Effect of 17β-Estradiol on Intracellular Ca²⁺ Levels in Renal Tubular Cells

Abstract

The effect of 17β-estradiol on intracellular Ca²⁺ concentrations ([Ca²⁺]_i) in Madin Darby canine kidney cells was investigated by using the fluorescent dye fura-2. 17β-Estradiol (5–100 µmol/l) induced instantaneous increases in [Ca²⁺]_i in a concentration-dependent manner. Ca²⁺ removal inhibited 45 ± 15% of the Ca²⁺ signal. In Ca²⁺-free medium, pretreatment with 50 µmol/l 17β-estradiol abolished the [Ca²⁺]_i increases induced by 2 µmol/l carbonylcyanide m-chlorophenylhydrazone (CCCP; a mitochondrial uncoupler), 1 µmol/l thapsigargin (an endoplasmic reticulum Ca²⁺ pump inhibitor) and 50 µmol/l brefeldin A (an antibiotic which disperses the Golgi complex), but pretreatment with brefeldin A, CCCP and thapsigargin only partly inhibited the 17β-estradiol-induced [Ca²⁺]_i signal. Adding 3 mmol/lCa²⁺ increased [Ca²⁺]_i in cells pretreated with 5–100 µmol/l 17β-estradiol in Ca²⁺-free medium. Pretreatment with 1 µmol/l U73122 to abolish the formation of inositol-1,4,5-trisphosphate inhibited 50% of the Ca²⁺ release induced by 50 µmol/l 17β-estradiol. 17β-Estradiol (20 µmol/l) also increased [Ca²⁺]_i in human bladder cancer cells and prostate cancer cells. Collectively, this study shows that 17β-estradiol evoked a significant internal Ca²⁺ release and external Ca²⁺ entry possibly in a nongenomic manner.

Estrogen Controls embryonic stem cell proliferation via store‐operated calcium entry and the nuclear factor of activated T‐cells (NFAT)

“…E2 was previously found to regulate mESC proliferation via both genomic and non‐genomic pathways (Han et al, 2006). E2 has been reported to trigger Ca 2+ release or Ca 2+ influx via non‐genomic pathway in various cell types (Picotto et al, 1999; Perret et al, 2001; Chen et al, 2002). In the present investigation, we found that E2 could not elicit any Ca 2+ influx within 10 min in mESCs (E2 at concentrations from 1 pM to 1 µM were tested; data not shown).…”

Mechanism of Paroxetine‐Induced Cell Death in Renal Tubular Cells

“…The inositol‐1,4,5‐trisphosphate‐sensitive Ca 2+ store is the major Ca 2+ store that releases Ca 2+ into the cytosol when cells are stimulated by endogenous agents, such as bradykinin and ATP [12,13]. But exogenous agents can release Ca 2+ from inositol‐1,4,5‐trisphosphate‐insensitive stores [15].…”

“…But exogenous Author for correspondence: Chung-Ren Jan, Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan (fax +886-7-3468056, e-mail crjan@isca.vghks.gov.tw). agents can release Ca 2+ from inositol-1,4,5-trisphosphateinsensitive stores [15].…”

Effect of Anandamide on Cytosolic Ca2+ Levels and Proliferation in Canine Renal Tubular Cells

“…The Madin Darby canine kidney (MDCK) cell line is a useful model for renal cell research. It has been shown that in this cell , [Ca 2+ ] i can be increased in response to the stimulation of various endogenous and exogenous compounds, such as ATP (Jan et al 1998a), linoleamide (Huang & Jan 2001), and oestrogens (Chen et al 2002) etc.…”