Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros










Base de datos
Intervalo de año de publicación
1.
Brain Inj ; 35(7): 850-862, 2021 06 07.
Artículo en Inglés | MEDLINE | ID: mdl-33780298

RESUMEN

OBJECTIVE: : A decrease in the blood flow below a current level in the brain results in ischemia. Studies demonstrated that human trophoblast progenitor cells (hTPCs) contribute to the treatment of many diseases. Therefore, hTPCs might be a promising source to repair ischemia in cerebral ischemia models. For this purpose, we evaluated the expression of many neurogenesis markers by performing hTPC transplantation after focal cerebral ischemia in rats. METHODS: : hTPCs, isolated from the term placentae, were characterized by immunofluorescent staining and differentiated into neuron-like cells. Differentiation was confirmed with immunostaining of GFAP and NeuN proteins. Cerebral ischemia models were generated in rats via middle cerebral artery occlusion and, after 24 hours, hTPCs were injected via the tail vein. Animals were sacrificed on day 3 or day 11. Immunohistochemical analysis was performed with proteins associated with neurogenesis and neuronal development, such as DLX2, DLX5, LHX6, NGN1, and NGN2, Olig1, Olig2, and PDGFRα. RESULTS: : According to our results, hTPCs may alleviate ischemic damage in the brain and contribute to the neurogenesis after ischemia. CONCLUSIONS: : Based on our findings, this topic should be further investigated as the hTPC-based therapies may be a reliable source that can be used in the treatment of stroke and ischemia.


Asunto(s)
Isquemia Encefálica , Trofoblastos , Animales , Humanos , Infarto de la Arteria Cerebral Media , Neurogénesis , Ratas , Ratas Sprague-Dawley , Células Madre
2.
Acta Histochem ; 123(3): 151694, 2021 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-33571695

RESUMEN

Our research aimed to compare the epigenetic alterations between placentae of in vitro fertilization (IVF) patients and spontaneous pregnancies. Additionally, the expression levels of proliferation markers (PCNA, Ki67) and glucose transporter proteins (GLUT1, GLUT3) were assessed in control and IVF placentae to examine the possible consequences of epigenetic alterations on placental development. Control group placentae were obtained from spontaneous pregnancies of healthy women (n = 16). IVF placentae were obtained from fresh (n = 16) and frozen (n = 16) embryo transfer pregnancies. A group of maternal and paternal imprint genes H19, IGF2, IGF2, IGF2R, PHLDA2, PLAGL1, MASH2, GRB10, PEG1, PEG3, and PEG10 were detected by Real-Time PCR. Additionally, PCNA, Ki67, GLUT1, and GLUT3 protein levels were assessed by immunohistochemistry and western blot. In the fresh embryo transfer placenta group (fETP), gene expression of paternal PEG1 and PEG10 was upregulated compared with the control group. Increased gene expression in paternal PEG1 and maternal IGFR2 genes was detected in the frozen embryo transfer placenta group (FET) compared with the control group. Conversely, expression levels of H19 and IGF2 genes were downregulated in the FET group. On the other hand, GLUT3 and PCNA expression was increased in FET group placentae. IVF techniques affect placental imprinted gene expressions which are important for proper placental development. Imprinted genes are differently expressed in fresh ET placentae and frozen ET placentae. In conclusion, these data indicate that altered imprinted gene expression may affect glucose transport and cell proliferation, therefore play an important role in placental development.


Asunto(s)
Transferencia de Embrión , Expresión Génica/fisiología , Factor II del Crecimiento Similar a la Insulina/metabolismo , Placenta/metabolismo , Adulto , Transferencia de Embrión/métodos , Femenino , Fertilización In Vitro/métodos , Perfilación de la Expresión Génica/métodos , Regulación del Desarrollo de la Expresión Génica/fisiología , Humanos , Masculino , Embarazo , Receptor IGF Tipo 2/metabolismo
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA