Characterization of the pathophysiology of voiding dysfunction in transgenic mice for sickle cell disease: molecular analysis

• Grant number: 23/03966-5
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: May 01, 2023
• End date: March 31, 2024
• Field of knowledge: Health Sciences - Pharmacy
• Principal Investigator: Fábio Henrique da Silva
• Grantee: Danillo Andrade Pereira
• Host Institution: Universidade São Francisco (USF). Campus Bragança Paulista. Bragança Paulista , SP, Brazil
• Associated research grant: 17/08122-9 - Priapism and voiding dysfunction in Sickle Cell Disease: pathophysiology and new drug candidates, AP.JP

Abstract

Epidemiological studies point to an association between sickle cell anemia andvoiding dysfunction, but the pathophysiological mechanisms involved remain unclear.understandable. There are only four experimental studies aimed at understanding thevoiding dysfunction in sickle cell anemia, and therefore the pathophysiology is still little known.explored. In an animal model, the excess of reactive oxygen species in thelower urinary tract appears to contribute to voiding dysfunction. In animal modelof overactive bladder, a previous study showed that NO-deficient male micethey present detrusor hypertrophy and hyperactivity. However, in sickle cell anemiathe molecular alterations of the contraction and relaxation signal pathway in the bladder waslittle explored, as well as oxidative stress. The objective of this project is to investigatethe main proteins involved in the contraction and relaxation of smooth muscledetrusor of sickle cell mice.