Novel perspectives on the therapeutic role of cryptotanshinone in the management of stem cell behaviors for high-incidence diseases.

Cryptotanshinone (CTS), a diterpenoid quinone, is found mostly in Bunge () and plays a crucial role in many cellular processes, such as cell proliferation/self-renewal, differentiation and apoptosis. In particular, CTS's profound physiological impact on various stem cell populations and their maintenance and fate determination could improve the efficiency and accuracy of stem cell therapy for high-incidence disease. However, as much promise CTS holds, these CTS-mediated processes are complex and multifactorial and many of the underlying mechanisms as well as their clinical significance for high-incidence diseases are not yet fully understood.

Direct retino-raphe projection alters serotonergic tone and affective behavior.

Light is a powerful modulator of higher-order cognitive processes such as mood but it remains unclear which neural circuits mediate the impact of light on affective behavior. We found that light deprivation produces a depressive-like behavioral state that is reversed by activation of direct retinal signals to the serotonergic dorsal raphe nucleus (DRN) in a manner equivalent to treatment with the selective serotonin reuptake inhibitor fluoxetine. Surprisingly, the DRN-projecting retinal ganglion cells (RGCs) are indistinguishable from the classic alpha/Y-like RGC type that contributes to image-forming visual pathways.

Caveolin-1 plays a crucial role in inhibiting neuronal differentiation of neural stem/progenitor cells via VEGF signaling-dependent pathway.

In the present study, we aim to elucidate the roles of caveolin-1(Cav-1), a 22 kDa protein in plasma membrane invaginations, in modulating neuronal differentiation of neural progenitor cells (NPCs). In the hippocampal dentate gyrus, we found that Cav-1 knockout mice revealed remarkably higher levels of vascular endothelial growth factor (VEGF) and the more abundant formation of newborn neurons than wild type mice. We then studied the potential mechanisms of Cav-1 in modulating VEGF signaling and neuronal differentiation in isolated cultured NPCs under normoxic and hypoxic conditions.

Caveolin-1 inhibits oligodendroglial differentiation of neural stem/progenitor cells through modulating β-catenin expression.

In the present study, we aim to elucidate the role of caveolin-1 (Cav-1) in modulating oligodendroglial differentiation of neural progenitor cells (NPCs) in vivo and in vitro. For in vivo experiments, we investigated oligodendroglial differentiation by detecting the expressions of 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) and β-catenin in the brains of wild type mice and Cav-1 knockout mice. Cav-1 knockout mice revealed more oligodendroglial differentiation, but lower levels of β-catenin expression than wild type mice.

Caveolin-1 promote astroglial differentiation of neural stem/progenitor cells through modulating Notch1/NICD and Hes1 expressions.

In the present study, we aim to elucidate the role of caveolin-1 in modulating astroglial differentiation of neural progenitor cells (NPCs) and the potential mechanisms involved. We first investigated astroglial differentiation and Notch signaling by detecting the expressions of S100β, GFAP, NICD and hairy enhancer of split 1 (Hes1) in the brains of wild-type and caveolin-1 knockout mice. Caveolin-1 knockout mice revealed remarkably less astroglial differentiation and lower levels of NICD and Hes1 expressions than wild type mice.

Retrograde labeling of retinal ganglion cells by application of fluoro-gold on the surface of superior colliculus.

Retinal ganglion cell (RGC) counting is essential to evaluate retinal degeneration especially in glaucoma. Reliable RGC labeling is fundamental for evaluating the effects of any treatment. In rat, about 98% of RGCs is known to project to the contralateral superior colliculus (SC) (Forrester and Peters, 1967).

Micro-dissection of rat brain for RNA or protein extraction from specific brain region.

Micro-dissection of rat brain into various regions is extremely important for the study of different neurodegenerative diseases. This video demonstrates micro-dissection of four major brain regions include olfactory bulb, frontal cortex, striatum and hippocampus in fresh rat brain tissue. Useful tips for quick removal of respective regions to avoid RNA and protein degradation of the tissue are given.

Modulation of the suppressive effect of corticosterone on adult rat hippocampal cell proliferation by paroxetine.

Objective: The literature has shown that cognitive and emotional changes may occur after chronic treatment with glucocorticoids. This might be caused by the suppressive effect of glucocorticoids on hippocampal neurogenesis and cell proliferation. Paroxetine, a selective serotonin reuptake transporter, is a commonly used antidepressant for alleviation of signs and symptoms of clinical depression.

Corticosteroid decreases subventricular zone cell proliferation, which could be reversed by paroxetine.

Purpose: Major depressive disorder is often associated with elevated glucocorticoid levels, which in turn suppress cell proliferation and neurogenesis in the hippocampus. Increasing evidence supports that antidepressants induce hippocampal neurogenesis and this induces speculation that decrease in hippocampal neurogenesis has causal relationship with depression. There is, however, a lack of information about neurogenic effects of antidepressants on the subventricular zone, which is another CNS region with continuous neurogenesis throughout adulthood.

Establishment and characterization of a human first-trimester extravillous trophoblast cell line (TEV-1).

Objective: Research into the biology of human trophoblast invasion has been hampered by a lack of in vitro models. The aim of this study was to establish and characterize a human extravillous trophoblast cell line from the first-trimester placenta.

Methods: Human papillomavirus type 16 (HPV16) E6/E7 genes were stably expressed in primary cultures of first-trimester placenta via a retroviral vector (pLXSN-E6/E7).