Filamina plaquetaria: una proteína del citoesqueleto integradora de la función celular / Platelet filamin: a cytoskeletal protein involved in cell signal integration and function

Activation of cellular receptors by diverse stimuli induces dramatic changes in shape and function to respond to the new circumstances of the cell. This modified behavior depends on the reorganization of the peripheral actin meshwork. An outstanding example of these processes can be found in platelets, from which much of the information available on cytoskeletal function has been obtained. Among the many actin-crosslinking proteins like spectrin, fimbrin or alpha actinin, filamin a (FLNa) emerges as the one with the highest potential in initiating the polimerization of actin filaments (F-actin) during the formation of tridimensional actin gels. FLNa also links actin filaments to the cytosolic domain of many membrane glycoproteins in platelets through its C-terminal region. In addition to participating in cell shape changes, FLNa is a scaffoldding protein that recruits numerous proteins involved in a completely different set of functions, including signal transduction, gene transcription regulation, and receptor translocation; however, the physiological role of FLNa in these processes has remained elusive. The purpose of the present communication is to briefly describe the characteristics of the macromolecules able to interact with FLNa and to discuss a possible role of FLNa during the transduction of signals from those molecular elements in platelets.

Trypanosoma cruzi isolates from Mexican and Guatemalan acute and chronic chagasic cardiopathy patients belong to Trypanosoma cruzi I

Trypanosoma cruzi is classified into two major groups named T. cruzi I and T. cruzi II. In the present work we analyzed 16 stocks isolated from human cases and four isolated from triatomines from diverse geographical origins (Mexico and Guatemala). From human cases four were acute cases, six indeterminates, and six from chronic chagasic cardiophatic patients with diagnosis of dilated cardiomyopathy established based on the left-ventricular end systolic dimension and cardiothoracic ratio on chest X-radiography and impaired contracting ventricle and different degree conduction/rhythm aberrations. DNA samples were analyzed based on mini-exon (ME) polymorphism, using a pool of three oligonucleotide for the amplification of specific intergenic region of T. cruzi ME gene. All the Mexican and Guatemalan isolates regardless their host or vector origin generated a 350 bp amplification product. In conclusion T. cruzi I is dominant in Mexico and Guatemala even in acute and chronic chagasic cardiopathy patients. To our knowledge, this is the first study describing predominance of T. cruzi I in human infection for North and Central America.

Fosforilación de tau y enfermedad de Alzheimer / Phosphorylation of Tau and Alzheimer's Disease

Tau forma parte importante del citoesqueleto en neuronas; estabilizando microtúbulos, manteniendo la forma celular y como via de transporte axonal. Sin embargo, por mecanismos desconocidos, tau sufre modificaciones importantes como son fosforilación anormal debida a la actividad desequilibrada de varias cinasas y fosfatasas, afectando su función biológica normal. Bajo estas circunstancias tau comienza a agregarse originando complejos proteicos denominados desarreglos neurofibrilares (NFTS) que son hallazgos histopatológicos característicos de la enfermedad de Alzheimer junto con las placas seniles. Esta revisión esta enfocada principalmente a describir la estructura de tau y la participación de diferentes cinasas en su regulación.

Tau is an important component of neuronal cytosqueleton; the protein stabilizas microtubules, maintains cell shape and axonal transport mechanisms. Howevwe, for unknown reasons tau experiments important postranslation modifications including enhanced phosphorylation due to unbalanced activity between kinases and phosphatases, affecting its normal biological function. Under these circumstances tau begins to aggregate into neurofibrillary tangles (NFTS) complexes which are pathological hallmarks of Alzheimer's disease together with senile plaques. This review is mainly concerned with the role that different kinase play into the regulation of tau structure and function.

Superoxide dismutase activity of the Salicylate-Iron complex

Background. Scavenging of superoxide radical by salicylate-iron complex was studied to determine whether or not the salicylate-iron complex was able to catalyze the dismutation of superoxide radicals, the result perhaps yielding an explanation of the antioxidant and anti-inflammatory properties of the drug. Methods. the scavenging was studied with an assay that generates Oú- 2 without the intervention of metal ions. Results. Results indicated that, in the presence of iron, salicylate was able to bring about the catalytic dismutation of the superoxide radiacal. The rate of superoxide removal was dependent on both the concentration of iron and the salicylate:iron molar ratio. Conclusions. these results may help to explain the interaction of nonsteroidal anti-inflammatory drugs with free radicals and the anti-inflammatory properties of these agents, inasmuch as accumulating evidence indicates that much of the injury observed during inflammatory disorders may be mediated by oxidative stress frequently induced by iron-dependent reactions

Captopril and Glutathione inhibit the superoxide dismutase activity of Hg(II)

El propósito de este estudio fue determinar si el captopril, un inhibidor de la enzima convertidora de angiotensina, y el glutatión podían reaccionar con iones mercúricos y así modificar la dismutación catalítica del superóxido llevada a cabo por este metal. Con un ensayo que genera radicales superóxido, sin la intervención de iones matálicos, concentraciones crecientes de ambos reactivos inhibieron de manera progresiva la dismutación del superóxico llevada a cabo por el mercurio. La inhibición máxima se observó con una relación molar de captopril (glutation): Hg (II) =1. Estos resultados pueden ayudar a explicar el efecto protector y/o antioxidante de los compuestos con tioles durante la intoxicación con mercurio

Bases moleculares de la hipertension arterial inducida por cadmio / Molecular basis of the cadmium induced by arterial hypertension

Con el fin de esclarecer los mecanismos bioquímicos involucrados en el establecimiento de la enfermedad hipertensiva inducida por el cadmio, en este trabajo se estudió el efecto del metal sobre diversas funciones mitocondriales, a saber: transporte de calcio y producción de energía. La presencia de cadmio en el medio inhibe ambas funciones debido a la unión de este metal a los grupos sulfhidrilo presentes en las proteínas de las cuales dependen estos procesos. En base a estos resultados es posible proponer un esquema en el cual el cadmio produce de manera directa un efecto de vasoconstricción renal el cual a su vez explica otros mecanismos que aparecen durante la enfermedad hipertensiva