Alquisiras-Burgos Iván, Peralta-Arrieta Irlanda, Espinoza-Rojo Mónica, Salazar-Salgado Alejandro, Antonino-Olguín Iván, Sánchez-Mendoza Alicia, Sánchez-Aguilar María, Ruiz-Tachiquín Martha-Eugenia, Valdez-Salazar Hilda-Alicia, Ortiz-Plata Alma, Franco-Pérez Javier, Hernández-Cruz Arturo, Aguilera Penélope
Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico.
Laboratorio de Transducción de Señales, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México, Mexico.
Front Mol Neurosci. 2025 Apr 17;18:1536409. doi: 10.3389/fnmol.2025.1536409. eCollection 2025.
The sulfonylurea receptor 1 (SUR1) has been classified as a member of the adenosine triphosphate (ATP)-binding cassette (ABC) transporter superfamily. SUR1, unlike the classic ABC transporters, assembles with Kir6.2, forming K channels to regulate the flux of potassium ions. In the central nervous system, SUR1 is weakly expressed in some brain regions but is induced by pathological conditions in the different cell types of the neurovascular unit. Therefore, we first analyzed the expression of SUR1 in various rat tissues and brain regions to identify SUR1 isoforms and their mRNA exon composition under physiological conditions. Later, we focused on the SUR1 expression in the brain and heart after ischemia/reperfusion. We observed two SUR1 isoforms (170 and 60-75 kDa) abundantly expressed in most rat tissues, except for the testis and brain, where basal expression of these isoforms was relatively low and exhibit a band of 100 kDa. Every exons coding for the functional domains of SUR1 mRNA were amplified from the tissues and brain regions analyzed. Results from and experiments indicated that SUR1 isoforms previously identified (170 and 60-75 kDa) were dramatically overexpressed in the brain after middle cerebral artery occlusion followed by reperfusion. In contrast, myocardial infarction followed by reperfusion significantly reduced SUR1 isoform expression in the heart. This study demonstrates the expression of at least two SUR1 isoforms in various tissues and suggests that ischemic processes may differentially regulate SUR1 expression depending on the tissue injured.
磺脲类受体1(SUR1)已被归类为三磷酸腺苷(ATP)结合盒(ABC)转运蛋白超家族的成员。与经典的ABC转运蛋白不同,SUR1与Kir6.2组装在一起,形成钾通道以调节钾离子通量。在中枢神经系统中,SUR1在某些脑区中弱表达,但在神经血管单元的不同细胞类型中会因病理状况而被诱导表达。因此,我们首先分析了SUR1在各种大鼠组织和脑区中的表达,以确定生理条件下SUR1同工型及其mRNA外显子组成。随后,我们重点研究了缺血/再灌注后大脑和心脏中SUR1的表达情况。我们观察到两种SUR1同工型(170 kDa和60 - 75 kDa)在大多数大鼠组织中大量表达,但睾丸和脑除外,在这些组织中这些同工型的基础表达相对较低,且呈现出一条100 kDa的条带。从所分析的组织和脑区中扩增出了编码SUR1 mRNA功能域的每个外显子。实验结果表明,先前鉴定出的SUR1同工型(170 kDa和60 - 75 kDa)在大脑中动脉闭塞后再灌注时会显著过度表达。相反,心肌梗死后再灌注会显著降低心脏中SUR1同工型的表达。本研究证明了至少两种SUR1同工型在各种组织中的表达,并表明缺血过程可能根据受损组织的不同而对SUR1表达进行差异性调节。