A5033997918- Connexins and lens biology
- Hearing, Cochlea, Tinnitus, Genetics
- Biochemical Analysis and Sensing Techniques
- Liver Disease Diagnosis and Treatment
- Hearing Loss and Rehabilitation
- Ion channel regulation and function
- Nicotinic Acetylcholine Receptors Study
- Cardiovascular Function and Risk Factors
- Cancer, Lipids, and Metabolism
- RNA regulation and disease
- Blood Pressure and Hypertension Studies
- Erythrocyte Function and Pathophysiology
- Organ Transplantation Techniques and Outcomes
- Heart Failure Treatment and Management
- Lipid metabolism and disorders
- Adipose Tissue and Metabolism
- Abdominal vascular conditions and treatments
- Acute Ischemic Stroke Management
- Venomous Animal Envenomation and Studies
- Diet and metabolism studies
- Neuroscience of respiration and sleep
- Cardiovascular Health and Disease Prevention
- Liver Disease and Transplantation
- bioluminescence and chemiluminescence research
- Effects of Radiation Exposure
Institute of Cell Biology and Neurobiology
2016-2022
Università Cattolica del Sacro Cuore
2017-2021
National Research Council
2016-2021
Veneto Institute of Molecular Medicine
2015-2017
University of Bologna
2013-2016
University of Padua
2014-2015
Policlinico S.Orsola-Malpighi
2013
Mutations in the genes encoding for gap junction proteins connexin 26 (Cx26) and 30 (Cx30) have been linked to syndromic nonsyndromic hearing loss mice humans. The release of ATP from hemichannels cochlear nonsensory cells has proposed be main trigger action potential activity immature sensory inner hair (IHCs), which is crucial refinement developing auditory circuitry. Using knock-out mice, we show that IHCs fire spontaneous potentials even absence ATP-dependent intercellular Ca 2+...
Mutations in GJB2, the gene that encodes connexin 26 (Cx26), are most common cause of sensorineural hearing impairment. The truncating variant 35delG, which determines a complete loss Cx26 protein function, is prevalent GJB2 mutation several populations. Here, we generated and analyzed Gjb2
Background: Mutations leading to changes in properties, regulation or expression of connexin–made channels have been implicated twenty-eight distinct human hereditary diseases. Eight these result from variants connexin 26 (Cx26), a protein critically involved cell-cell signaling the inner ear and skin. Lack non-toxic drugs with defined mechanisms action poses serious obstacle therapeutic interventions for diseases caused by mutant connexins. In particular, molecules that specifically...
Numerous currently incurable human diseases have been causally linked to mutations in connexin (Cx) genes. In several instances, pathological generate abnormally active Cx hemichannels, referred also as "leaky" hemichannels. The goal of this study was assay the vivo efficacy a potent antagonist antibody targeting
// Bianca Calì 1,2 , Stefano Ceolin 3 Federico Ceriani 1,3 Mario Bortolozzi Andrielly H.R. Agnellini Veronica Zorzi Andrea Predonzani 4 Vincenzo Bronte 1,5 Barbara Molon 4,* and Fabio Mammano 1,3,6,* 1 Foundation for Advanced Biomedical Research, Venetian Institute of Molecular Medicine, Padua, Italy 2 University Department Surgery Oncology Gastroenterology, Immunology Section, Physics Astronomy, IRCCS, Istituto Oncologico Veneto, 5 Verona Hospital, Pathology Diagnostics, Verona, 6 Present...
Using microfluidics, ATP biosensors, multiphoton microscopy and genetically targeted mice, we show that release through connexin hemichannels, not pannexin 1 channels, underlies spontaneous Ca<sup>2+</sup> wave propagation in the greater epithelial ridge of developing cochlea.
We have previously shown that in vitro transduction with bovine adeno-associated viral (BAAV) vectors restores connexin expression and rescues gap junction coupling cochlear organotypic cultures from connexin-deficient mice are models DFNB1 nonsyndromic hearing loss deafness. The aims of this study were to manipulate inner ear vivo using BAAV vectors, identify the optimal route vector delivery. Injection a encoding bacterial Cre recombinase via canalostomy adult floxed 26 (Cx26) alleles...
Background Many risk factors are known to predict ischaemic events and mortality in the elderly people, but their ranking of importance remains uncertain. This study was designed identify compare main predictors total (TM), cardiovascular (CVM) non-cardiovascular (NCVM) older adults. Methods Nine hundred seventy-nine community resident adults aged ≥ 65 years, free previous heart failure events, participated study. The univariate multivariate (Cox regression) relationships baseline factors,...
Panx1 forms plasma membrane channels in brain and several other organs, including the inner ear. Biophysical properties, activation mechanisms modulators of have been characterized detail, however impact on auditory function is unclear due to conflicts published results. To address this issue, hearing performance cochlear Panx1−/− mouse strain, first with a reported global ablation Panx1, were scrutinized. Male female homozygous (Panx1−/−), hemizygous (Panx1+/−) their wild type (WT) siblings...
Pathogenic mutations in the Gjb2 and Gjb6 genes, encoding connexin 26 (Cx26) 30 (Cx30), respectively, have been linked to most frequent monogenic hearing impairment, nonsyndromic loss, deafness DFNB1. It is known that Cx26 plays an important role auditory development, while of Cx30 remains controversial. Previous studies found partial deletion can accelerate age-related loss (ARHL), a multifactorial complex disorder, with both environmental genetic factors contributing etiology disease....
Objectives The ultrasound investigation of carotid and vertebral arteries is routinely performed in stroke patients to determine the etiopathogenetic classification possible need revascularization. However, medium long-term prognostic implications ischemic are not yet known. Methods This study included 309 (mean age 76.3; 160 men). They all had undergone (carotid stenoses were measured according European Carotid Surgery Trial [ECST] method). After a median interval 9.4 months, telephone...
Pathogenic mutations in the non-syndromic hearing loss and deafness 1 (DFNB1) locus are primary cause of monogenic inheritance for prelingual loss. To unravel molecular pathways involved etiopathology look early degeneration biomarkers, we used a system biology approach to analyze Cx30-/- mice at an cochlear post-natal developmental stage. These DFNB1 mouse model with severely reduced expression levels two connexins inner ear, Cx30, Cx26. Integrated analysis miRNA mRNA profiles cochleae day...
Mutations in the genes encoding for gap junction proteins connexin 26 (Cx26) and 30 (Cx30) have been linked to syndromic nonsyndromic hearing loss mice humans. The release of ATP from hemichannels cochlear nonsensory cells has proposed be main trigger action potential activity immature sensory inner hair (IHCs), which is crucial refinement developing auditory circuitry. Using knock-out mice, we show that IHCs fire spontaneous potentials even absence ATP-dependent intercellular...