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Seminars

Type of Event: Evaluation Examination
Speaker: M.Sc. Brisa Rodope Alarcón Sánchez
Day: 2024-02-26, at 10:00:00 hrs.
Place: Cell Biology´s seminar classroom
Title: A model of alcoholic liver disease based on different hepatotoxics leading to liver cancer
Abstract:

The worst-case scenario related to alcoholic liver disease (ALD) arises after a long period of exposure to the harmful effect of alcohol consumption along with other hepatotoxics. ALD encompasses a broad spectrum of liver-associated disorders, such as steatosis, steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Based on the chronic administration of different hepatotoxics, including ethanol, sucrose, lipopolysaccharide, and low doses of diethylnitrosamine over a short period, here we aimed to develop a multiple hepatotoxic (MHT)-ALD model in the mouse that recapitulates the human ALD-associated disorders. We demonstrated that the MHT-ALD model induces ADH1A and NXN, an ethanol metabolizer and a redox-sensor enzyme, respectively; promotes steatosis associated with the induction of the lipid droplet forming FSP27, inflammation identified by the infiltration of hepatic neutrophils-positive to LY-6G marker, and the increase of MYD88 level, a protein involved in inflammatory response; and stimulates the early appearance of cellular senescence identified by the senescence markers SA-β-gal activity and p-H2A.XSer139. It also induces fibrosis associated with increased desmin, a marker of hepatic stellate cells whose activation leads to the deposition of collagen fibers, accompanied by cell death and compensatory proliferation revealed by increased CASP3-mediated apoptosis, and KI67- and PCNA-proliferation markers, respectively. It also induces histopathological traits of malignancy and the level of the HCC marker, GSTP1. In conclusion, we provide a useful model for exploring the chronological ALD-associated alterations and stages, and addressing therapeutic approaches.

Exams

Type of Event: Final Doctoral Examination
Speaker: M.Sc. Nínive Tanairy Rodríguez Ochoa
Day: 2024-01-19, at 12:00:00 hrs.
Place: Cell Biology´s Conference Classroom
Title: Effect of lactoferrin on migration, invasion, and secretion of extracellular vesicles in MDA-MB-231 cells and murine model
Abstract:

Breast cancer is the most frequently diagnosed type of cancer and the leading cause of death among women around the world and in Mexico. Incidence and mortality rates are projected to continue increasing in the coming years. The treatments that are currently available generate a large number of side effects, so it is important to look for options that do not generate harmful effects on the quality of life of patients. Lactoferrin is a protein with high nutritional value that has anticancer properties and that we can find mainly in milk and various secretions. The objective of this study was to evaluate the effect of bovine lactoferrin (BLf) in a breast cancer model in vivo and in vitro. Our results demonstrate that BLf negatively regulates the expression of Epithelial-Mesenchymal Transition markers, inhibits migration and invasion through the reduction of phosphorylation in FAK Tyr-397, inhibiting the turnover of focal adhesions, and thus decreasing the migratory capacity of breast cancer cells decreasing their metastatic potential. In addition to this, BLf is capable of increasing the number of EVs secreted by MDA-MB-231 cells without altering their structure or secretion pattern.

Type of Event: Predoctoral Examination
Speaker: M.Sc. Enrique Nicolai Darquea Bustillos
Day: 2024-01-23, at 11:00:00 hrs.
Place: Department of Cell Biology´s Videoconference Classroom
Title: Activity of bovine lactoferrin on the adhesion and cytopathic effect of Acanthamoeba genotype T4 in corneal epithelial cells
Abstract:

Acanthamoeba is a genus of protozoans with ubiquitous distribution, belonging to the phylum Amebozoa and the family Acanthamoebidae. These microorganisms are included the in free-living amoeba gruoup, and more specifically in the group of amphizoic amoebas. These amoebas are characterized by carrying out their life cycle freely in nature, as well as by their adaptation to parasitic life, where they can cause serious health problems in the organisms they infect. Acanthamoeba has a life cycle with two phases: an active trophozoite and a cyst with little metabolic activity. From a health point of view, Acanthamoeba is the causative agent of amoebic keratitis or Acanthamoeba keratitis, a chronic disease that affects corneal cells in immunocompetent people. Furthermore, this amoeba is the cause of the rare but fatal amoebic granulomatous encephalitis (GAE) caused by Acanthamoeba in immunocompromised people. Amoebic keratitis is considered a misdiagnosed entity, which leads to the administration of erroneous treatments, causing serious conditions in which the patient loses vision, even requiring ocular enucleation. Furthermore, this amoeba is the cause of the rare but fatal granulomatous amebic encephalitis (GAE) caused by Acanthamoeba in immunocompromised people. Amoebic keratitis is considered a misdiagnosed entity, which leads to the administration of erroneous treatments, causing serious conditions in which the patient loses vision, even requiring ocular enucleation. The treatment for this pathology can become long and painful, which is why many patients abandon it, complicating its development. In this sense, several alternative lines of treatment have been investigated, including the use of lactoferrin. This glycoprotein of the mammalian innate immune system is present in high concentrations in colostrum and milk, as well as to a lesser extent in tears and other fluids. Lactoferrin has been shown to have potent antimicrobial activity, including an important antiparasitic role. In this sense, in the present research project, we will seek to evaluate the effect of bovine lactoferrin on adhesion, as well as the cytopathic effect of Acanthamoeba genotype T4 in corneal epithelial cells. For this purpose, we will first seek to analyze the effect of bovine apo-lactoferrin (apo-BLf) and bovine holo-lactoferrin (holo-BLf) on the viability and growth of the amoeba. Subsequently, adhesion assays of the amoeba to the corneal epithelial cell line RCE1-(5T5) will be developed, using different doses of apo-BLf and holo-BLf. Furthermore, the cytopathic effect of the parasite will be evaluated in RCE1-(5T5) cells, by analyzing the proteolytic activity by 10% SDS-PAGE copolymerized with various substrates. In this way, a much more comprehensive view of the role of bovine lactoferrin on the virulence factors of this microorganism will be obtained.

Type of Event: Predoctoral Examination
Speaker: M.Sc. Cristhina Estefanía Jaramillo Ordóñez
Day: 2024-02-08, at 12:00:00 hrs.
Place: Department of Cell Biology´s Classroom
Title: EVALUATION OF THE EFFECT OF AMYLOID BETA OLIGOMERS ON THE EXPRESSION AND FUNCTIONALITY OF LATROPHILINS AND THEIR LIGANDS IN MODELS OF ALZHEIMER´S DISEASE
Abstract:

Alzheimer´s disease (AD) is the main cause of dementia among older adults and is a complex disease which is characterized by the accumulation of neuropathological structures such as amyloid-ß plaques and neurofibrillary tangles that generate cellular toxicity, loss of synapses and neuronal death. In the early stages of the disease, it has been reported that there is a structural and functional alteration of the neuronal synapse, where the expression of several receptors and adhesion molecules is deregulated. Latrophilins are adhesion receptors coupled to G proteins, and two of their isoforms are expressed mainly in the brain, participating in various neuronal processes such as the stabilization of synapses, intercellular adhesion and in the activation of different signaling pathways. Previous studies report that amyloid-ß (Aß) oligomers can abnormally interact with various receptors and adhesion molecules, altering their expression and activation; however, to date there are no published studies about the effects of these oligomers on the activity of the latrophilins. Therefore, this study aims to study the effect of Aß oligomers on the expression and functionality of latrophilins and associated ligands, in order to determine if this is an additional mechanism of pathogenicity of Aß on other receptor families.

Type of Event: Predoctoral Examination
Speaker: M.Sc. Jesús Yaniel Ayala Camejo
Day: 2024-02-26, at 12:00:00 hrs.
Place: Department of Cell Biology´s Classroom
Title: Proteomic analysis of the nuclear and cytoplasmic fractions of healthy and progeroid fibroblasts treated with Selinexor
Abstract:

Hutchinson-Gilford progeroid syndrome (HGPS) is characterized by accelerated and premature aging that mimics the characteristics of biological aging. This disease´s most common genetic origin lies in the mutation c.1824C>T in the LMNA gene, which codes for lamin A/C. This change activates a cryptic splicing site that causes the deletion of 50 amino acids in the mutated protein, also known as progerin. Progerin causes multiple cellular alterations that lead to cellular senescence and general aging. Recently, our work group demonstrated that in individuals with HGPS, the export of nuclear proteins is increased by the overexpression of the exportin XPO1 and that treatment of progeroid fibroblasts with Selinexor, a specific XPO1 inhibitor, normalizes nuclear export and decreases several characteristics of cellular senescence. However, it is still unknown which proteins are involved in the recovery of the normal phenotype. To answer this question, we plan to study the sub-proteomes of the nuclear and cytoplasmic fractions of progeroid fibroblasts when treated with and in the absence of Selinexor. We previously implemented a cell fractionation strategy to obtain nuclear and cytoplasmic extracts with the purity necessary for proteomic studies. Furthermore, we confirmed the effectiveness of Selinexor to retain proteins with a nuclear export signal in the nucleus. We corroborated that p53 is an excellent candidate to verify the effect of selective inhibitors of nuclear export on nuclear-cytoplasmic traffic. The next step is to obtain the subproteomes and the subsequent mass analysis, from which candidate pathways and proteins will be selected to be evaluated as possible indirect targets of Selinexor that mediate the recovery of the normal phenotype in progeroid cells. Once concluded, this study will contribute to elucidate the molecular mechanisms that are affected in individuals with HGPS, which could be extrapolated to what happens during physiological aging.

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