Expression of SUR1 isoforms in the brain and heart after ischemia/reperfusion
Por:
Alquisiras-Burgos, I, Peralta-Arrieta, I, Espinoza-Rojo, M, Salazar-Salgado, A, Antonino-Olguín, I, Sánchez-Mendoza, A, Sánchez-Aguilar, M, Ruiz-Tachiquín, ME, Valdez-Salazar, HA, Ortiz-Plata, A, Franco-Pérez, J, Hernández-Cruz, A, Aguilera, P
Publicada:
17 abr 2025
Resumen:
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 KATP 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 in vitro and in vivo 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.
Filiaciones:
Alquisiras-Burgos, I:
Inst Nacl Neurol & Neurocirug, Clin Enfermedad Vasc Cerebral, Manuel Velasco Suarez, Mexico
Peralta-Arrieta, I:
Inst Nacl Enfermedades Respiratorias Ismael Cosio, Lab Transducc Senales, Mexico City, Mexico
Espinoza-Rojo, M:
Univ Autonoma Guerrero, Fac Ciencias Quim Biol, Lab Biol Mol & Genomica, Chilpancingo De Los Bravo, Mexico
Salazar-Salgado, A:
Univ Nacl Autonoma Mexico, Dept Neuropatol Mol, Inst Fisiol Celular, Mexico City, Mexico
Antonino-Olguín, I:
Inst Nacl Neurol & Neurocirug, Clin Enfermedad Vasc Cerebral, Manuel Velasco Suarez, Mexico
Univ Autonoma Guerrero, Fac Ciencias Quim Biol, Lab Biol Mol & Genomica, Chilpancingo De Los Bravo, Mexico
Sánchez-Mendoza, A:
Inst Nacl Cardiol Ignacio Chavez, Dept Farmacol, Mexico City, Mexico
Sánchez-Aguilar, M:
Inst Nacl Cardiol Ignacio Chavez, Dept Farmacol, Mexico City, Mexico
Ruiz-Tachiquín, ME:
Hosp Especial, Ctr Med Nacl Siglo XXI, Unidad Invest Med Enfermedades Endocrinas, Inst Mexicano Seguro Social, Ciudad Mex, Mexico City, Mexico
Valdez-Salazar, HA:
Ctr Med Nacl Siglo XXI, Unidad Invest Med Enfermedades Infecciosas & Paras, Inst Mexicano Seguro Social, Mexico City, Mexico
Ortiz-Plata, A:
Inst Nacl Neurol & Neurocirugia Manuel Velasco Sua, Lab Patol Expt, Mexico City, Mexico
Franco-Pérez, J:
Inst Nacl Neurol & Neurocirug, Clin Enfermedad Vasc Cerebral, Manuel Velasco Suarez, Mexico
Hernández-Cruz, A:
Univ Nacl Autonoma Mexico, Dept Neuropatol Mol, Inst Fisiol Celular, Mexico City, Mexico
Aguilera, P:
Inst Nacl Neurol & Neurocirug, Clin Enfermedad Vasc Cerebral, Manuel Velasco Suarez, Mexico
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