Journal: iScience

Article Title: The role of arachidonic acid metabolites in the subtype classification and pathogenesis of primary aldosteronism

doi: 10.1016/j.isci.2025.114598

Figure Lengend Snippet: Arachidonic acid promotes Ca 2+ uptake and increases CYP11B2 expression in adrenal cortical cells (A) Confirmation of the expression of CYP11B2 in primary adrenal cortical cells. Scale bars, 50 μm. (B) Cell viability of primary adrenal cortical cells treated with different doses of arachidonic acid (AA) ( n = 4). (C) Aldosterone levels in cellular supernatant of primary adrenal cortical cells treated with different doses of AA ( n = 6). (D) Aldosterone levels in cellular supernatant of primary adrenal cortical cells treated with different doses of Ang II (left) or endothelin-1 (right) along with AA ( n = 3). (E) Representative western blots showing levels of CYP11B2, CYP11B1, CYP17A1, and HSD3B2 in primary adrenal cortical cells treated with vehicle or AA. The quantitative results are shown on the right ( n = 3). (F) Changes of cytoplasmic Ca 2+ , labeled with Fura-2 AM, in primary adrenal cortical cells treated with 1 mM thapsigargin (TG) stimulation in a 1 mM extracellular Ca 2+ solution after preincubation with vehicle or AA ( n = 12). (G) Changes of mitochondrial Ca 2+ , labeled with Rhod-2 AM, in digitonin-permeabilized primary adrenal cortical cells treated with 200 μM ATP stimulation in a 300 μM extracellular Ca 2+ solution after preincubation with vehicle or AA ( n = 12). (H) Changes of endoplasmic reticulum (ER) Ca 2+ , labeled with Mag Fura-2 AM, in digitonin-permeabilized primary adrenal cortical cells treated with ATP stimulation in a Ca 2+ -free extracellular solution after preincubation with vehicle or AA ( n = 12). (I) Representative western blots showing levels of KCNJ5, Na + /K + ATPase alpha-1 subunit, NCX-1, Letm 1, MCU, VDAC, RyR2, and IP 3 R in primary adrenal cortical cells treated with vehicle or AA. (Left) Representative western blots showing levels of TRPC1, TRPC3, TRPC6, TRPV1, and TRPV4 in primary adrenal cortical cells treated with vehicle or AA. (Right) The quantitative results are shown on the left ( n = 3). The results are expressed as the mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001 compared with vehicle group; # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 compared with 1 μM AA group by one-way ANOVA (B and C) and by Student’s t test (D–I).

Article Snippet: TRPC1 , Alomone , Cat#ACC-010; RRID: AB_2040234.

Techniques: Expressing, Western Blot, Labeling

Journal: Animal Bioscience

Article Title: Oxidative stress impairs the meat quality of broiler by damaging mitochondrial function, affecting calcium metabolism and leading to ferroptosis

doi: 10.5713/ab.22.0019

Figure Lengend Snippet: (a, b) Effects of H 2 O 2 exposure on the contents of Ca 2+ . (c, d) Effects of H 2 O 2 exposure on the relative protein expression levels of TRPC1, PMCA, NCX, SERCA1, and MCU. The control group was the non-injected treatment. The saline group: birds were injected with physiological saline buffer (0.75%) with a dosage of 1.0 mL/kg BW. The H 2 O 2 group: birds were given an injection of 10.0% H 2 O 2 with a dosage of 1.0 mL/kg BW. Data were reported as mean±standard error (n = 6). TRPC1, transient receptor potential channel 1; PMCA, plasma membrane Ca 2+ -ATPase; NCX, sodium-calcium exchanger; SERCA1, sarcoplasmic/endoplasmic reticulum calcium ATPase 1; MCU, mitochondrial calcium uniporter; BW, body weight. a,b denoted p<0.05.

Article Snippet: The antibodies of plasma membrane Ca 2+ -ATPase (PMCA bs-4978R), transient receptor potential channel 1 (TRPC1 bs-10404R), and sodium-calcium exchanger (NCX bs-1550R) were produced by Bioss biotechnology company (Beijing, China).

Techniques: Expressing, Control, Injection, Saline, Membrane

Journal:

Article Title:

doi:

Figure Lengend Snippet: Potential mechanism of Tv1 antitumor activity inhibits COX2 and PGE2 function. In our model of Tv1 antitumor activity in liver cancer cells, overexpression of TRP channels (TRPC6 and V6) stimulates COX-2-dependent PGE2 production via enhanced [Ca 2+ ] dynamics. Influx of Ca 2+ can occur through voltage gated (VGC), receptor operated (ROC), and store operated (SOC) calcium channels. Transient receptor potential (TRP) channels contribute to store operated calcium (SOC) channels. Ca 2+ -dependent transcription factor NFAT is activated via dephosphorylation by calcineurin, which is activated upon binding of Ca 2+ /calmodulin. Ubiquitously present transcription factor NFAT regulates COX-2 expression and further prostaglandin E2 (PGE2) release in different cancer cells and its activation occurs through Ca 2+ influx associated with TRPC1-, TRPC3-, or TRPC6-associated SOC or ROC activities. PGE2 release plays multiple roles in cancer as shown. Upon Tv1 application to liver cancer (HCC) cells the pictured downstream pathways leading to proliferation inhibition and apoptosis are encountered.

Article Snippet: Rabbit polyclonal Anti-HERG (Kv11.1)-APC109, Anti TRPV6-ACC036, Anti TRPV2-ACC039, Anti TRPC1-ACC-118 were purchased from Alomone lab, Israel.

Techniques: Activity Assay, Over Expression, De-Phosphorylation Assay, Binding Assay, Expressing, Activation Assay, Inhibition