, mainly found in black cumin, which has been found to have potential anti-cancer activities. TQ targets numerous signaling pathways, including AKT, in different cancers. In fact, many studies revealed that AKT is one of the major targets of TQ. The preclinical success of TQ suggests its clinical studies on cancer. Conclusion: This review article summarizes the role of AKT in carcinogenesis, its potent inhibitors in clinical trials, and how TQ acts as an inhibitor of AKT and TQ’s future as a cancer therapeutic drug.

scholarly journals Akt signaling is activated by TGFβ2 and impacts tenogenic induction of mesenchymal stem cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sophia K. Theodossiou ◽  
Jett B. Murray ◽  
LeeAnn A. Hold ◽  
Jeff M. Courtright ◽  
Anne M. Carper ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathways ◽  
Transforming Growth Factor ◽  
Akt Signaling ◽  
Cell Alignment ◽  
Limited Information ◽  
Akt Inhibitor ◽  
Tenogenic Differentiation

Abstract Background Tissue engineered and regenerative approaches for treating tendon injuries are challenged by the limited information on the cellular signaling pathways driving tenogenic differentiation of stem cells. Members of the transforming growth factor (TGF) β family, particularly TGFβ2, play a role in tenogenesis, which may proceed via Smad-mediated signaling. However, recent evidence suggests some aspects of tenogenesis may be independent of Smad signaling, and other pathways potentially involved in tenogenesis are understudied. Here, we examined the role of Akt/mTORC1/P70S6K signaling in early TGFβ2-induced tenogenesis of mesenchymal stem cells (MSCs) and evaluated TGFβ2-induced tenogenic differentiation when Smad3 is inhibited. Methods Mouse MSCs were treated with TGFβ2 to induce tenogenesis, and Akt or Smad3 signaling was chemically inhibited using the Akt inhibitor, MK-2206, or the Smad3 inhibitor, SIS3. Effects of TGFβ2 alone and in combination with these inhibitors on the activation of Akt signaling and its downstream targets mTOR and P70S6K were quantified using western blot analysis, and cell morphology was assessed using confocal microscopy. Levels of the tendon marker protein, tenomodulin, were also assessed. Results TGFβ2 alone activated Akt signaling during early tenogenic induction. Chemically inhibiting Akt prevented increases in tenomodulin and attenuated tenogenic morphology of the MSCs in response to TGFβ2. Chemically inhibiting Smad3 did not prevent tenogenesis, but appeared to accelerate it. MSCs treated with both TGFβ2 and SIS3 produced significantly higher levels of tenomodulin at 7 days and morphology appeared tenogenic, with localized cell alignment and elongation. Finally, inhibiting Smad3 did not appear to impact Akt signaling, suggesting that Akt may allow TGFβ2-induced tenogenesis to proceed during disruption of Smad3 signaling. Conclusions These findings show that Akt signaling plays a role in TGFβ2-induced tenogenesis and that tenogenesis of MSCs can be initiated by TGFβ2 during disruption of Smad3 signaling. These findings provide new insights into the signaling pathways that regulate tenogenic induction in stem cells.

scholarly journals Retraction Note: Chemopreventive Potential of Resveratrol in Mouse Skin Tumors Through Regulation of Mitochondrial and PI3K/AKT Signaling Pathways

2021 ◽  
Vol 38 (2) ◽  
pp. 375-375
Author(s):  
Preeti Roy ◽  
Neetu Kalra ◽  
Sahdeo Prasad ◽  
Jasmine George ◽  
Yogeshwer Shukla
Keyword(s):  
Signaling Pathways ◽  
Mouse Skin ◽  
Akt Signaling ◽  
Skin Tumors

Brown alga Ecklonia cava attenuates type 1 diabetes by activating AMPK and Akt signaling pathways

2010 ◽  
Vol 48 (2) ◽  
pp. 509-516 ◽  
Author(s):  
Changkeun Kang ◽  
Yeung Bae Jin ◽  
Hyunkyoung Lee ◽  
Mijin Cha ◽  
Eun-tae Sohn ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Signaling Pathways ◽  
Brown Alga ◽  
Akt Signaling ◽  
Ecklonia Cava

scholarly journals Veratrilla baillonii Franch exerts anti-diabetic activity and improves liver injury through IRS/PI3K/AKT signaling pathways in type 2 diabetic db/db mice

2020 ◽  
Vol 75 ◽  
pp. 104204
Author(s):  
Cai-Jing He ◽  
Li-Qun Ma ◽  
Muhammad Sarfaraz Iqbal ◽  
Xian-Ju Huang ◽  
Jun Li ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathways ◽  
Akt Signaling ◽  
Type 2 Diabetic
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