ArticleBiological research2019
IcarisideII facilitates the differentiation of ADSCs to SCs via let-7i/STAT3 axis to preserve erectile function.
Article in Biological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- An updated narrative review on revolutionizing erectile dysfunction treatment: the crucial role of trophic factors in Adipose-Derived stem cell therapy.BMC urology · 2025Review
- Diversity and epimedium biotransformation potential of cultivable endophytic fungi associated with Epimedium brevicornum Maxim in the Qinling Mountains, China.Microbial cell factories · 2025Article
- Lacosamide alleviates bilateral cavernous nerve injury-induced erectile dysfunction in the rat model by ameliorating pathological changes in the corpus cavernosum.International journal of impotence research · 2024Article
- Flavonoids in Combination with Stem Cells for the Treatment of Neurological Disorders.Neurochemical research · 2023Review
- Advancements in the Biotransformation and Biosynthesis of the Primary Active Flavonoids Derived fromMolecules (Basel, Switzerland) · 2023Review
- Therapies Based on Adipose-Derived Stem Cells for Lower Urinary Tract Dysfunction: A Narrative Review.Pharmaceutics · 2022Review
- The role of microRNAs in erectile dysfunction: From pathogenesis to therapeutic potential.Frontiers in endocrinology · 2022Review
- Let-7i-5p enhances cell proliferation, migration and invasion of ccRCC by targeting HABP4.BMC urology · 2021Article
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3 authors.
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Abstract
backgroundIcarisideII (ICAII) could promote the differentiation of adipose tissue-derived stem cells (ADSCs) to Schwann cells (SCs), leading to improvement of erectile function (EF) and providing a realistic therapeutic option for the treatment of erectile dysfunction (ED). However, the underlying molecular mechanisms of ADSCs and ICAII in this process remain largely unclear.
methodsADSCs were treated with different concentrations of ICAII. Cell proliferation was determined by MTT assay. qRT-PCR and western blot were performed to detect expressions of SCs markers, signal transducer and activator of transcription-3 (STAT3), and microRNA-let-7i (let-7i). Luciferase reporter assay was conducted to verify the regulatory relationship between let-7i and STAT3. The detection of intracavernosal pressure (ICP) and the ratio of ICP/mean arterial pressure (MAP) were used to evaluate the EF in bilateral cavernous nerve injury (BCNI) rat models.
resultsICAII promoted cell proliferation of ADSCs in a dose-dependent manner. The mRNA and protein levels of SCs markers were increased by ICAII treatment in a dose-dependent manner in ADSCs. Moreover, let-7i was significantly decreased in ICAII-treated ADSCs and upregulation of let-7i attenuated ICAII-induced promotion of SCs markers. In addition, STAT3 was a direct target of let-7i and upregulated in ICAII-treated ADSCs. Interestingly, overexpression of STAT3 abated the let-7i-mediated inhibition effect on differentiation of ADSCs to SCs and rescued the ICAII-mediated promotion effect on it. Besides, combination treatment of ADSCs and ICAII preserved the EF of BCNI rat models, which was undermined by let-7i overexpression.
conclusionICAII was effective for preserving EF by promoting the differentiation of ADSCs to SCs via modulating let-7i/STAT3 pathway.
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