Related Experiment Video
Updated: Dec 6, 2025
Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology
Published on: August 18, 2014
Estrogen-regulated expression of SK3 channel in rat colonic smooth muscle contraction
Wenjie Xiong1, Ya Jiang1, Ting Yu1
1Department of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Aims:
Estrogen can induce inhibition of colonic smooth muscle contraction in male and female mice, which may lead to constipation; however, the mechanisms of inhibition are poorly understood. Hence, this study investigated the effect of estrogen on rat colonic smooth muscle contraction and role of small-conductance Ca2+-activated K+ 3 (SK3) and transcription factors (Sp1 and Sp3) in the underlying mechanisms.
Main Methods:
The experiment included 24 female Sprague-Dawley (SD) rats divided into 4 groups. The rats were oophorectomized surgically, and a silicone tube containing blank solvent, 0.3 mg/mL estrogen (E2), equal-concentration of estrogen and estrogen receptor antagonist (EI), and bovine serum albumin-E2 (BSA-E2) was implanted. The rats were sacrificed on day 14. The molecular insights were confirmed using real-time quantitative reverse transcription PCR (qRT-PCR) and western blot analyses to determine the effect of estrogenic stimulation on gene and protein expression analyses, respectively.
Key Findings:
The E2 group showed significantly greater SK3 expression (P < .005) compared with other groups and significantly lowers smooth muscle cell (SMC) contractility (P < .005). Estrogen stimulation and SK3 overexpression resulted in a significant decrease (P < .05) in Ca2+ mobilization in the E2 group versus the control group. Further, the E2 group showed significantly higher Sp1 mRNA (P < .05) but lower Sp3 mRNA expression (P < .05) and protein expression (P < .001) compared with other groups.
Significance:
E2 may promote SK3 expression by its genomic effect and inhibit colonic contraction by affecting SK3 expression via an interaction between Sp1 and Sp3.
Insights
Estrogen inhibits colonic smooth muscle contraction by increasing small-conductance Ca2+-activated K+ 3 (SK3) channel expression, influenced by transcription factors Sp1 and Sp3.
Area of Science:
- Physiology
- Molecular Biology
- Gastroenterology
Background:
- Estrogen is known to inhibit colonic smooth muscle contraction, potentially causing constipation.
- The precise molecular mechanisms underlying estrogen-induced colonic inhibition remain unclear.
Purpose of the Study:
- To investigate the effect of estrogen on rat colonic smooth muscle contraction.
- To elucidate the role of small-conductance Ca2+-activated K+ 3 (SK3) channels and transcription factors Sp1 and Sp3 in this process.
Main Methods:
- Oophorectomized Sprague-Dawley rats were treated with estrogen (E2), estrogen antagonist (EI), or control.
- Gene and protein expression of SK3, Sp1, and Sp3 were analyzed using qRT-PCR and Western blot.
- Colonic smooth muscle contractility and intracellular Ca2+ mobilization were measured.
Main Results:
- Estrogen treatment significantly increased SK3 expression and decreased colonic smooth muscle contractility.
- Estrogen stimulation led to reduced Ca2+ mobilization.
- Estrogen increased Sp1 mRNA and protein expression while decreasing Sp3 mRNA and protein expression.
Conclusions:
- Estrogen likely promotes SK3 expression through genomic effects.
- Estrogen-induced colonic inhibition may involve SK3 modulation via an interaction between Sp1 and Sp3 transcription factors.
More Related Videos
11:02Exploring Arterial Smooth Muscle Kv7 Potassium Channel Function using Patch Clamp Electrophysiology and Pressure Myography
Published on: September 14, 2012
08:30Preparation and Utilization of Freshly Isolated Human Detrusor Smooth Muscle Cells for Characterization of 9-Phenanthrol-Sensitive Cation Currents
Published on: January 31, 2020
