Investigación FAME UACh

Dr. Hans Richter Becerra | Investigador FAME UACh

Dr. Hans G. Richter Becerra

Información Académica:

  • 1994: Licenciado en Bioquímica. Escuela de Bioquímica, Universidad Austral de Chile. Valdivia, Chile.
  • 2001: Doctor en Ciencias, Mención Biología Celular y Molecular. Escuela de Graduados. Facultad de Ciencias, Universidad Austral de Chile. Valdivia, Chile.
  • 2001-2003: Becado de postdoctorado. Grupo de investigación liderado por la Dra. María J. Serón-Ferré. Unidad de Reproducción y Desarrollo, Departamento de Ciencias Fisiológicas, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile.
  • 2007-2010: Senior postdoctoral fellow. Research team led by Dr Dino A. Giussani. Department of Physiology, Development & Neuroscience, University of Cambridge, UK.

Interés Científico (resumen)

Our ongoing investigation associates a group of Chilean, German, Scottish and English senior and young researchers with a common interest in developmental aspects of chronobiology as well as fetal programming of adult disease and their probable underlying mechanisms: chromatin remodeling, inflammation and oxidative stress. As for the latter prenatal insult, in recent reports we have demonstrated that the long term cardiovascular adverse effects of fetal hypoxia and undernutrition are programmed by oxidative stress and may be ameliorated by treatment of the pregnant dams with vitamin C or melatonin. However, the core long term goal of our research network, which is coordinated from our Laboratory of Developmental Chronobiology  (Valdivia, Chile), is establishing the risks of shift work, and how this system enforced by modern 24/7 society does impact our health at different levels. In this context, we are mainly interested in modeling the adverse pregnancy outcomes imposed by shift worker women on their offspring, particularly those which carry on into adulthood (i.e., developmental programming of adult chronic disease by gestational chronodisruption). Previously, epidemiological studies on the effects of chronodisruption on gestational outcomes had reported increased preterm delivery and low birth weight at term; both being strong predictors of late onset chronic disease. These findings prompted us to address the impact of chronodisruption during pregnancy on fetal global gene expression in different tissues. Using an integrative approach applied to longitudinal cohorts, at the behavioral, pathophysiological, systems, isolated organ, cellular and molecular levels, we are now determining whether and how metabolism, inflammatory response, transcriptional regulation, epigenetics, neuroendocrinology, circadian rhythms, cognitive behavior and cardiovascular physiology are individually or collectively affected in the adult offspring gestated under chronodisruption conditions. Our functional genomics analyses of genome-wide fetal gene expression have uncovered a number of pathophysiological deregulations inside different gene networks, which strongly correlate with our findings in the adult offspring which had been gestated under altered photoperiod, including: hypertrophic cardiomyopathy, significant differences in spatial cognitive skills and fasting glucose level, a prolonged response to intraperitoneal glucose, as well as decreased plasma levels of melatonin, corticosterone and C3/C4 complement factors. Notably, several of these fetal and adult pathophysiological alterations were reversed in the fetal and adult offspring of mothers receiving melatonin every day during gestation.

Líneas de Investigación

  • Cronobiología del desarrollo y programación fetal de enfermedades del adulto.

Proyectos Vigentes

2011-2015 : Developmental programming of chronic diseases in adult and aging individuals: The role of maternal melatonin in the regulation of fetal transcriptional and gene promoter activity. Proyecto Regular FONDECYT 1110220. Investigador Responsable.

2012-2016 : Decoding the rat fetal circadian system and the link of fetal chronodisruption to disease in adulthood. Proyecto Regular FONDECYT 1120938 (Dra. Claudia Torres-Farfán). Co-investigador

2012-2016 : Mecanismos fisiopatológicos de enfermedades crónicas del adulto impuestas por la alteración circadiana prenatal: valor terapéutico del tratamiento con melatonina a la madre expuesta a turnos nocturnos durante la gestación. Proyecto ANILLO ACT1116, Programa de Investigación Asociativa CONICYT. Director Alterno

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