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In 2023, UNamur opened a fourth CaNDLE call funded through the joint support of the Fonds Jérôme pour le développement durable and the Assemblée des Cercles of UNamur students. Discover one of the 7 selected projects.

In 2023, UNamur opened a fourth CaNDLE call funded through the joint support of the Fonds Jérôme pour le développement durable and the Assemblée des Cercles of UNamur students. Discover one of the 7 selected projects.

Summary: Impact of the UPR pathway on the establishment of the UVB-induced senescent phenotype Skin aging, influenced by a combination of intrinsic and extrinsic factors, leads to damage capable of altering skin functions. Among extrinsic factors, ultraviolet (UV) radiation is responsible for skin photoaging. In particular, these elements lead to an accumulation of senescent cells capable of contributing to the development of age-related pathologies such as skin cancers. Indeed, senescence is accompanied by profound morphological and molecular changes within the cell. This includes a modification of its secretome, which becomes enriched with pro-inflammatory cytokines, growth factors and extracellular matrix remodeling enzymes, altering the characteristics of tissues as they age. Nevertheless, the precise mechanisms leading to the senescent phenotype induced by UVB remain largely unknown. In this context, the main objective of this work was to identify molecular mechanisms underlying the establishment of UVB-induced senescence in normal human dermal fibroblasts (NHDFs), mechanisms that could contribute to skin aging. In vitro, we confirmed that repeated UVB exposures induce premature senescence in NHDFs and that this state is associated with activation of the three branches of the UPR (Unfolded Protein Response) pathway responsible for maintaining homeostasis of the endoplasmic reticulum (ER), the primary secretory compartment. These observations were supported by transcriptomic analysis, revealing regulatory elements linked to major senescence pathways and ER functions in UVB-exposed NHDFs. Subsequently, we showed that the ATF6α branch plays a central role in the occurrence of biomarkers of the UVB-induced senescent phenotype. Indeed, ATF6α invalidation not only protects against UVB-induced morphological changes, but reduces the percentage of SA-βgalactosidase (SA-βgal)-positive cells, prevents persistent DNA damage, and alters the expression of major factors of the senescence-associated secretory phenotype (SASP). As SASP exerts, among other things, a pro-tumoral action, we sought to assess whether the conditioned medium (CM) of UVB-exposed fibroblasts invalidated for ATF6α could impact the migration and invasion potential of melanoma-derived cells. However, we did not observe any ATF6α-dependent pro-migratory or pro-invasive effects.To highlight a potential role for ATF6α in another biological process, we exploited our transcriptomic and secretomic analyses and identified a possible effect of ATF6α on the paracrine control of the skin environment. To explore this, we focused on SASP factors (cytokines and metalloproteases) regulated by ATF6α and whose impact on the tissue environment was known. Next, we treated a reconstructed human epidermis (RHE) model with MC derived from NHDFs exposed to UVB or not, and invalidated or not for ATF6α. Surprisingly, we observed that MC from UVB-exposed NHDFs increased RHE thickness and basal keratinocyte proliferation, via an ATF6α-dependent mechanism. Finally, we identified IL8 as a major paracrine factor involved in this process, since IL-8 blockade by neutralizing antibodies prevents excessive keratinocyte proliferation. In conclusion, we report the role of ATF6α in UVB-induced senescence as well as its impact on the preservation of skin homeostasis under stress conditions notably through the regulation of the expression of SASP components. This suggests that ATF6α and its effectors could be promising targets controlling the effects of skin aging.Abstract: Impact of the UPR pathway on the establishment of the senescent phenotype induced by UVBSkin aging, influenced by a combination of intrinsic and extrinsic factors, can result in damage that has the potential to alter skin functions. Among extrinsic factors, ultraviolet (UV) radiation is responsible for skin photoaging. These factors notably contribute to the accumulation of senescent cells which in turn can contribute to the development of age-related pathologies, including skin cancers. Indeed, senescence is characterized by profound morphological and molecular changes within the cell. This includes a modification of its secretome, which becomes enriched in pro-inflammatory cytokines, growth factors, and matrix-remodeling enzymes, altering tissue characteristics during aging. However, the exact mechanisms driving the senescent phenotype induced by UVB remain largely unknown. In this context, the main objective of this work was to identify the underlying molecular mechanisms responsible for the establishment of UVB-induced senescence in normal human dermal fibroblasts (NHDFs), mechanisms that may play a role in skin aging. In vitro, we confirmed that repeated exposures to UVB induce premature senescence of NHDFs and that this state is associated with the activation of the three branches of the Unfolded Protein Response (UPR), which are responsible for maintaining endoplasmic reticulum (ER) homeostasis, the primary cellular secretion compartment. These observations were supported by transcriptomic analysis, revealing regulatory elements related to major senescence pathways and ER functions in UVB-exposed NHDFs. Subsequently, we demonstrated that the ATF6α branch plays a central role in the development of the UVB-induced senescent phenotype. Indeed, the silencing of ATF6α not only protects against morphological changes induced by UVB, but also reduces the percentage of senescence-associated β-galactosidase (SA-βgal) positive cells, prevents the persistence of DNA damage, and alters the expression of major factors associated with the senescence-associated secretory phenotype (SASP).The SASP, exerting a pro-tumoral action, led us to assess whether the conditioned medium (CM) from UVB-exposed fibroblasts invalidated for ATF6α could impact the migration and invasion potential of melanoma cells. However, we did not observe any ATF6α-dependent pro-migratory or pro-invasive effects. To highlight a potential role of ATF6α in another biological process, we further analyzed our transcriptomic and secretomic analyses and identified a possible effect of ATF6α on the paracrine control of the skin environment. To explore this, we focused on SASP factors (cytokines and metalloproteinases) regulated by ATF6α and whose impact on tissue environment was known. Subsequently, we treated a reconstructed human epidermis (RHE) model with CM from NHDFs exposed or not to UVB and invalidated or not for ATF6α. Surprisingly, we observed that the CM from UVB-exposed NHDFs increased the thickness of the RHE as well as the proliferation of basal keratinocytes, via an ATF6α-dependent mechanism. Finally, we identified IL8 as a major paracrine factor involved in this process, as blocking IL-8 with neutralizing antibodies prevented excessive proliferation of keratinocytes. In conclusion, we report the role of ATF6α in UVB-induced senescence and its impact on the preservation of skin homeostasis under stress conditions, particularly through the regulation of the expression of SASP components. This suggests that ATF6α and its effectors could be promising targets for controlling the effects of skin aging. Jury Prof. Yves POUMAY (Department of Medicine, UNamur), chairmanProf. Florence CHAINIAUX (Department of Biology, UNamur), promoter and secretaryProf. Olivier PLUQUET (Canther, University of Lille), co-promoterProf. Isabelle PETROPULOS (Adaptation Biologique et Vieillissement, Sorbonne Université)Prof. Jérôme LAMARTINE (Laboratoire de Biologie Tissulaire et d'Ingénierie thérapeutique, Université Claude Bernard Lyon 1)Prof. Fabienne FOUFELLE (Maladies métaboliques, diabète et comorbidités, Sorbonne Université)

What environmental impact can a contraceptive molecule have? Recent work by Professor Patrick Kestemont, Director of UNamur's Environmental and Evolutionary Biology Research Unit (URBE) and his team answers this question, and has just been published in the journal Environment International. The article's lead author is Sébastien Baekelandt, postdoctoral researcher at URBE.

Courses, exercise sessions, practical laboratory work, field days and internships... everything is done to ensure excellent mastery of concepts and the development of practical skills.

A multidisciplinary research team from the University of Namur (UNamur) and the UCL Namur University Hospital (Godinne campus) has just published a study in the journal Acta Neuropathologica that sheds light on some of the mysteries surrounding the origin of the pain experienced by patients with long COVID. Their findings suggest that these painful symptoms may be mediated by an autoimmune response. In other words: patients produce antibodies that attack their own neurons—those responsible for pain perception and deep body sensation, located along the spine. These highly promising results represent a major scientific breakthrough that opens new avenues for better understanding the disease and, ultimately, developing a treatment targeting the painful symptoms of long COVID.

On Monday February 19, students in Block 3 of Medicine at UNamur and Midwifery in the Paramedical Department at Hénallux took part in the second edition of a project to raise awareness of domestic violence. Conceived by the two institutions, the project takes the form of an escape game entitled "Oseras-tu poser la question" ("Dare to ask the question"). Used as part of the practical work on "Professional communication in healthcare" in the Medical Psychology course taught by Martin Desseilles, professor at the Faculty of Medicine at UNamur, this escape game aims to train future healthcare professionals to detect signs of domestic violence in patients during consultations and to act accordingly.

Lately, and thanks to LUMI, one of Europe's largest supercomputers, the limits of our knowledge of cell lipid membranes have been pushed back. A team of Namur researchers, including Professor Benoît Champagne and Drs. Pierre Beaujean and Charlotte Bouquiaux, has just published in the Journal of Chemical Information and Modeling. The results of this study pave the way for new approaches in the field of membrane lipid therapy.

At the 12th International Congress on Mesostructured Materials (IMMA), held from July 8 to 12 in Montpellier, Prof. Bao-Lian Su was re-elected President of the International Mesostructured Materials Association (IMMA).

In 2021, the European Union has embarked on a titanic project to safeguard the genomes of all eukaryotic species in Europe. In other words, all living organisms, with the exception of bacteria and archaea (micro-organisms). Called ERGA, for European Reference Genome Atlas, and in which UNamur is participating thanks to Professor Alice Dennis, this project hopes to help safeguard biodiversity, at a time when a fifth of European species are in danger of extinction..

COVID-19 is an infectious disease caused by SARS-CoV-2. COVID-19 was quickly declared a pandemic by the World Health Organization (WHO) on March 11, 2020.At the start of the pandemic, healthcare professionals were faced with the marketing of numerous kits designed to measure binding antibodies. The role of neutralizing antibodies as the best correlate of protection against SARS-CoV-2 infection was quickly highlighted. A neutralization assay with the use of pseudovirus was therefore developed by our team and compared with several binding assays.There have been considerable efforts to produce and clinically validate new vaccines against COVID-19. The CRO-VAX HCP study was designed to assess the humoral response in a population of healthcare professionals who had received two doses of COVID-19 BNT162b2 vaccine.Given the decline in vaccine efficacy over time and the emergence of variants likely to evade immunity, a third dose was quickly recommended by the authorities to boost immunity. This was administered to 155 volunteers in the CRO-VAX HCP study.Still facing a decline in vaccine efficacy over time and the emergence of new variants, a second adapted booster was proposed. In September 2022, 54 participants in the CRO-VAX HCP study received this second booster. The humoral response was assessed and neutralizing antibodies against several variants were measured. In addition, we also measured the cellular response using an interferon-gamma release assay. Compared with the humoral response, which declines considerably over time, the cellular response remained fairly stable. This could therefore explain why individuals with low antibody titers can still be protected against a severe form of the disease .