Related Experiment Video
Updated: Jul 17, 2025
Cavernous Nerve Stimulation and Recording of Intracavernous Pressure in a Rat
Published on: April 23, 2018
Effects of endoplasmic reticulum stress on erectile function in rats with cavernous nerve injury
Shanjie Guo1, Danfeng Zhao1,2, Zhenjie Zang3
1Department of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, China.
Background:
Erectile dysfunction (ED) occurs in an increasing number of patients after radical prostatectomy and cystectomy, and the phenotypic modulation of corpus cavernosum smooth muscle cells is closely related to ED.
Aim:
To determine whether endoplasmic reticulum stress (ERS) is implicated in the phenotypic modulation of ED induced by bilateral cavernous nerve injury (BCNI).
Methods:
In total, 36 Sprague-Dawley rats were randomly divided into 3 groups: sham, in which rats received sham surgery with bilateral cavernous nerve exposure plus phosphate-buffered saline; control, in which rats received BCNI plus phosphate-buffered saline; and experimental, in which rats received BCNI plus 4-phenylbutyric acid. Analysis of variance and a Bonferroni multiple-comparison test were utilized to evaluate differences among groups.
Outcomes:
Erectile function, smooth muscle/collagen ratios, and the expression levels of phenotypic modulation and ERS were measured.
Results:
Two ratios-maximum intracavernosal pressure/mean arterial pressure and smooth muscle/collagen-were decreased in the control group as compared with the sham group. In penile tissue, there was increased expression of GRP78 (78-kDa glucose-regulated protein), p-PERK/PERK (phosphorylated protein kinase R-like endoplasmic reticulum kinase/protein kinase R-like endoplasmic reticulum kinase), caspase 3, CHOP (C/EBP homologous protein), and OPN (osteopontin) but decreased expression of nNOS (neuronal nitric oxide synthase) and α-SMA (α-smooth muscle actin). As compared with the control group, erectile function was improved and pathologic changes were partially recovered in the experimental group.
Clinical Translation:
The present study demonstrated that ERS is involved in ED caused by cavernous nerve injury, thereby providing a new target and theoretical basis for clinical treatment.
Strengths And Limitations:
The present study demonstrated for the first time that ERS is related to ED caused by cavernous nerve injury. Inhibition of ERS reverses phenotypic modulation and improves erectile function in rats with BCNI. Additional in vitro studies should be performed to verify these conclusions and explore the specific mechanism of phenotypic modulation.
Conclusion:
The present study demonstrated that inhibiting ERS reverses phenotypic modulation and enhances erectile function in rats with BCNI.
Related Concept Videos
01:17Role of ER in the Secretory Pathway
Components of the secretory pathway
About a third of proteins synthesized in the cell are sorted via the secretory route. They shuffle between different compartments in membrane-bound vesicles until they reach their final destination. The main intracellular compartments involved...
01:17Male Sexual Response: Erection & Ejaculation
The blood filling the erectile tissues compresses the veins, which helps to prevent blood from leaving...
01:28Nitric Oxide Signaling Pathway