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Upcoming Seminars

Luis JV. Galietta, MSc - "Therapeutic strategies to correct the basic defect in cystic fibrosis"

Principal Investigator and Head of Cell Culture and Cytogenetics Core, Tigem, Naples, Italy
When Dec 18, 2018
from 12:00 PM to 01:30 PM
Where Tigem, Vesuvius Auditorium
Contact Name
Contact Phone 081-19230659
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Abstract
Cystic fibrosis (CF), one of the most frequent genetic diseases (approximately 6,000 patients in Italy), is caused by the defective function of CFTR, an epithelial anion channel.  Loss of chloride and bicarbonate secretion leads to a multi-organ disease that is particularly severe in the lungs.  Here, loss of CFTR causes impairment of antimicrobial defense mechanisms with consequent development of airway colonization by antibiotic-resistant bacteria.
Mutant CFTR protein can ben rescued with small molecules that can target the different defects caused by CF mutations.  One of our goals is to find novel “correctors”, i.e. small molecules that improve the folding, stability, and trafficking of CFTR with F508del or other similar mutations.  Recently, we identified compounds that, in combination with first generation correctors, markedly enhance chloride secretion in bronchial and nasal epithelial cells from CF patients.
A second goal of our studies is to develop alternative therapeutic strategies in CF.  For this purpose, we are considering two alternative targets.  The first target, TMEM16A, is another type of anion channel expressed in epithelial cells.  Its pharmacological stimulation could represent a strategy to bypass CF basic defect.  Recently, we screened a chemical library with the identification of putative TMEM16A activators.  These compounds are now under evaluation.  The second target, ATP12A, acts as a proton/potassium pump.  Its activity leads to abnormal acidification of CF airways.  We are studying ATP12A expression/role in the airway epithelium and developing a suitable functional assay with the final goal to identify pharmacological inhibitors.  These compounds could become novel drugs to normalize pH in the airways of CF patients.

Iain W. Mattaj, PhD, FRS, FMedSci - "Introducing Human Technopole"

Director General EMBL - European Molecular Biology Laboratory, Heidelberg, Germany
When Jan 14, 2019
from 12:00 PM to 01:00 PM
Where Tigem, Vesuvius Auditorium
Contact Name
Contact Phone 081-19230659
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Technological advances over the past decade have transformed opportunities for research in human systems as well as on models with direct relevance to human biology, thereby boosting possibilitiesfor scientists to develop improved, more targeted strategies for promoting human health and healthy ageing. The Human Technopole, a new institute for life science research that is coming into being in Milan, has the overarching goal of developing stratified approaches to improve patient care (personalised medicine) and quality of life. Research at the Human Technopole will take a comprehensive and interdisciplinary approach to health and ageing by integrating cutting-edge technologies with basic and translational science, starting with critical areas including genomics, computational biology, structural biology and neuroscience. In my talk I will introduce the Human Technopole project, outline future plans and how these will contribute to scientific development in Italy and Europe, and present the many opportunities the new institute offers to young scientists.

Florian Sennlaub, MD, PhD - "How genetic-risk variants of age–related macular degeneration shape pathogenic inflammation"

Sorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France
When Apr 09, 2019
from 12:00 PM to 01:30 PM
Where Tigem, Vesuvius Auditorium
Contact Name
Contact Phone 081-19230659
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Abstract
CD47 activation by Thrombospondin 1 (TSP-1) is essential in maintaining the subretinal immunosuppressive environment and prevents the subretinal accumulation of macrophages. Age-related Macular Degeneration (AMD), a highly heritable, major cause of blindness, is characterized by the breakdown of the immune-suppression and an accumulation of pathogenic MPs. Of all genetic factors, a variant of Complement factor H (CFH) and a risk haplotype of 10q26 are associated with greatest linkage to AMD. We recently showed that complement factor H (CFH) and in particular the AMD-associated CFH variant, curbs Thrombospondin 1 (TSP-1) activation of CD47. We now demonstrate that monocytes from homozygous carriers of the major AMD-risk haplotype of the 10q26 locus significantly overexpress the High-Temperature Requirement A Serine Peptidase 1 (HTRA1). Mechanistically we demonstrate that HTRA1 hydrolyses TSP-1, preventing its ability to activate CD47 and induce MP elimination. Our study reveals a comprehensive mechanism how CFH and HTRA1 participate in the pathogenesis of AMD and opens new therapeutic avenues to restore subretinal immunosuppressivity and inhibit the pathogenic subretinal inflammation.