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Reactive Astrocytes Expressing Intense Estrogen Receptor-alpha Immunoreactivities Have Much Elongated Cytoplasmic Processes: An Autopsy Case of Human Cerebellar Tissue with Multiple Genitourinary and Gastrointestinal Anomalies

We performed an immunohistochemical study on the estrogen receptor alpha (ER-α) distribution in the cerebellum of a human neonate with multiple congenital anomalies, that had been acquired during autopsy. Although the exact pathology in the brain was not clearly elucidated in this study, an unidenti...

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Detalles Bibliográficos
Autores principales: Kim, Eo-Jin, Oh, Chang Seok, Kim, Jaehyup, Kim, Wu Ho, Chung, Yoon Hee, Shin, Dong Hoon
Formato: Texto
Lenguaje:English
Publicado: The Korean Academy of Medical Sciences 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693869/
https://www.ncbi.nlm.nih.gov/pubmed/17982251
http://dx.doi.org/10.3346/jkms.2007.22.5.936
Descripción
Sumario:We performed an immunohistochemical study on the estrogen receptor alpha (ER-α) distribution in the cerebellum of a human neonate with multiple congenital anomalies, that had been acquired during autopsy. Although the exact pathology in the brain was not clearly elucidated in this study, an unidentified stressful condition might have induced the astrocytes into reactive states. In this immunohistochemical study on the neonatal cerebellum with multiple congenital anomalies, intense ER-α immunoreactivities (IRs) were localized mainly within the white matter even though ER-α IRs were known to be mainly localized in neurons. Double immunohistochemical staining showed that ER-α IR cells were reactive astrocytes, but not neurons. Interestingly, there were differences in the process length among the reactive astrocytes showing ER-α IRs. Our quantitative data confirmed that among the glial fibrillary acidic protein (GFAP)-expressing reactive astrocytes, the cells exhibiting intense ER-α IRs have much longer cytoplasmic processes and relatively weaker GFAP IRs. Taken together, the elongated processes of reactive astrocytes might be due to decreased expression of GFAP, which might be induced by elevated expression of ER-α even though the elucidation of the exact mechanism needs further studies.