Dataset Information

A possible mechanism of erectile dysfunction in coronavirus disease-19: Cavernosal smooth muscle damage: A pilot study.

ABSTRACT:

Introduction

Studies have reported that coronavirus disease 2019 (COVID-19) may cause erectile dysfunction (ED), however, its role in the pathophysiology of ED has not yet been fully elucidated. We aimed to elucidate COVID-19's effects on cavernosal smooth muscle, which has a pretty important role in erection physiology, by corpus cavernosum electromyography (cc-EMG).

Materials and methods

Twenty-nine male patients aged 20-50 years who applied to the urology outpatient clinic due to ED were included in the study. Nine patients that had COVID-19 and were treated as outpatients were classified as group 1, 10 patients who were hospitalized due to COVID-19 were classified as group 2, and 10 patients who did not have COVID-19 were classified as the control group (group 3). Patients underwent diagnostic evaluation including International Index of Erectile Function (IIEF)-5 form, penile color Doppler ultrasonography (CDUS), cc-EMG, and fasting serum levels of reproductive hormones (07-11am).

Results

According to penile CDUS and hormonal values results, there was no significant difference between the groups. According to cc-EMG results, amplitudes and relaxation capacities of the cavernosal smooth muscle of patients in group 3 were significantly higher than those in the other groups.

Conclusions

COVID-19 can cause ED not only by psychogenic and hormonal factors but also with cavernosal smooth muscle damage.

Clinical trial registration number

NCT04980508.

SUBMITTER: Unal S

PROVIDER: S-EPMC10261716 | biostudies-literature | 2023 Oct-Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

A possible mechanism of erectile dysfunction in coronavirus disease-19: Cavernosal smooth muscle damage: A pilot study.

Unal Selman S Uzundal Halil H Soydas Turker T Kutluhan Musab A MA Ozayar Asim A Okulu Emrah E Kayigil Onder O

Revista internacional de andrologia 20230613 4

<h4>Introduction</h4>Studies have reported that coronavirus disease 2019 (COVID-19) may cause erectile dysfunction (ED), however, its role in the pathophysiology of ED has not yet been fully elucidated. We aimed to elucidate COVID-19's effects on cavernosal smooth muscle, which has a pretty important role in erection physiology, by corpus cavernosum electromyography (cc-EMG).<h4>Materials and methods</h4>Twenty-nine male patients aged 20-50 years who applied to the urology outpatient clinic due ...[more]

PMID: 37413939

Similar Datasets

Project description:IntroductionHydrochlorothiazide has a negative influence on penile erection but little is known about the mechanism(s) involved.AimsTo characterize the effects of this diuretic on mouse corpus cavernosum (CC) smooth muscle in vitro and ex vivo.MethodsCC strips of C57BL/6 mice (12-16 weeks old) were mounted in organ baths containing Krebs-Henseleit solution and tissue reactivity was evaluated. Expression of genes encoding diuretic targets and enzymes involved in penile erection were evaluated by polymerase chain reaction.Main outcome measuresStimulation-response curves to phenylephrine (10 nmol/L-100 μmol/L) or to electrical field stimulation (1-32 Hz) were constructed, with or without hydrochlorothiazide. Strips of CC from mice after long-term hydrochlorothiazide treatment (6 mg/kg/day for 4 weeks) with or without amiloride (0.6 mg/kg/day for 4 weeks) in vivo also were studied. Nitric oxide and Rho-kinase pathways were evaluated.ResultsHydrochlorothiazide (100 μmol/L) increased the maximum response to phenylephrine by 64% in vitro. This effect was unaffected by the addition of indomethacin (5 μmol/L) but was abolished by N((ω))-nitro-L-arginine methyl ester (100 μmol/L). Hydrochlorothiazide (100 μmol/L) potentiated electrical field stimulation-induced contraction in vitro, but not ex vivo. Long-term treatment with hydrochlorothiazide increased the maximum response to phenylephrine by 60% and resulted in a plasma concentration of 500 ± 180 nmol/L. Amiloride (100μmol/L) caused rightward shifts in concentration-response curves to phenylephrine in vitro. Long-term treatment with hydrochlorothiazide plus amiloride did not significantly increase the maximum response to phenylephrine (+13%). Reverse transcriptase polymerase chain reaction did not detect the NaCl cotransporter in mouse CC. Hydrochlorothiazide did not change Rho-kinase activity, whereas amiloride decreased it in vitro and ex vivo (approximately 18% and 24% respectively). A 40% decrease in Rock1 expression also was observed after long-term treatment with hydrochlorothiazide plus amiloride.ConclusionHydrochlorothiazide potentiates contraction of smooth muscle from mouse CC. These findings could explain why diuretics such as hydrochlorothiazide are associated with erectile dysfunction.

Project description:Long-term daily administration of phosphodiesterase type 5 (PDE5) inhibitors in the rat prevents or reverses corporal veno-occlusive dysfunction (CVOD) and smooth muscle cell (CSMC) loss and fibrosis, in both aging and bilateral cavernosal nerve resection (BCNR) models for erectile dysfunction. In the aging rat model, corporal implantation of skeletal muscle-derived stem cells (MDSC) reverses CVOD. Nitric oxide (NO) and cyclic guanosine monophosphate can modulate stem cell lineage.To investigate in the BCNR model the effects of sildenafil at lower doses, alone or in combination with MDSC or the NO donor molsidomine, on CVOD and the underlying corporal histopathology.CVOD, histological, and biochemical markers in rat corporal tissue. Methods.? Rats subjected to BCNR were maintained for 45 days either untreated, or received sildenafil in the water or retrolingually at 10, 2.5, and 1.25 mg/kg/day (medium, low, and very low doses), or intraperitoneal molsidomine, or MDSC implantation into the corpora cavernosa separately or in combination. Cavernosometry evaluated CVOD. Histopathology was assessed on penile sections by Masson trichrome, immunohistochemistry for ?-smooth muscle actin (ASMA), or immunofluorescence for neuronal nitric oxide synthase (nNOS)/neurofilament 70, and in fresh tissue by Western blot for various markers and picrosirius red for collagen.All treatments normalized erectile function (drop rate), and most increased the CSMC/collagen ratio and ASMA expression in corporal tissue sections, and reduced collagen content in the penile shaft. MDSC also increased nNOS and brain-derived neurotrophic factor. The combination treatment was not superior to MDSC or sildenafil given alone, and upregulated PDE5.Lowering the dose of a continuous long-term sildenafil administration still maintained the prevention of CVOD in the BCNR rat previously observed, but it was less effective on the underlying histopathology. As in the aging rat model, MDSC also counteracted CVOD, but supplementation with very low-dose sildenafil did not improve the outcome.

Project description:ObjectiveTo construct a corpus cavemosum smooth muscle cell (CCSMCs) line with TEAD1 knockout from diabetic rats with erectile dysfunction (ED) using CRISPR/Cas9 technology and explore the role of TEAD1 in phenotypic modulation of CCSMCs in diabetic rats with ED.ObjectiveModels of diabetic ED were established in male Sprague-Dawley rats by intraperitoneal injection of streptozotocin. CCSMCs from the rat models were primarily cultured and identified with immunofluorescence assay. Three sgRNAs (sgRNA-1, sgRNA-2 and sgRNA-3) were transfected via lentiviral vectors into 293T cells to prepare the sgRNA-Cas9 lentivirus. CCSMCs from diabetic rats with ED were infected by the lentivirus, and the cellular expression of TEAD1 protein was detected using Western blotting. In CCSMCs infected with the sgRNA-Cas9 lentivirus (CCSMCs-sgRNA-2), or the empty lentiviral vector (CCSMCs-sgRNA-NC) and the blank control cells (CCSMCs-CK), the expressions of cellular phenotypic markers SMMHC, calponin and PCNA at the mRNA and protein levels were detected using real-time fluorescence quantitative RT-PCR (qRT-PCR) and Western blotting, respectively.ObjectiveThe primarily cultured CCSMCs from diabetic rats with ED showed a high α-SMA-positive rate of over 95%. The recombinant lentivirus of TEAD1-sgRNA was successfully packaged, and stable TEAD1-deficient CCSMC lines derived from diabetic rat with ED were obtained. Western blotting confirmed that the protein expression of TEAD1 in TEAD1-sgRNA-2 group was the lowest (P < 0.05), and this cell line was used in subsequent experiment. The results of qRT-PCR and Western blotting showed significantly up-regulated expressions of SMMHC and calponin (all P < 0.05) and down-regulated expression of PCNA (all P < 0.05) at both the mRNA and protein levels in TEAD1-deficient CCSMCs from diabetic rats with ED.ObjectiveWe successfully constructed a stable CCSMCs line with CRISPR/Cas9-mediated TEAD1 knockout from diabetic rats with ED. TEAD1 gene knockout can induce phenotype transformation of the CCSMCs from diabetic rats with ED from the synthetic to the contractile type.

Dataset Information

A possible mechanism of erectile dysfunction in coronavirus disease-19: Cavernosal smooth muscle damage: A pilot study.

Introduction

Materials and methods

Results

Conclusions

Clinical trial registration number

Publications

A possible mechanism of erectile dysfunction in coronavirus disease-19: Cavernosal smooth muscle damage: A pilot study.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets