• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

The loss of endothelin-2 exhibits an anticancer effect in A549 human lung adenocarcinoma cell line
This study aimed to investigate the pathophysiological functions of ET-2 in A549 human lung adenocarcinoma cells. We analyzed the expression of ET-2 mRNA in lung adenocarcinoma tissues compared to that in non-tumor lung tissues using public online databases. The function of ET-2 in A549 cells was investigated using siRNA. ET-2 mRNA level was upregulated in lung adenocarcinoma tissues, and high ET-2 level was associated with poor overall survival in patients with lung adenocarcinoma. ET-2 silencing reduced the proliferation, migration, invasion, and enhanced apoptosis in A549 cells. Mechanistically, ET-2 silencing reduced t...
Source: Canadian Journal of Physiology and Pharmacology - June 9, 2022 Category: Drugs & Pharmacology Authors: Ratih Paramita Suprapto Yoko Suzuki Tatsuya Nagano Ken-Ichi Hirata Noriaki Emoto Source Type: research

Metformin alleviates hydrogen peroxide-induced inflammation and oxidative stress via inhibiting P2X7R signaling in spinal cord tissue cells neurons.
In conclusion, our results show that metformin can alleviate H2O2-induced inflammation and oxidative stress via modulating the P2X7R signaling pathway. PMID: 33201730 [PubMed - as supplied by publisher]
Source: Canadian Journal of Physiology and Pharmacology - November 17, 2020 Category: Drugs & Pharmacology Authors: Wang G, Chen S, Shao Z, Li Y, Wang W, Mao L, Li J, Mei X Tags: Can J Physiol Pharmacol Source Type: research

TMEM98, a novel secretory protein, promotes endothelial cell adhesion as well as vascular smooth muscle cell proliferation and migration.
Abstract Transmembrane protein 98 (TMEM98) is a novel gene. In a prior study, we have shown that siRNA-mediated knockdown of TMEM98 inhibited interleukin (IL)-8-promoted endothelial cell (EC) adhesion as well as vascular smooth muscle cell (VSMC) proliferation and migration in the vascular endothelial and smooth muscle cells dysfunction. Herein, we used gain- and loss-of-function approaches combined with biochemical techniques to further explore the role of TMEM98 in the vascular wall cell. The expression and secretion of TMEM98 was increased in cultured human umbilical vein endothelial cells (HUVECs) and VSMCs tr...
Source: Canadian Journal of Physiology and Pharmacology - September 4, 2020 Category: Drugs & Pharmacology Authors: Li M, Zhu H, Hu X, Gao F, Hu X, Cui Y, Wei X, Xie C, Lv G, Zhao Y, Gao Y Tags: Can J Physiol Pharmacol Source Type: research

Galectin-3 inhibition attenuates doxorubicin-induced cardiac dysfunction by upregulating the expression of peroxiredoxin-4.
In conclusion, Gal-3 mediated Dox-induced cardiotoxicity and Gal-3 inhibition attenuated Dox-induced cardiac dysfunction by upregulating the expression of Prx-4 to reduce myocardial oxidative stress. PMID: 32516552 [PubMed - as supplied by publisher]
Source: Canadian Journal of Physiology and Pharmacology - June 8, 2020 Category: Drugs & Pharmacology Authors: Tian Y, Lv W, Lu C, Jiang Y, Yang X, Song M Tags: Can J Physiol Pharmacol Source Type: research

Knockout of the Circadian Clock Protein PER1 Results in Sex-Dependent Alterations of ET-1 Production in Mice in Response to a High Salt Diet plus Mineralocorticoid Treatment.
Abstract Previously, we showed that global knockout (KO) of the circadian clock transcription factor PER1 in male, but not female, mice fed a high salt diet plus mineralocorticoid treatment (HS/DOCP) resulted in non-dipping hypertension and decreased night/day ratio of sodium (Na) excretion. Additionally, we have shown that the endothelin-1 (ET-1) gene is targeted by both PER1 and aldosterone. We hypothesized that ET-1 would exhibit a sex-specific response to HS/DOCP treatment in PER1 KO. Here we show that male, but not female, global PER1 KO mice exhibit a decreased night/day ratio of urinary ET-1. Gene expressio...
Source: Canadian Journal of Physiology and Pharmacology - May 20, 2020 Category: Drugs & Pharmacology Authors: Douma LG, Crislip GR, Cheng KY, Barral D, Masten S, Holzworth MR, Roig E, Glasford K, Beguiristain K, Li W, Bratanatawira P, Lynch IJ, Cain BD, Wingo CS, Gumz ML Tags: Can J Physiol Pharmacol Source Type: research

Elevated Aldolase 1A, retrogene 1 expression induces cardiac apoptosis in rat experimental autoimmune myocarditis model.
Abstract Acute myocarditis is an unpredictable heart disease, which is caused by inflammation-associated cell death. Although viral infection and drug exposure are known to induce acute myocarditis, the molecular basis for its development remains undefined. Using proteomics and molecular analyses in myosin-induced rat experimental autoimmune myocarditis (EAM), we identified that elevated expression of aldolase 1A, retrogene 1 (Aldoart1) is critical to induce mitochondrial dysfunction and acute myocarditis development. Here, we demonstrate that cardiac cell death is associated with increased expressions of pro-apop...
Source: Canadian Journal of Physiology and Pharmacology - January 29, 2020 Category: Drugs & Pharmacology Authors: Choi S, Chung JH, Nam MH, Bang E, Hong KS, Kim YH, Seo JB, Chi SG Tags: Can J Physiol Pharmacol Source Type: research

Allyl isothiocyanate up-regulates MRP1 expression through Notch1 signaling in human bronchial epithelial cells.
In conclusion, Notch1 signaling positively regulated MRP1 in 16HBE cells, and AITC induced MRP1 expression and function may be attributed to Notch1 signaling. These findings show that Notch1 and MRP1 might have a potential protective effect in the COPD process and become a new therapeutic target for COPD or other lung diseases. It also provides theoretical basis for the therapeutic effects of AITC. PMID: 31747319 [PubMed - as supplied by publisher]
Source: Canadian Journal of Physiology and Pharmacology - November 19, 2019 Category: Drugs & Pharmacology Authors: Li N, Guo Y, Jiang C, Zhou Y, Li C, Li Z, Wang D Tags: Can J Physiol Pharmacol Source Type: research

Role of Brd4 in the production of inflammatory cytokines in mouse macrophages treated with titanium particles.
In conclusion, Brd4 expression increases in interface membrane and Brd4 participates in the production of pro-inflammatory cytokines induced by Ti particles via promoting the activation of NF-B signaling and binding to acetylated NF-κB p65 (lysine-310) in mouse macrophages. PMID: 31330113 [PubMed - as supplied by publisher]
Source: Canadian Journal of Physiology and Pharmacology - July 21, 2019 Category: Drugs & Pharmacology Authors: Ren Y, Zhang Y, Wang Z, Wang C, Zhang H, Wang Y, Zhao Z Tags: Can J Physiol Pharmacol Source Type: research

miRNA-218 Targets Lipin-1 and Glucose Transporter Type 4 Genes in 3T3-L1 Cells Treated With Lopinavir/Ritonavir
Conclusion: 3T3-L1 cells, treated with LPV/RTV, show altered lipid content due to increased miRNA-218 levels, which affects lipin-1 mRNA. Moreover, increased miRNA-218 levels were inversely correlated with changes in GLUT-4 expression, which suggests a role for miRNA-218 in mediating the insulin resistance consequent to cART. Introduction Metabolic syndrome is a serious consequence of combined Antiretroviral Therapy (cART). HIV-associated metabolic syndrome is often accompanied by lipodystrophy (LS), the redistribution of body fat with loss of subcutaneous adipose tissue in face, limbs and buttocks, concomitant wit...
Source: Frontiers in Pharmacology - April 29, 2019 Category: Drugs & Pharmacology Source Type: research

Auranofin, an Anti-rheumatic Gold Drug, Aggravates the Radiation-Induced Acute Intestinal Injury in Mice
Conclusion In this study, we found that a non-toxic dose of auranofin significantly aggravated the severity of the radiation-induced intestinal injury. This suggests that auranofin treatment can be an independent factor that influences the risk of intestinal complications after pelvic or abdominal radiotherapy. Ethics Statement All the protocols used in this study were approved by the Institutional Animal Care and Use Committee of the Korean Institute of Radiological and Medical Sciences (IACUC permit number: KIRAMS217-0007). Author Contributions H-JL, JS, and Y-BL designed the experiments. EL and JK conducted the exp...
Source: Frontiers in Pharmacology - April 23, 2019 Category: Drugs & Pharmacology Source Type: research

Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway
In conclusion, our research results indicate that DAPT activates PI3K/AKT/Cdc42 signaling by non-canonical Notch pathway, and the activated Cdc42 promotes the filopodia formation and inhibits lamellipodia assembly, resulting in reduced migration of breast cancer cells. The results imply that non-canonical Notch signaling may play a very important role in the rapid response of cells to the extracellular signals. Author Contributions LG, JD, and LL designed the study and wrote and revised the manuscript. LL and LZ performed most of the experiments and data analysis. SZ, X-YZ, P-XM, Y-DM, Y-YW, YC, S-JT, and Y-JZ assisted i...
Source: Frontiers in Pharmacology - April 15, 2019 Category: Drugs & Pharmacology Source Type: research

Pages: 1  2