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El péptido intestinal vasoactivo reduce la hipertensión ocular mediante la regulación de la unión estrecha de la
Liwen Chen1, Xiaoqin Yan1, Zhaoxia Luo1
1Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Annals of medicine
|August 27, 2025
Resumen
El péptido intestinal vasoactivo (VIP) reduce la presión intraocular alta (IOP) inhibiendo la unión estrecha (TJ) en la malla trabecular (TM) a través de la vía Rab13-PKA, ofreciendo nuevos conocimientos terapéuticos para la hipertensión ocular.
Área de la Ciencia:
- Oftalmología
- Biología celular
- Fisiología
Sus antecedentes:
- El canal de Schlemm y la malla trabecular (TM) son clave para mantener la homeostasis de la presión intraocular (IOP).
- El péptido intestinal vasoactivo (VIP, por sus siglas en inglés) previamente mostró potencial para reducir la presión arterial interna alta al afectar a la F-actina en el endotelio del canal de Schlemm.
- Este estudio investiga el mecanismo de VIP en las uniones cerradas de TM (TJ).
Objetivo del estudio:
- Para aclarar el mecanismo por el cual VIP influye en las uniones estrechas de TM.
- Para determinar el papel de VIP en la regulación de la hipertensión ocular a través de la MT.
- Para explorar la vía de señalización Rab13-PKA en el efecto de VIP en TM.
Principales métodos:
- Se han establecido modelos de alta PIO en ratas y células de malla trabecular humana (CTMH).
- Se evaluó la PIO utilizando TonoLab y la densidad de tejido TM mediante tinción H&E.
- Se utilizó el bloqueo occidental, la qRT-PCR, la inmunofluorescencia y la inmunohistoquímica para analizar la expresión de ZO-1, Claudin-1, Rab13 y PKA.
Principales resultados:
- Aumento de la expresión de las proteínas TJ ZO-1 y Claudin-1 en modelos de alta PIO.
- La sobreexpresión de VIP y Rab13 redujo ZO-1 y Claudin-1 en los HTMC estimulados por presión.
- VIP disminuyó las proteínas TJ y la densidad TM en ratas, aliviando la hipertensión ocular.
Conclusiones:
- VIP inhibe las uniones tensas TM mediante la regulación del complejo de señalización Rab13-PKA.
- Este mecanismo reduce efectivamente la hipertensión ocular en ratas.
- Los hallazgos ofrecen nuevas estrategias terapéuticas para el tratamiento de la hipertensión ocular.
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