scholarly journals Short-term effects of triiodothyronine on thyroid hormone receptor alpha by PI3K pathway in adipocytes, 3T3-L1

2014 ◽  
Vol 58 (8) ◽  
pp. 833-837 ◽  
Author(s):  
Miriane de Oliveira ◽  
Regiane Marques Castro Olimpio ◽  
Maria Teresa De Sibio ◽  
Fernanda Cristina Fontes Moretto ◽  
Renata de Azevedo Mello Luvizotto ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Thyroid Hormone Receptor ◽  
Pi3k Pathway ◽  
Control Group ◽  
Pi3k Signaling ◽  
Pi3k Inhibitor Ly294002 ◽  
Receptor Alpha ◽  
Pi3k Signaling Pathway

Objective The present study aimed to examine the effects of thyroid hormone (TH), more precisely triiodothyronine (T3), on the modulation of TH receptor alpha (TRα) mRNA expression and the involvement of the phosphatidyl inositol 3 kinase (PI3K) signaling pathway in adipocytes, 3T3-L1, cell culture. Materials and methods: It was examined the involvement of PI3K pathway in mediating T3 effects by treating 3T3-L1 adipocytes with physiological (P=10nM) or supraphysiological (SI =100 nM) T3 doses during one hour (short time), in the absence or the presence of PI3K inhibitor (LY294002). The absence of any treatment was considered the control group (C). RT-qPCR was used for mRNA expression analyzes. For data analyzes ANOVA complemented with Tukey’s test was used at 5% significance level. Results T3 increased TRα mRNA expression in P (1.91±0.13, p<0.001), SI (2.14±0.44, p<0.001) compared to C group (1±0.08). This increase was completely abrogated by LY294002 in P (0.53±0.03, p<0.001) and SI (0.31±0.03, p<0.001). To examine whether TRα is directly induced by T3, we used the translation inhibitor cycloheximide (CHX). The presence of CHX completely abrogated levels TRα mRNA in P (1.15±0.05, p>0.001) and SI (0.99±0.15, p>0.001), induced by T3. Conclusion These results demonstrate that the activation of the PI3K signaling pathway has a role in T3-mediated indirect TRα gene expression in 3T3-L1 adipocytes.

scholarly journals BRCA1 subcellular localization regulated by PI3K signaling pathway in triple-negative breast cancer MDA-MB-231 cells and hormone-sensitive T47D cells

2020 ◽  
Vol 15 (1) ◽  
pp. 501-510
Author(s):  
Bin Ma ◽  
Wenjia Guo ◽  
Meihui Shan ◽  
Nan Zhang ◽  
Binlin Ma ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Nuclear Localization ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Pi3k Pathway ◽  
Pi3k Signaling ◽  
T47d Cells ◽  
Pi3k Signaling Pathway ◽  
Hormone Sensitive

AbstractThis study is to investigate the effect of the PI3K/Akt signaling pathway on the regulation of BRCA1 subcellular localization in triple-negative breast cancer (TNBC) MDA-MB-231 cells and hormone-sensitive T47D cells. We found that heregulin-activated T47D cells showed more nuclear localization of BRCA1, but BRCA1 nuclear localization decreased after the inhibition of the PI3K signaling pathway. In MDA-MB-231 cells, activation or inhibition of the PI3K signaling pathway did not significantly affect cell apoptosis and BRCA1 nuclear translocation (P > 0.05). However, in T47D cells, the activation of the PI3K pathway significantly increased cell apoptosis (P < 0.05). In the heregulin-activated MDA-MB-231 and T47D cells, the phosphorylation of Akt and BRCA1 was significantly increased (P < 0.05), while that was significantly reduced after PI3K pathway inhibition (P < 0.05). The changing trends of the mRNA levels of Akt and BRCA1 in MDA-MB-231 and T47D cells after PI3K pathway activation or inhibition were consistent with the trends of their proteins. In both MDA-MB-231 and T47D cells, BRCA1 phosphorylation is regulated by the PI3K signaling pathway, but the nuclear localization of BRCA1 is different in these two cell lines. Moreover, the apoptosis rates of these two cell lines are different.

The Role of miRNAs in PI3K Signaling Pathway in Blood Malignancies: A Review Article

2021 ◽  
Author(s):  
Haniyeh Gaffari-Nazari ◽  
Samira Karami ◽  
Leila Noorazar ◽  
Sayeh Parkhideh ◽  
Elham Roshandel ◽  
...  
Keyword(s):  
Treatment Failure ◽  
Signaling Pathway ◽  
Intracellular Signaling ◽  
Pi3k Pathway ◽  
Pi3k Signaling ◽  
Laboratory Findings ◽  
A Cell ◽  
Pi3k Signaling Pathway ◽  
Relationship Of

Background: The PI3K/Akt/mTOR signaling pathway is one of the most important intracellular signaling pathways by regulating the cell cycle process. The direct relationship of this pathway with important mechanisms such as cell quiescence, longevity, and proliferation has been established. The overactive PI3K pathway with decreased and increased apoptosis and cell proliferation respectively is involved in pathogenesis of many cancers, including blood malignancies such as leukemia. Methods: Laboratory findings have shown that different factors, such as miRNAs, play a role in regulating PI3K signaling pathway. These molecules can alter the fate of a cell by interfering in suppression/overexpression of mRNA, transcription factors or stimulating the transcription of some genes. In this article, we reviewed the role of miRNAs in regulating the PI3K/Akt/mTOR pathway and its effect on leukemic progression and treatment failure. Conclusion: At present, miRNAs are known to be one of the causes of treatment failure and relapse in cancers.

scholarly journals Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium

2007 ◽  
Vol 195 (3) ◽  
pp. 429-438 ◽  
Author(s):  
C R Liu ◽  
L Y Li ◽  
F Shi ◽  
X Y Zang ◽  
Y M Liu ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Mrna Expression ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Developmental Process ◽  
Control Group ◽  
Rat Myocardium ◽  
Receptor Mrna ◽  
Close Relationship ◽  
Heart Lesions

Thyroid dysfunction is classified into hyperthyroidism and congenital hypothyroidism (CH). Both hyperthyroidism and CH can cause heart lesions; however, the mechanisms involved remain unclear. The left ventricle was collected from eu-, hyper-, and hypothyroid rat. RNA was extracted and reverse-transcripted to cDNA. Real-time fluorescence quantitation-PCR was used to quantify the differential expression of thyroid hormone receptor (TR) subtype mRNA among eu-, hyper-, and hypothyroid rat myocardium. Here, we show that compared with the normal myocardium, TRα1 mRNA expression was upregulated by 51% (P<0.01), TRα2 mRNA expression was downregulated by 58% (P<0.01), and TRβ1 mRNA expression remained unchanged in hyperthyroid rat myocardium (P>0.05). TRα1, TRα2, and TRβ1 were expressed in normal and hypothyroid rat myocardium throughout the developmental process. In hypothyroid rats, myocardial TRα1 mRNA expression was generally downregulated and the expression peak appeared late. Myocardial TRα2 mRNA expression was generally upregulated and the expression peak appeared late. Myocardial TRβ1 mRNA expression was generally downregulated and changed similarly with the control group. In addition, the hypogenetic myocardium can be seen in the hypothyroid rat by pathology study. Taken together, the abnormal expression of TR subtype mRNA may have a close relationship with the pathogenesis of CH and hyperthyroidism heart disease.

scholarly journals Quercetin Prevents Primordial Follicle Loss via Suppression of PI3K/Akt/Foxo3a Pathway Activation in Cyclophosphamide - Treated Mouse

2020 ◽  
Author(s):  
Jianghui Li ◽  
Hui Long ◽  
Yanyan Cong ◽  
Hongyuan Gao ◽  
Qifeng Lyu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Survival Rates ◽  
Primordial Follicle ◽  
Pi3k Pathway ◽  
Pi3k Signaling ◽  
Primordial Follicles ◽  
Pathway Activation ◽  
Pi3k Signaling Pathway ◽  
Induced Apoptosis ◽  
Immunohistochemistry Stain

Abstract Background: Chemotherapy improves survival rates but often causes some adverse effects associated with ovarian damage, characterized by a decreased of primordial follicle stockpiles. Recent studies reveal that chemotherapy may stimulate the PI3K signaling pathway, who has roles in manipulating the dormancy and activation of mammalian primordial follicles, resulting in accelerated primordial follicles activation followed by the loss of ovarian reserve. As an inhibitor of PI3K pathway, whether quercetin has protective properties against chemotherapy - induced follicle loss in mice is worth to be explored.Methods: The effects of quercetin on the mouse model of cyclophosphamide-induced ovarian dysfunction were investigated. Paraffin sections of mouse ovary were stained with hematoxylin and eosin for differential follicles count and TUNEL assay for apoptosis detection. Immunohistochemistry stain with ki67 and Foxo3a were used to evaluate the activation of primordial follicles. The function of PI3K signaling pathway were assessed via the western blot of ovary.Results: Quercetin cotreatment rescued the reduction number of dormant primordial follicles induced by cyclophosphamide. Moreover, analysis of the PI3K/Akt/Foxo3a pathway demonstrated that quercetin co - administration decreased phosphorylation of proteins that stimulate follicle activation in ovary induced by cyclophosphamide. Meanwhile, Quercetin prevents cyclophosphamide - induced apoptosis in early growing follicles and early antral follicles, maintaining AMH level secreted by these follicles, preserving the quiescence of the primordial follicle pool, characterized by the intranuclear staining of Foxo3a in primordial follicle. Conclusions: Quercetin attenuates cyclophosphamide - induced follicle loss by preventing the phosphorylation of PI3K/Akt/Foxo3a pathway members and maintaining AMH level secreted by growing follicles.

Abstract 222: Intralipid-induced Cardioprotection In Late Pregnancy Is Fully Abolished By Inhibition Of Stat3, But Not Pi3k Signaling Pathway

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Jingyuan li ◽  
Mansoureh Eghbali
Keyword(s):  
Infarct Size ◽  
Signaling Pathway ◽  
Therapeutic Potential ◽  
Heart Function ◽  
Ischemia Reperfusion ◽  
Late Pregnancy ◽  
Pi3k Signaling ◽  
Pi3k Inhibitor Ly294002 ◽  
Pi3k Signaling Pathway ◽  
Group 2

We have recently shown that the heart of late pregnant (LP) rodent is more prone to ischemia/reperfusion (I/R) injury compared to non-pregnant. Here we explored the therapeutic potential of Intralipid (ITLD) in the protection of LP hearts against I/R injury, and investigate the involvement of the signal transducer and activator of transcription-3 (STAT3) and phosphoinositide 3-kinase (PI3K) signaling pathways in ITLD-induced cardioprotetion. Isolated LP mouse hearts were subjected to 20 min ischemia followed by 40 min reperfusion with 1) Krebs Henseleit buffer (CTRL group), 2) 1% intralipid (ITLD group) or 3) ITLD+STAT3 inhibitor Stattic (20 μM, Stattic group), and 4) ITLD+PI3K inhibitor LY294002 (45 μM). The heart function and the infarct size were measured. The Intralipid-induced cardioprotection was fully abolished by Stattic, as RPP was significantly lower in the presence of Stattic (RPP=8881±1331 mmHg*beats/min vs. 1186±563 mmHg*beats/min in ITLD+Stattic, p<0.01) at the end of reperfusion. In fact, all of the hemodynamic indexes in ITLD+Stattic were not significantly different from CTRL. The infarct size was also significantly larger in ITLD+Stattic group when compared to Intralipid alone (47.9±2.5% in ITLD+Stattic vs. 21.7±2.6 % in ITLD, p<0.01). The Intralipid-induced cardioprotection was only partially abolished by LY294002, as at the end of 40 min reperfusion the RPP was significantly lower compared to the group treated with Intralipid alone, but still significantly higher than ITLD+Stattic ((RPP=8881±1331 mmHg*beats/min in ITLD vs. 5212±1955 mmHg*beats/min in ITLD+LY, p<0.05; RPP=5212±1955 mmHg*beats/min in ITLD+LY vs.1186±563 mmHg*beats/min in ITLD+Stattic, p<0.05). The infarct size was also larger when compared to Intralipid alone (32.8±3.1% in ITLD+LY vs. 21.7±2.6% in ITLD, p<0.05), but lower than ITLD+Stattic group (32.8±3.1% in ITLD+LY vs 47.9±2.5%, p<0.05). In conclusion, Intralipid protects the late pregnant heart against I/R injury via the STAT3 rather than the PI3K signaling pathway.

scholarly journals KISS1 Suppresses Apoptosis and Stimulates the Synthesis of E2 in Porcine Ovarian Granulosa Cells

Animals ◽  
2019 ◽  
Vol 9 (2) ◽  
pp. 54 ◽  
Author(s):  
Xiaoping Xin ◽  
Zhonghui Li ◽  
Yuyi Zhong ◽  
Qingqing Li ◽  
Jiaying Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Granulosa Cells ◽  
Cell Apoptosis ◽  
Pi3k Signaling ◽  
Mrna Levels ◽  
Ovarian Granulosa Cells ◽  
Estrogen Synthesis ◽  
Pi3k Signaling Pathway

Previous studies have strongly recommended that KISS-1 metastasis suppressor (KISS1) plays an essential gatekeeper of the initiation of reproductive maturation in mammals. However, KISS1 has been recently reported to highly express in ovarian granulosa cells (GCs). But the biological functionalities of KISS1 on cell apoptosis, cell cycle, and synthesis of estradiol-17β (E2) have not been explored in GCs. In this study, using porcine GCs as a cellular model, the overexpression plasmid of KISS1 was built to explore the biological effects of KISS1 on the PI3K signaling pathway, estrogen signaling pathway, cell apoptosis, cell cycle, and E2 secretion. We found that mRNA of KISS1 highly expressed in the ovary and significantly increased from immature to mature follicles in gilts. Overexpression of KISS1 could significantly increase the mRNA expression of PIK3CG, PIK3C1, and PDK1, and significantly decreased the mRNA levels of FOXO3, TSC2, and BAD of PI3K signaling pathway. Furthermore, results of the flow cytometry showed that overexpression of KISS1 significantly inhibited the apoptosis of GCs and decreased the percentage of GCs at G0/G1 phase of the cell cycle. Additionally, overexpression of KISS1 could increase the mRNA levels of Star, CYP17, 3B-HSD, 17B-HSD of estrogen synthesis signaling pathway, significantly increase the concentration of E2 in the supernatant of the cultured GCs, and up-regulate the mRNA expression levels of ESR1 and ESR2. These results suggested that KISS1 might suppress cell apoptosis through activating the PI3K signaling pathway and stimulate synthesis of E2 via boosting the estrogen synthesis signaling pathway. This study would be of great interests for exploring the biological functionalities of KISS1 in the folliculogenesis and sex steroid production of the ovaries in mammals.

Thyroid hormone inhibits the proliferation of piglet Sertoli cell via PI3K signaling pathway

2015 ◽  
Vol 83 (1) ◽  
pp. 86-94 ◽  
Author(s):  
Yan Sun ◽  
WeiRong Yang ◽  
HongLin Luo ◽  
XianZhong Wang ◽  
ZhongQiong Chen ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Signaling Pathway ◽  
Sertoli Cell ◽  
Pi3k Signaling ◽  
Pi3k Signaling Pathway

scholarly journals Quercetin Prevents Primordial Follicle Loss via Suppression of PI3K/Akt/Foxo3a Pathway Activation in Cyclophosphamide - Treated Mouse

2020 ◽  
Author(s):  
Sha Yu ◽  
Jianghui Li ◽  
Hui Long ◽  
Yanyan Cong ◽  
Hongyuan Gao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Survival Rates ◽  
Primordial Follicle ◽  
Pi3k Pathway ◽  
Pi3k Signaling ◽  
Primordial Follicles ◽  
Pathway Activation ◽  
Pi3k Signaling Pathway ◽  
Induced Apoptosis ◽  
Immunohistochemistry Stain

Abstract Background: Chemotherapy improves survival rates but often causes some adverse effects associated with ovarian damage, characterized by a decreased of primordial follicle stockpiles. Recent studies reveal that chemotherapy may stimulate the PI3K signaling pathway, who has roles in manipulating the dormancy and activation of mammalian primordial follicles, resulting in accelerated primordial follicles activation followed by the loss of ovarian reserve. As an inhibitor of PI3K pathway, whether quercetin has protective properties against chemotherapy - induced follicle loss in mice is worth to be explored.Methods：The effects of quercetin on the mouse model of cyclophosphamide-induced ovarian dysfunction were investigated. Paraffin sections of mouse ovary were stained with hematoxylin and eosin for differential follicles count and TUNEL assay for apoptosis detection. Immunohistochemistry stain with ki67 and Foxo3a were used to evaluate the activation of primordial follicles. The function of PI3K signaling pathway were assessed via the western blot of ovary.Results: Quercetin cotreatment rescued the reduction number of dormant primordial follicles induced by cyclophosphamide. Moreover, analysis of the PI3K/Akt/Foxo3a pathway demonstrated that quercetin co - administration decreased phosphorylation of proteins that stimulate follicle activation in ovary induced by cyclophosphamide. Meanwhile, Quercetin prevents cyclophosphamide - induced apoptosis in early growing follicles and early antral follicles, maintaining AMH level secreted by these follicles, preserving the quiescence of the primordial follicle pool, characterized by the intranuclear staining of Foxo3a in primordial follicle. Conclusions: Quercetin attenuates cyclophosphamide - induced follicle loss by preventing the phosphorylation of PI3K/Akt/Foxo3a pathway members and maintaining AMH level secreted by growing follicles.

scholarly journals The PI3K signaling pathway mediates the biological effects of leptin

2010 ◽  
Vol 54 (7) ◽  
pp. 591-602 ◽  
Author(s):  
Jose Donato Jr. ◽  
Renata Frazão ◽  
Carol Fuzeti Elias
Keyword(s):  
Food Intake ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Intracellular Signaling ◽  
Leptin Receptor ◽  
Biological Effects ◽  
Pi3k Pathway ◽  
Pi3k Signaling ◽  
Electrophysiological Properties ◽  
Pi3k Signaling Pathway

The activation of the leptin receptor recruits several intracellular signaling pathways, including the phosphatidylinositol 3-kinase (PI3K) pathway. While some of the leptin-induced signaling pathways, such as the JAK2/STAT3 pathway, induce cellular responses primarily through changes in gene expression, the PI3K pathway affects cellular properties more rapidly, through post-translational changes such as protein phosphorylation. Accordingly, several studies have shown that the PI3K pathway is required for the acute effects of leptin, such as a leptin-induced decrease in food intake. Leptin signaling through PI3K also affects the electrophysiological properties of neurons, including changes in their membrane potential and firing rates. In this review, we summarize the recent advances in our understanding of the role played by the PI3K signaling pathway in controlling food intake and energy balance. In particular, we focus on the importance of the PI3K signaling pathway as a mediator of the effects of leptin on hypothalamic neurons.

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