EphrinB3 regulates cell proliferation and survival in adult neurogenesis

2006 ◽  
Vol 31 (4) ◽  
pp. 713-722 ◽  
Author(s):  
Jerome Ricard ◽  
Jessica Salinas ◽  
Lissette Garcia ◽  
Daniel J. Liebl
2016 ◽  
Vol 87 (3) ◽  
pp. 175-183 ◽  
Author(s):  
Alice Schade Powers

Studies of the relationship between behavioral plasticity and new cells in the adult brain in amphibians and reptiles are sparse but demonstrate that environmental and hormonal variables do have an effect on the amount of cell proliferation and/or migration. The variables that are reviewed here are: enriched environment, social stimulation, spatial area use, season, photoperiod and temperature, and testosterone. Fewer data are available for amphibians than for reptiles, but for both groups many issues are still to be resolved. It is to be hoped that the questions raised here will generate more answers in future studies.


2021 ◽  
Author(s):  
Show-Li Chen

Abstract Background Breast carcinoma-amplified sequence 2 (BCAS2) regulates β-catenin gene splicing. The conditional knockout of BCAS2 expression in the forebrain (BCAS2 cKO) of mice confers impaired learning and memory along with decreased β-catenin expression. Because β-catenin reportedly regulates adult neurogenesis, we wondered whether BCAS2 could regulate adult neurogenesis via β-catenin. Methods BCAS2 regulating neurogenesis was investigated by characterizing BCAS2 cKO mice. Also, lentivirus-shBCAS2 was intracranially injected into the hippocampus of wild-type mice to knock down BCAS2 expression. We evaluated the rescue effects of BCAS2 cKO by intracranial injection of adeno-associated virus encoding BCAS2 (AAV-DJ8-BCAS2) and AAV-β-catenin gene therapy. Results To show that BCAS2-regulating adult neurogenesis via β-catenin, first, BCAS2 cKO mice showed low SRY-box 2–positive (Sox2+) neural stem cell proliferation and doublecortin-positive (DCX+) immature neurons. Second, stereotaxic intracranial injection of lentivirus-shBCAS2 knocked down BCAS2 in the hippocampus of wild-type mice, and we confirmed the BCAS2 regulation of adult neurogenesis via β-catenin. Third, AAV-DJ8-BCAS2 gene therapy in BCAS2 cKO mice reversed the low proliferation of Sox2+ neural stem cells and the decreased number of DCX+ immature neurons with increased β-catenin expression. Moreover, AAV-β-catenin gene therapy restored neuron stem cell proliferation and immature neuron differentiation, which further supports BCAS2 regulating adult neurogenesis via β-catenin. In addition, cells targeted by AAV-DJ8 injection into the hippocampus included Sox2 and DCX immature neurons, interneurons, and astrocytes. BCAS2 may regulate adult neurogenesis by targeting Sox2+ and DCX+ immature neurons for autocrine effects and interneurons or astrocytes for paracrine effects. Conclusions BCAS2 can regulate adult neurogenesis in mice via β-catenin.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Hyongjun Jeon ◽  
Sun Ryu ◽  
Dongsoo Kim ◽  
Sungtae Koo ◽  
Ki-Tae Ha ◽  
...  

Adult neurogenesis has recently been considered a new therapeutic paradigm of Parkinson’s disease. In this study, we investigated whether acupuncture restores 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) induced impaired neurogenesis in the subventricular zone (SVZ). Male C57BL/6 mice were given 30 mg/kg of MPTP intraperitoneally once a day for 5 days, after which they were intraperitoneally injected with 50 mg/kg of bromodeoxyuridine (BrdU) and given acupuncture stimulation at HT7 or GB34 for 12 consecutive days. Dopaminergic neuronal survival in the nigrostriatal pathway and cell proliferation in the SVZ was then evaluated by immunostaining. MPTP administration induced dopaminergic neuronal death in the nigrostriatal pathway, which was suppressed by acupuncture stimulation at GB34. MPTP administration also suppressed the number of BrdU-positive cells and glial fibrillary acidic protein/BrdU-positive cells and increased the number of doublecortin/BrdU-positive cells in the SVZ, which were restored by acupuncture stimulation at GB34. These results indicate that acupuncture stimulation at GB34 restores MPTP-induced neurogenesis impairment.


2021 ◽  
Vol 22 (7) ◽  
pp. 3449
Author(s):  
Mikhail Semenov

We studied cell proliferation in the postnatal mouse brain between the ages of 2 and 30 months and identified four compartments with different densities of proliferating cells. The first identified compartment corresponds to the postnatal pallial neurogenic (PPN) zone in the telencephalon; the second to the subpallial postnatal neurogenic (SPPN) zone in the telencephalon; the third to the white matter bundles in the telencephalon; and the fourth to all brain parts outside of the other three compartments. We estimated that about 3.4 million new cells, including 0.8 million in the subgranular zone (SGZ) in the hippocampus, are produced in the PPN zone. About 21 million new cells, including 10 million in the subependymal zone (SEZ) in the lateral walls of the lateral ventricle and 2.7 million in the rostral migratory stream (RMS), are produced in the SPPN zone. The third and fourth compartments together produced about 31 million new cells. The analysis of cell proliferation in neurogenic zones shows that postnatal neurogenesis is the direct continuation of developmental neurogenesis in the telencephalon and that adult neurogenesis has characteristics of the late developmental process. As a developmental process, adult neurogenesis supports only compensatory regeneration, which is very inefficient.


2015 ◽  
Vol 19 (1) ◽  
pp. pyv085 ◽  
Author(s):  
Noelia Geribaldi-Doldán ◽  
Eugenia Flores-Giubi ◽  
Maribel Murillo-Carretero ◽  
Francisco García-Bernal ◽  
Manuel Carrasco ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e84838 ◽  
Author(s):  
Ariel B. Abraham ◽  
Robert Bronstein ◽  
Avanish S. Reddy ◽  
Mirjana Maletic-Savatic ◽  
Adan Aguirre ◽  
...  

Author(s):  
C. W. Kischer

The morphology of the fibroblasts changes markedly as the healing period from burn wounds progresses, through development of the hypertrophic scar, to resolution of the scar by a self-limiting process of maturation or therapeutic resolution. In addition, hypertrophic scars contain an increased cell proliferation largely made up of fibroblasts. This tremendous population of fibroblasts seems congruous with the abundance of collagen and ground substance. The fine structure of these cells should reflect some aspects of the metabolic activity necessary for production of the scar, and might presage the stage of maturation.A comparison of the fine structure of the fibroblasts from normal skin, different scar types, and granulation tissue has been made by transmission (TEM) and scanning electron microscopy (SEM).


Author(s):  
Venita F. Allison

In 1930, Moore, Hughes and Gallager reported that after castration seminal vesicle epithelial cell atrophy occurred and that cell regeneration could be achieved with daily injections of testis extract. Electron microscopic studies have confirmed those observations and have shown that testosterone injections restore the epithelium of the seminal vesicle in adult castrated male rats. Studies concerned with the metabolism of androgens point out that dihydrotestosterone stimulates cell proliferation and that other metabolites of testosterone probably influence secretory function in certain target cells.Although the influence of androgens on adult seminal vesicle epithelial cytology is well documented, little is known of the effect of androgen depletion and replacement on those cells in aging animals. The present study is concerned with the effect of castration and testosterone injection on the epithelium of the seminal vesicle of aging rats.


Author(s):  
S.S. Poolsawat ◽  
C.A. Huerta ◽  
S.TY. Lae ◽  
G.A. Miranda

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.


Sign in / Sign up

Export Citation Format

Share Document