Downregulation of miR-29b is associated with Peyronie's disease
Nenhuma Miniatura disponível
Citações na Scopus
Tipo de produção
article
Data de publicação
2022
Título da Revista
ISSN da Revista
Título do Volume
Editora
SAGE PUBLICATIONS LTD
Citação
UROLOGIA JOURNAL, v.89, n.3, p.451-455, 2022
Resumo
Background: Peyronie's disease (PD) is characterized by the formation of fibrous plaque in tunica albuginea, causing several problems in patients. The etiology of this disease is not fully understood, and there are few effective treatments. To better understand the molecular pathways of PD, we studied miR-29b, a microRNA that could be involved with this illness. MicroRNAs are endogenous molecules that act by inhibiting messenger RNA. MiR-29b regulates 11 of 20 collagen genes and the TGF-beta 1 gene, which are related to PD progression. Methods: We compared miR-29b expression in 11 patients with PD and 14 patients without PD (control group). For the patients with PD, we utilized samples from the fibrous plaque (n = 9), from the tunica albuginea (n = 11), and from the corpus cavernosum (n = 8). For the control group, we utilized samples from the tunica albuginea (n = 14) and from the corpus cavernosum (n = 10). MiR-29b expression was determined by q-PCR. Results: We found a downregulation of miR-29b in the fibrous plaque, tunica albuginea and corpus cavernosum of patients with PD in comparison with the control group (p = 0.0484, p = 0.0025, and p = 0.0016, respectively). Conclusion: Although our study has a small sample, we showed for the first time an evidence that the downregulation of miR-29b is associated with PD.
Palavras-chave
Peyronie's disease, microRNA, miR-29b
Referências
- Cai Yimei, 2009, Genomics Proteomics & Bioinformatics, V7, P147, DOI 10.1016/S1672-0229(08)60044-3
- Camelo A, 2016, ACTA UROLOGICA PORTU, V33, P75
- Cao W, 2019, BIOL RES, V52, DOI 10.1186/s40659-019-0260-5
- Cushing L, 2011, AM J RESP CELL MOL, V45, P287, DOI 10.1165/rcmb.2010-0323OC
- ElSakka AI, 1997, J UROLOGY, V158, P1391, DOI 10.1016/S0022-5347(01)64223-X
- Gelbard M, 2013, J UROLOGY, V190, P199, DOI 10.1016/j.juro.2013.01.087
- Haag SM, 2007, EUR UROL, V51, P255, DOI 10.1016/j.eururo.2006.05.002
- He Y, 2013, BIOCHIMIE, V95, P1355, DOI 10.1016/j.biochi.2013.03.010
- Hyun J, 2014, J MOL HISTOL, V45, P103, DOI 10.1007/s10735-013-9532-5
- Ivanovic RF, 2018, CANCER CELL INT, V18, DOI 10.1186/s12935-018-0516-0
- Katz D, 2019, MED SCI BASEL, V7, P2019
- Kriegel AJ, 2012, PHYSIOL GENOMICS, V44, P237, DOI 10.1152/physiolgenomics.00141.2011
- Li JX, 2016, MOL MED REP, V13, P4229, DOI 10.3892/mmr.2016.5062
- Luna C, 2011, INVEST OPHTH VIS SCI, V52, P3567, DOI 10.1167/iovs.10-6448
- Luna C, 2009, MOL VIS, V15, P2488
- Milenkovic U, 2019, SEX MED REV, V7, P679, DOI 10.1016/j.sxmr.2019.02.004
- Qin W, 2011, J AM SOC NEPHROL, V22, P1462, DOI 10.1681/ASN.2010121308
- Roderburg C, 2011, HEPATOLOGY, V53, P209, DOI 10.1002/hep.23922
- Steele Robert, 2010, Genes Cancer, V1, P381
- Taylor FL, 2007, UROL CLIN N AM, V34, P517, DOI 10.1016/j.ucl.2007.08.017
- van Rooij E, 2008, P NATL ACAD SCI USA, V105, P13027, DOI 10.1073/pnas.0805038105