@article {710,
	title = {Transcriptomic Analysis of a Diabetic Skin-Humanized Mouse Model Dissects Molecular Pathways Underlying the Delayed Wound Healing Response.},
	journal = {Genes (Basel)},
	volume = {12},
	year = {2020},
	month = {2020 12 31},
	abstract = {<p>Defective healing leading to cutaneous ulcer formation is one of the most feared complications of diabetes due to its consequences on patients{\textquoteright} quality of life and on the healthcare system. A more in-depth analysis of the underlying molecular pathophysiology is required to develop effective healing-promoting therapies for those patients. Major architectural and functional differences with human epidermis limit extrapolation of results coming from rodents and other small mammal-healing models. Therefore, the search for reliable humanized models has become mandatory. Previously, we developed a diabetes-induced delayed humanized wound healing model that faithfully recapitulated the major histological features of such skin repair-deficient condition. Herein, we present the results of a transcriptomic and functional enrichment analysis followed by a mechanistic analysis performed in such humanized wound healing model. The deregulation of genes implicated in functions such as angiogenesis, apoptosis, and inflammatory signaling processes were evidenced, confirming published data in diabetic patients that in fact might also underlie some of the histological features previously reported in the delayed skin-humanized healing model. Altogether, these molecular findings support the utility of such preclinical model as a valuable tool to gain insight into the molecular basis of the delayed diabetic healing with potential impact in the translational medicine field.</p>},
	keywords = {Animals, Diabetes Mellitus, Experimental, Gene Expression Profiling, Gene Expression Regulation, Gene ontology, Humans, Metabolic Networks and Pathways, Mice, Mice, Nude, Microarray Analysis, Molecular Sequence Annotation, Principal Component Analysis, Signal Transduction, Skin, Skin Transplantation, Skin Ulcer, Streptozocin, Tissue Engineering, Transcriptome, Transplantation, Heterologous, Wound Healing},
	issn = {2073-4425},
	doi = {10.3390/genes12010047},
	author = {Le{\'o}n, Carlos and Garcia-Garcia, Francisco and Llames, Sara and Garc{\'\i}a-P{\'e}rez, Eva and Carretero, Marta and Arriba, Mar{\'\i}a Del Carmen and Dopazo, Joaquin and Del Rio, Marcela and Escamez, Maria Jos{\'e} and Mart{\'\i}nez-Santamar{\'\i}a, Luc{\'\i}a}
}
@article {410,
	title = {LRH-1 agonism favours an immune-islet dialogue which protects against diabetes mellitus.},
	journal = {Nat Commun},
	volume = {9},
	year = {2018},
	month = {2018 04 16},
	pages = {1488},
	abstract = {<p>Type 1 diabetes mellitus (T1DM) is due to the selective destruction of islet beta cells by immune cells. Current therapies focused on repressing the immune attack or stimulating beta cell regeneration still have limited clinical efficacy. Therefore, it is timely to identify innovative targets to dampen the immune process, while promoting beta cell survival and function. Liver receptor homologue-1 (LRH-1) is a nuclear receptor that represses inflammation in digestive organs, and protects pancreatic islets against apoptosis. Here, we show that BL001, a small LRH-1 agonist, impedes hyperglycemia progression and the immune-dependent inflammation of pancreas in murine models of T1DM, and beta cell apoptosis in islets of type 2 diabetic patients, while increasing beta cell mass and insulin secretion. Thus, we suggest that LRH-1 agonism favors a dialogue between immune and islet cells, which could be druggable to protect against diabetes mellitus.</p>},
	keywords = {Animals, Apoptosis, Cell Communication, Cell Survival, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Female, Gene Expression Regulation, Humans, Hypoglycemic Agents, Immunity, Innate, insulin, Insulin-Secreting Cells, Islets of Langerhans, Islets of Langerhans Transplantation, Macrophages, Male, Mice, Mice, Inbred C57BL, Phenalenes, Receptors, Cytoplasmic and Nuclear, Streptozocin, T-Lymphocytes, Regulatory, Transplantation, Heterologous},
	issn = {2041-1723},
	doi = {10.1038/s41467-018-03943-0},
	author = {Cobo-Vuilleumier, Nadia and Lorenzo, Petra I and Rodr{\'\i}guez, Noelia Garc{\'\i}a and Herrera G{\'o}mez, Irene de Gracia and Fuente-Martin, Esther and L{\'o}pez-Noriega, Livia and Mellado-Gil, Jos{\'e} Manuel and Romero-Zerbo, Silvana-Yanina and Baqui{\'e}, Mathurin and Lachaud, Christian Claude and Stifter, Katja and Perdomo, German and Bugliani, Marco and De Tata, Vincenzo and Bosco, Domenico and Parnaud, Geraldine and Pozo, David and Hmadcha, Abdelkrim and Florido, Javier P and Toscano, Miguel G and de Haan, Peter and Schoonjans, Kristina and S{\'a}nchez Palaz{\'o}n, Luis and Marchetti, Piero and Schirmbeck, Reinhold and Mart{\'\i}n-Montalvo, Alejandro and Meda, Paolo and Soria, Bernat and Berm{\'u}dez-Silva, Francisco-Javier and St-Onge, Luc and Gauthier, Benoit R}
}
