Sichuan Da Xue Xue Bao Yi Xue Ban
March 2019
Objective: To explore the effect and mechanism of human adipose-derived mesenchymal stem cells (hADMSCs) on phenotypic polarization of microglia.
Methods: BV-2 microglia of C57/BL6 mice were co-cultured with hADMSCs+lipopolysaccharide (LPS), or cultured with LPS alone. Cell morphology was observed under an inverted microscope.
Background: Antigen-specific and MHCII-restricted CD4+ αβ T cells have been shown or suggested to play an important role in the transition from acute to chronic mechanical allodynia after peripheral nerve injuries. However, it is still largely unknown where these T cells infiltrate along the somatosensory pathways transmitting mechanical allodynia to initiate the development of chronic mechanical allodynia after nerve injuries. Therefore, the purpose of this study was to ascertain the definite neuroimmune interface for these T cells to initiate the development of chronic mechanical allodynia after peripheral nerve injuries.
View Article and Find Full Text PDFCorneal integrity, transparency and vision acuity are maintained by corneal epithelial cells (CECs), which are continuously renewed by corneal limbal stem cells (LSCs). Deficiency of CECs and/or LSCs is associated with numerous ocular diseases. Paired box (PAX)6 is an eye development-associated transcription factor that is necessary for cell fate determination and differentiation of LSCs and CECs.
View Article and Find Full Text PDFSchwann cell migration, including collective migration and chemotaxis, is essential for the formation of coordinate interactions between Schwann cells and axons during peripheral nerve development and regeneration. Moreover, limited migration of Schwann cells imposed a serious obstacle on Schwann cell-astrocytes intermingling and spinal cord repair after Schwann cell transplantation into injured spinal cords. Recent studies have shown that mature brain-derived neurotrophic factor, a member of the neurotrophin family, inhibits Schwann cell migration.
View Article and Find Full Text PDFBackground: Inflammatory injury plays a critical role in intracerebral hemorrhage (ICH)-induced neurological deficits; however, the signaling pathways are not apparent by which the upstream cellular events trigger innate immune and inflammatory responses that contribute to neurological impairments. Toll-like receptor 4 (TLR4) plays a role in inflammatory damage caused by brain disorders.
Methods: In this study, we investigate the role of TLR4 signaling in ICH-induced inflammation.
Objective: To establish an artificial somatic-autonomic reflex arc in rats and observe the following distributive changes of neural fibers in the bladder.
Methods: Adult Sprague-Dawley rats were randomly divided into three groups: control group, spinal cord injury (SCI) group, and reinnervation group. DiI retrograde tracing was used to verify establishment of the model and to investigate the transport function of the regenerated efferent axons in the new reflex arc.
Objective To investigate the role of poly-lactic acid and agarose gelatin in promoting the functional recovery of the injured spinal cord. Methods Poly-lactic acid (PLA) or agarose was embedded in the space between two stumps of the hemisectioned spinal cord. Immunohistochemistry was used to show astroglia proliferation and the infiltration of RhoA-positive cells.
View Article and Find Full Text PDFShi Yan Sheng Wu Xue Bao
March 2002
The localization of the new estrogen receptor, ER-beta, in the rat brain was studied by immunocytochemical technique, and the results revealed that ER-beta immunoactive material was predominantly localized in the neuronal nucleus, but it was also detectable in the cytoplasm and neuronal processes. High levels of ER-beta immunopositive signals were detected in the cerebral cortex, vertical limb of the diagonal band, Purkinje cells, locus ceruleus, and motor trigeminal nucleus. Moderate levels were found in the medial septum, lateral amygdaloid nucleus, substantia nigra, and central gray.
View Article and Find Full Text PDFPrevious studies have shown that estrogen receptor beta (ERbeta) is the predominant estrogen receptor in the hypothalamic paraventricular nucleus (PVN) of mouse, mediating estrogen regulation of the neuroendocrine activities of the PVN, but the exact roles that ERbeta plays in the PVN remain unclear. In this study, we used immunocytochemistry to investigate the expression of ERbeta in the maternal PVN of mice during pregnancy (pregnant days 8, 10, 12, 15 and 18), lactation (postpartum days 1, 4 and 8) as well as in the PVN of the females from postnatal days 1, 3, 5, 7, 9, 15, 30 and 70. We found out that ERbeta was predominantly localized in the magnocellular divisions of PVN.
View Article and Find Full Text PDFThe last 5-6 years have seen the emergence of a new gene family that currently comprises CTGF, Cyr61, nov, elm1, HICP and WISP-3. The translational products of most CCN family members are secreted proteins that contain 343 to 381 amino-acid residues to compose 4 distinct structural modules, each having 38 conserved cysteine residues. These proteins have a variety of properties to affect the cellular behaviors such as growth, differentiation, adhesion and locomotion.
View Article and Find Full Text PDFStudies have shown that estrogen plays important roles in regulating neural structure and function in the brain, but the mechanism remains unclear. The actions of estrogen were thought to be mediated by a single estrogen receptor until the identification of another estrogen receptor, namely estrogen receptor-beta (ER-beta). Here we report a comprehensive study of the localization of ER-beta immunoreactivity and differences in the brains of adult male and female rats on the basis of a nickel ammonium sulfate-enhanced immunocytochemical method using a polyclonal antiserum sc-8974.
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