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1.
Int J Mol Sci ; 25(7)2024 Mar 29.
Artículo en Inglés | MEDLINE | ID: mdl-38612616

RESUMEN

Niemann-Pick Type C (NPC) represents an autosomal recessive disorder with an incidence rate of 1 in 150,000 live births, classified within lysosomal storage diseases (LSDs). The abnormal accumulation of unesterified cholesterol characterizes the pathophysiology of NPC. This phenomenon is not unique to NPC, as analogous accumulations have also been observed in Alzheimer's disease, Parkinson's disease, and other neurodegenerative disorders. Interestingly, disturbances in the folding of the mutant protein NPC1 I1061T are accompanied by the aggregation of proteins such as hyperphosphorylated tau, α-synuclein, TDP-43, and ß-amyloid peptide. These accumulations suggest potential disruptions in proteostasis, a regulatory process encompassing four principal mechanisms: synthesis, folding, maintenance of folding, and protein degradation. The dysregulation of these processes leads to excessive accumulation of abnormal proteins that impair cell function and trigger cytotoxicity. This comprehensive review delineates reported alterations across proteostasis mechanisms in NPC, encompassing changes in processes from synthesis to degradation. Additionally, it discusses therapeutic interventions targeting pharmacological facets of proteostasis in NPC. Noteworthy among these interventions is valproic acid, a histone deacetylase inhibitor (HDACi) that modulates acetylation during NPC1 synthesis. In addition, various therapeutic options addressing protein folding modulation, such as abiraterone acetate, DHBP, calnexin, and arimoclomol, are examined. Additionally, treatments impeding NPC1 degradation, exemplified by bortezomib and MG132, are explored as potential strategies. This review consolidates current knowledge on proteostasis dysregulation in NPC and underscores the therapeutic landscape targeting diverse facets of this intricate process.


Asunto(s)
Enfermedades por Almacenamiento Lisosomal , Enfermedad de Niemann-Pick Tipo C , Humanos , Proteostasis , Enfermedad de Niemann-Pick Tipo C/tratamiento farmacológico , Pliegue de Proteína , Proteolisis
2.
BMC Ophthalmol ; 23(1): 335, 2023 Jul 27.
Artículo en Inglés | MEDLINE | ID: mdl-37501105

RESUMEN

PURPOSE: Ocular surface squamous neoplasia (OSSN) comprises a wide spectrum of squamous tumors, from which corneal/conjunctival intraepithelial neoplasia (CIN) is the most common one. The classic treatment is complete excision, but recurrence rates are high. Antineoplastic drugs such as mitomycin C (MMC) and interferon alpha 2b (IFNα2b) have been used as adjuvants or as primary treatment. To evaluate the efficacy and safety of topical IFNα2b and MMC in patients with CIN, a phase IIb double-blind clinical trial was performed. METHODS: Patients diagnosed with localized CIN were evaluated by slit lamp and impression cytology and were randomly given MMC 0.04% or INF2b (1 million IU/mL) 4 times daily until neoplasia resolution. Time of resolution and frequency of adverse effects were analyzed to determine the pharmacological efficacy and safety of both medications. RESULTS: Seventeen patients were included. Nine patients were treated with MMC and 8 with IFNα2b. All patients responded to treatment. The resolution time in days was 59.11 ± 24.02 in patients treated with MMC and 143.50 ± 47.181 in those treated with IFNα2b (p < 0.001). In the MMC group, one recurrence was reported (11%). There were no recurrences at 2 years of follow-up in the IFNα2b group. Regarding adverse effects, one or more mild adverse reaction occurred in 77% of patients managed with MMC and in 50% of patients managed with IFNα2b (p > 0.05). No serious adverse effects were reported. CONCLUSIONS: Topical chemotherapy with MMC and IFNα2b demonstrate pharmacological safety and efficacy. Therefore, these drugs could be considered as primary therapies for localized CIN .


Asunto(s)
Antineoplásicos , Carcinoma in Situ , Carcinoma de Células Escamosas , Neoplasias de la Conjuntiva , Enfermedades de la Córnea , Neoplasias del Ojo , Humanos , Administración Tópica , Antineoplásicos/uso terapéutico , Antineoplásicos/efectos adversos , Carcinoma in Situ/tratamiento farmacológico , Carcinoma in Situ/patología , Carcinoma de Células Escamosas/tratamiento farmacológico , Carcinoma de Células Escamosas/patología , Neoplasias de la Conjuntiva/tratamiento farmacológico , Enfermedades de la Córnea/patología , Neoplasias del Ojo/inducido químicamente , Interferón alfa-2/uso terapéutico , Interferón-alfa/uso terapéutico , Interferón-alfa/efectos adversos , Mitomicina , Resultado del Tratamiento
3.
Cells ; 11(19)2022 09 26.
Artículo en Inglés | MEDLINE | ID: mdl-36230953

RESUMEN

Establishing the role of non-coding RNA (ncRNA), especially microRNAs (miRNAs), in the regulation of cell function constitutes a current research challenge. Two to six miRNAs can act in clusters; particularly, the miR-17-92 family, composed of miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a is well-characterized. This cluster functions during embryonic development in cell differentiation, growth, development, and morphogenesis and is an established oncogenic cluster. However, its role in the regulation of cellular metabolism, mainly in lipid metabolism and autophagy, has received less attention. Here, we argue that the miR-17-92 cluster is highly relevant for these two processes, and thus, could be involved in the study of pathologies derived from lysosomal deficiencies. Lysosomes are related to both processes, as they control cholesterol flux and regulate autophagy. Accordingly, we compiled, analyzed, and discussed current evidence that highlights the cluster's fundamental role in regulating cellular energetic metabolism (mainly lipid and cholesterol flux) and atherosclerosis, as well as its critical participation in autophagy regulation. Because these processes are closely related to lysosomes, we also provide experimental data from the literature to support our proposal that the miR-17-92 cluster could be involved in the pathogenesis and effects of lysosomal storage diseases (LSD).


Asunto(s)
Aterosclerosis , Enfermedades por Almacenamiento Lisosomal , MicroARNs , Humanos , Aterosclerosis/genética , Autofagia , Colesterol , Lípidos , MicroARNs/genética , MicroARNs/metabolismo
4.
Cells ; 11(16)2022 08 21.
Artículo en Inglés | MEDLINE | ID: mdl-36010679

RESUMEN

Behavioural and psychological symptoms of dementia (BPSD) are presented in 95% of Alzheimer's Disease (AD) patients and are also associated with neurotrophin deficits. The molecular mechanisms leading to age-related diseases are still unclear; however, emerging evidence has suggested that epigenetic modulation is a key pathophysiological basis of ageing and neurodegeneration. In particular, it has been suggested that G9a methyltransferase and its repressive histone mark (H3K9me2) are important in shaping learning and memory by modulating autophagic activity and synaptic plasticity. This work deepens our understanding of the epigenetic mechanisms underlying the loss of cognitive function and BPSD in AD. For this purpose, several tasks were performed to evaluate the parameters of sociability (three-chamber test), aggressiveness (resident intruder), anxiety (elevated plus maze and open field) and memory (novel object recognition test) in mice, followed by the evaluation of epigenetic, autophagy and synaptic plasticity markers at the molecular level. The behavioural alterations presented by senescence-accelerated mice prone 8 (SAMP8) of 12 months of age compared with their senescence-accelerated mouse resistant mice (SAMR1), the healthy control strain was accompanied by age-related cognitive deficits and alterations in epigenetic markers. Increased levels of G9a are concomitant to the dysregulation of the JNK pathway in aged SAMP8, driving a failure in autophagosome formation. Furthermore, lower expression of the genes involved in the memory-consolidation process modulated by ERK was observed in the aged male SAMP8 model, suggesting the implication of G9a. In any case, two of the most important neurotrophins, namely brain-derived neurotrophic factor (Bdnf) and neurotrophin-3 (NT3), were found to be reduced, along with a decrease in the levels of dendritic branching and spine density presented by SAMP8 mice. Thus, the present study characterizes and provides information regarding the non-cognitive and cognitive states, as well as molecular alterations, in aged SAMP8, demonstrating the AD-like symptoms presented by this model. In any case, our results indicate that higher levels of G9a are associated with autophagic deficits and alterations in synaptic plasticity, which could further explain the BPSD and cognitive decline exhibited by the model.


Asunto(s)
Enfermedad de Alzheimer , Disfunción Cognitiva , N-Metiltransferasa de Histona-Lisina/metabolismo , Envejecimiento/metabolismo , Enfermedad de Alzheimer/genética , Animales , Autofagia , Disfunción Cognitiva/genética , Disfunción Cognitiva/metabolismo , Masculino , Ratones , Factores de Crecimiento Nervioso
5.
Arch Med Res ; 53(1): 59-68, 2022 01.
Artículo en Inglés | MEDLINE | ID: mdl-34247888

RESUMEN

BACKGROUND: Multiple Sclerosis (MS) is an immune-mediated demyelinating disease mainly affecting the Central Nervous System (CNS). 80% of MS patients present the Relapsing-Remitting form (RRMS). Pleiotrophin (PTN), a cytokine previously associated with other autoimmune and neurological diseases, could play a role in the pathophysiology of RRMS due to its neuro and immunomodulatory effect. However, PTN has never been explored in RRMS patients. AIM OF THE STUDY: To determine PTN serum levels in patients with RRMS, treated with Glatiramer acetate (GA) or Interferon-beta (IFN-ß), as well as in non-treated patients and healthy controls as a first attempt to explore PTN in RRMS. METHODS: PTN serum levels were quantified by ELISA in 57 patients and 18 controls. RESULTS: We demonstrated that PTN serum levels are significantly higher in RRMS patients. In IFN-ß treated patients alone, PTN correlated positively with time of disease evolution and time of IFN-ß use and correlated negatively with the MS severity score (MSSS). When comparing groups according to weight status, we observed that PTN is statistically increased in overweight female patients and that weight does not affect male patients. The Area Under the Curve (AUC) of the Receiver Operating Characteristic (ROC) curve analysis was higher for males compared to females. CONCLUSION: PTN serum level is higher in RRMS patients and that is associated with sex, BMI and IFN-ß treatment. Therefore, we propose that PTN could be playing a role in MS. Further studies must be performed to identify the exact role of PTN in this pathology.


Asunto(s)
Esclerosis Múltiple Recurrente-Remitente , Esclerosis Múltiple , Índice de Masa Corporal , Proteínas Portadoras , Citocinas , Femenino , Humanos , Masculino , Esclerosis Múltiple Recurrente-Remitente/tratamiento farmacológico
6.
Int J Mol Sci ; 22(7)2021 Mar 26.
Artículo en Inglés | MEDLINE | ID: mdl-33810307

RESUMEN

Niemann-Pick type C (NPC) disease is a rare autosomal recessive inherited childhood neurodegenerative disease characterized by the accumulation of cholesterol and glycosphingolipids, involving the autophagy-lysosome system. Inhibition of soluble epoxide hydrolase (sEH), an enzyme that metabolizes epoxy fatty acids (EpFAs) to 12-diols, exerts beneficial effects in modulating inflammation and autophagy, critical features of the NPC disease. This study aims to evaluate the effects of UB-EV-52, an sEH inhibitor (sEHi), in an NPC mouse model (Npc) by administering it for 4 weeks (5 mg/kg/day). Behavioral and cognitive tests (open-field test (OF)), elevated plus maze (EPM), novel object recognition test (NORT) and object location test (OLT) demonstrated that the treatment produced an improvement in short- and long-term memory as well as in spatial memory. Furthermore, UB-EV-52 treatment increased body weight and lifespan by 25% and reduced gene expression of the inflammatory markers (i.e., Il-1ß and Mcp1) and enhanced oxidative stress (OS) markers (iNOS and Hmox1) in the treated Npc mice group. As for autophagic markers, surprisingly, we found significantly reduced levels of LC3B-II/LC3B-I ratio and significantly reduced brain protein levels of lysosomal-associated membrane protein-1 (LAMP-1) in treated Npc mice group compared to untreated ones in hippocampal tissue. Lipid profile analysis showed a significant reduction of lipid storage in the liver and some slight changes in homogenated brain tissue in the treated NPC mice compared to the untreated groups. Therefore, our results suggest that pharmacological inhibition of sEH ameliorates most of the characteristic features of NPC mice, demonstrating that sEH can be considered a potential therapeutic target for this disease.


Asunto(s)
Antiinflamatorios/uso terapéutico , Antioxidantes/uso terapéutico , Inhibidores Enzimáticos/uso terapéutico , Epóxido Hidrolasas/antagonistas & inhibidores , Enfermedad de Niemann-Pick Tipo C/tratamiento farmacológico , Animales , Autofagia , Cognición , Femenino , Masculino , Memoria , Ratones , Ratones Endogámicos C57BL , Fenotipo
7.
Exp Appl Acarol ; 79(2): 255-266, 2019 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-31659545

RESUMEN

Rhipicephalus microplus is a hematophagous ectoparasite that significantly affects parasitized cattle. As a one-host tick its entire life cycle consists of free-living and parasitic forms. Its extraordinary ability to survive during prolonged off-host periods has been related to the process of cytoplasmic degradation called autophagy. In order to deepen our understanding of this process during R. microplus non-parasitic stages, we determined the expression dynamics of a set of five autophagy-related genes (ATG genes) during embryonic development and over an increasing larval starvation period of 50 days. We found two apparent successive waves of ATG genes transcriptional activation, which paralleled key embryonic changes such as cellularization and organogenesis, as well as nutrient utilization. Moreover, during increasing larval starvation, ATG genes were up-regulated cyclically every 10-15 days. Taken together, our results suggest that autophagy is playing a major role in embryo development and energy metabolism during starvation in R. microplus.


Asunto(s)
Proteínas de Artrópodos/genética , Autofagia/genética , Expresión Génica , Rhipicephalus/genética , Animales , Proteínas de Artrópodos/metabolismo , Bovinos/parasitología , Desarrollo Embrionario/genética , Larva/genética , México , Rhipicephalus/embriología , Rhipicephalus/crecimiento & desarrollo
8.
Front Genet ; 9: 596, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30619445

RESUMEN

A growing body of research shows that epigenetic mechanisms are critically involved in normal and pathological aging. The Senescence-Accelerated Mouse Prone 8 (SAMP8) can be considered a useful tool to better understand the dynamics of the global epigenetic landscape during the aging process since its phenotype is not fully explained by genetic factors. Here we investigated dysfunctional age-related transcriptional profiles and epigenetic programming enzymes in the hippocampus of 2- and 9-month-old SAMP8 female mice using the Senescent-Accelerated Resistant 1 (SAMR1) mouse strain as control. SAMP8 mice presented 1,062 genes dysregulated at 2 months of age, and 1,033 genes at 9 months, with 92 genes concurrently dysregulated at both ages compared to age-matched SAMR1. SAMP8 mice showed a significant decrease in global DNA methylation (5-mC) at 2 months while hydroxymethylation (5-hmC) levels were increased in SAMP8 mice at 2 and 9 months of age compared to SAMR1. These changes were accompanied by changes in the expression of several enzymes that regulate 5-mC and methylcytosine oxidation. Acetylated H3 and H4 histone levels were significantly diminished in SAMP8 mice at 2-month-old compared to SAMR1 and altered Histone DeACetylase (HDACs) profiles were detected in both young and old SAMP8 mice. We analyzed 84 different mouse miRNAs known to be altered in neurological diseases or involved in neuronal development. Compared with SAMR1, SAMP8 mice showed 28 and 17 miRNAs differentially expressed at 2 and 9 months of age, respectively; 6 of these miRNAs overlapped at both ages. We used several bioinformatic approaches to integrate our data in mRNA:miRNA regulatory networks and functional predictions for young and aged animals. In sum, our study reveals interplay between epigenetic mechanisms and gene networks that seems to be relevant for the progression toward a pathological aging and provides several potential markers and therapeutic candidates for Alzheimer's Disease (AD) and age-related cognitive impairment.

9.
J Mol Neurosci ; 64(1): 51-61, 2018 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-29170997

RESUMEN

In mammals, the neural control of breathing is attributed to circuits distributed along the ventral respiratory column (VRC) in the ventrolateral medulla. The VRC contains the kernel for generation of the inspiratory phase of respiratory rhythm and nuclei involved in central chemoreception. During development, the respiratory rhythm, as well as central chemosensitivity, adjusts to meet the changing physiological requirements associated with increased body weight and size. Gene expression in VRC ontogeny is well characterized. However, little is known about gene expression in the VRC during postnatal development. Here, we sought to characterize the changes in gene expression that occur in the VRC of the adult rat (5-6 months of age) in comparison with the VRC of neonate rat (1-4 days old). We isolated total RNA from VRC tissue punches collected from thick transversal slices. We hybridized cDNA to a 5000-oligonucleotide rat microarray. We found that 218 genes (4.4%) of the 5000 genes in the microarray changed their expression in adult VRC with respect to that from neonate. To further analyze the modified expression of specific genes, we quantified the differential expression of 84 genes of neuronal ion channels using a quantitative RT-PCR array. This analysis confirmed the overexpression of 68 genes and the underexpression of 14 genes in the VRC from adult compared with that from neonate. Our findings may help to explain the functional changes in respiratory rhythm and chemosensitivity occurring throughout life.


Asunto(s)
Regulación del Desarrollo de la Expresión Génica , Canales Iónicos/genética , Centro Respiratorio/metabolismo , Animales , Canales Iónicos/metabolismo , Masculino , Ratas , Ratas Wistar , Centro Respiratorio/crecimiento & desarrollo
10.
Exp Parasitol ; 170: 227-235, 2016 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-27729251

RESUMEN

Rhipicephalus (Boophilus) microplus ticks are obligatory hematophagous ectoparasites of cattle and act as vectors for disease-causing microorganisms. Conventional tick control is based on the use of chemical acaricides; however, their uncontrolled use has increased tSresistant tick populations, as well as food and environmental contamination. Alternative immunological tick control has shown to be partially effective. The only anti-tick vaccine commercially available at present in the world is based on intestinal Bm86 protein, and shows a variable effectiveness depending on tick strains or geographic isolates. Therefore, there is a need to characterize new antigens in order to improve immunological protection. The aim of this work was to identify immunogenic proteins from ovarian tissue extracts of R. microplus, after cattle immunization. Results showed that ovarian proteins complexed with the adjuvant Montanide ISA 50 V generated a strong humoral response on vaccinated cattle. IgG levels peaked at fourth post-immunization week and remained high until the end of the experiment. 1D and 2D SDS-PAGE-Western blot assays with sera from immunized cattle recognized several ovarian proteins. Reactive bands were cut and analyzed by LC-MS/MS. They were identified as Vitellogenin, Vitellogenin-2 precursor and Yolk Cathepsin. Our findings along with bioinformatic analysis indicate that R. microplus has several Vitellogenin members, which are proteolytically processed to generate multiple polypeptide fragments. This apparent complexity of vitellogenic tick molecular targets gives the opportunity to explore their potential usefulness as vaccine candidates but, at the same time, imposes a challenge on the selection of the appropriate set of antigens.


Asunto(s)
Vectores Arácnidos/inmunología , Proteínas de Artrópodos/inmunología , Rhipicephalus/inmunología , Control de Ácaros y Garrapatas/métodos , Animales , Western Blotting , Bovinos , Enfermedades de los Bovinos/prevención & control , ADN Complementario/biosíntesis , Electroforesis/métodos , Desarrollo Embrionario/inmunología , Ensayo de Inmunoadsorción Enzimática , Femenino , Inmunoglobulina G/sangre , Larva/inmunología , Oogénesis/inmunología , Ovario/inmunología , Reacción en Cadena de la Polimerasa , Proteómica/métodos , ARN/genética , ARN/aislamiento & purificación , Reproducción/inmunología , Espectrometría de Masas en Tándem , Infestaciones por Garrapatas/prevención & control , Infestaciones por Garrapatas/veterinaria , Vacunas , Vitelogeninas/biosíntesis , Vitelogeninas/inmunología
11.
Parasitology ; 143(13): 1802-1809, 2016 11.
Artículo en Inglés | MEDLINE | ID: mdl-27609093

RESUMEN

The cattle tick Rhipicephalus (Boophilus) microplus is a hematophagous ectoparasite of major importance for the livestock industry. It shows a remarkable ability to survive over long periods without feeding. However, the mechanisms used to endure long-term starvation are poorly understood. It is believed that autophagy, a process of intracellular protein degradation, may play a significant role to confront adverse environmental conditions. To advance our understanding of autophagy in R. microplus, in the present study we report the molecular characterization of three autophagy-related (ATG) genes, namely, RmATG3, RmATG4 and RmATG6, as well as their expression profiles in different developmental stages and organs of the parasite. The deduced amino acid sequences derived from the characterized gene sequences were subjected to Basic Local Alignment Search Tool analysis. The testing produced significant alignments with respective ATG proteins from Haemaphysalis longicornis and Ixodes scapularis ticks. Real-time polymerase chain reaction assays revealed that RmATG4 and RmATG6 transcripts were elevated in egg and ovary tissue, when compared with larva and midgut samples, while RmATG3 expression in midgut was 2-fold higher than in egg, larva and ovary samples.


Asunto(s)
Proteínas Relacionadas con la Autofagia/genética , Perfilación de la Expresión Génica , Rhipicephalus/embriología , Rhipicephalus/genética , Animales , Larva/genética , Larva/crecimiento & desarrollo , Reacción en Cadena en Tiempo Real de la Polimerasa , Cigoto/crecimiento & desarrollo
12.
Mol Cell Neurosci ; 75: 113-21, 2016 09.
Artículo en Inglés | MEDLINE | ID: mdl-27468976

RESUMEN

Pleiotrophin (PTN) is a secreted growth factor recently proposed to act as a neuromodulatory peptide in the Central Nervous System. PTN appears to be involved in neurodegenerative diseases and neural disorders, and it has also been implicated in learning and memory. Specifically, PTN-deficient mice exhibit a lower threshold for LTP induction in the hippocampus, which is attenuated in mice overexpressing PTN. However, there is little information about the signaling systems recruited by PTN to modulate neural activity. To address this issue, the gene expression profile in hippocampus of mice lacking PTN was analyzed using microarrays of 22,000 genes. In addition, we corroborated the effect of the absence of PTN on the expression of these genes by silencing this growth factor in primary neuronal cultures in vitro. The microarray analysis identified 102 genes that are differentially expressed (z-score>3.0) in PTN null mice, and the expression of eight of those modified in the hippocampus of KO mice was also modified in vitro after silencing PTN in cultured neurons with siRNAs. The data obtained indicate that the absence of PTN affects AKT pathway response and modulates the expression of genes related with neuroprotection (Mgst3 and Estrogen receptor 1, Ers 1) and cell differentiation (Caspase 6, Nestin, and Odz4), both in vivo and in vitro.


Asunto(s)
Proteínas Portadoras/metabolismo , Cerebelo/metabolismo , Citocinas/metabolismo , Hipocampo/metabolismo , Neuronas/metabolismo , Transcriptoma , Animales , Proteínas Portadoras/genética , Caspasa 6/genética , Caspasa 6/metabolismo , Células Cultivadas , Cerebelo/citología , Citocinas/deficiencia , Citocinas/genética , Hipocampo/citología , Proteínas Quinasas JNK Activadas por Mitógenos/genética , Proteínas Quinasas JNK Activadas por Mitógenos/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Proteínas Proto-Oncogénicas c-akt/metabolismo , ARN Ribosómico 18S/genética , ARN Ribosómico 18S/metabolismo , Ratas , Ratas Sprague-Dawley , Transducción de Señal , Sinaptofisina/genética , Sinaptofisina/metabolismo
13.
Front Cell Neurosci ; 8: 443, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25620911

RESUMEN

Pleiotrophin (PTN) is a secreted growth factor, and also a cytokine, associated with the extracellular matrix, which has recently starting to attract attention as a significant neuromodulator with multiple neuronal functions during development. PTN is expressed in several tissues, where its signals are generally related with cell proliferation, growth, and differentiation by acting through different receptors. In Central Nervous System (CNS), PTN exerts post-developmental neurotrophic and -protective effects, and additionally has been involved in neurodegenerative diseases and neural disorders. Studies in Drosophila shed light on some aspects of the different levels of regulatory control of PTN invertebrate homologs. Specifically in hippocampus, recent evidence from PTN Knock-out (KO) mice involves PTN functioning in learning and memory. In this paper, we summarize, discuss, and contrast the most recent advances and results that lead to proposing a PTN as a neuromodulatory molecule in the CNS, particularly in hippocampus.

14.
Res Vet Sci ; 93(3): 1293-300, 2012 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-22840333

RESUMEN

Bovine respiratory disease (BRD) complex is a major cause of economic losses for the cattle backgrounding and feedlot industries. Mannheimia haemolytica is considered the most important pathogen associated with this disease. Vaccines against M. haemolytica have been prepared and used for many decades, but traditional bacterins have failed to demonstrate effective protection and their use has often exacerbated disease in vaccinated animals. Thus, the BRD complex continues to exert a strong adverse effect on the health and wellbeing of stocker and feeder cattle. Therefore, generation of recombinant proteins has been helpful in formulating enhanced vaccines against M. haemolytica, which could confer better protection against BRD. In the present study, we formulated a vaccine preparation enriched with recombinant small fragments of leukotoxin A (LKTA) and outer-membrane lipoprotein (PlpE) proteins, and demonstrated its ability to generate high antibody titers in rabbits and sheep, which protected against M. haemolytica bacterial challenge in mice.


Asunto(s)
Proteínas de la Membrana Bacteriana Externa/inmunología , Proteínas Bacterianas/inmunología , Vacunas Bacterianas/inmunología , Proteínas Hemolisinas/inmunología , Lipoproteínas/inmunología , Mannheimia haemolytica/inmunología , Infecciones por Pasteurellaceae/veterinaria , Animales , Anticuerpos Antibacterianos , Proteínas de la Membrana Bacteriana Externa/química , Proteínas Bacterianas/química , Clonación Molecular , Ensayo de Inmunoadsorción Enzimática/veterinaria , Proteínas Hemolisinas/química , Lipoproteínas/química , Ratones , Ratones Endogámicos BALB C , Infecciones por Pasteurellaceae/prevención & control , Conejos , Proteínas Recombinantes , Ovinos
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