Melatonin ameliorates neural function by promoting endogenous neurogenesis through the MT2 melatonin receptor in ischemic-stroke mice

Chern, Chang‐Ming; Liao, Jyh‐Fei; Wang, Yea‐Hwey; Shen, Yung Kang

doi:10.1016/j.freeradbiomed.2012.01.030

Cited by 133 publications

(110 citation statements)

References 31 publications

Supporting

Mentioning

104

Contrasting

Unclassified

Order By: Relevance

“…Moreover, melatonin has demonstrated that it could protect BBB by ischemic and hemorrhagic stroke, and sepsis or inflammatory responses to infection (Chen et al, 2006;Reiter et al, 2010;Tocharus et al, 2010;Chern et al, 2012;Acuna-Castroviejo et al, 2014;Garcia et al, 2014;Wang et al, 2014aWang et al, , 2014bLacoste et al, 2015;Nguyen et al, 2015;Manchester et al, 2015;Zhao et al, 2015). According to its exerting effects, melatonin might be beneficial for protecting BBB in METH administration.…”

Section: Introductionmentioning

confidence: 99%

Melatonin promotes blood-brain barrier integrity in methamphetamine-induced inflammation in primary rat brain microvascular endothelial cells

et al. 2016

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Melatonin promotes blood-brain barrier integrity in methamphetamine-induced inflammation in primary rat brain microvascular endothelial cells

et al. 2016

View full text Add to dashboard Cite

“…In the case of Erlandsson et al, CsA administration led to newly formed tissue at the site of the infarct that contained only newborn glial cells [104] . In Chern et al, intraperitoneal administration of melatonin after MCAO stroke in mice resulted in a reduction in neurological deficit, even though the increase in mature neurons was not significant [93] . These studies support the possibility that NPCs contribute to recovery through other mechanisms, such as providing factors that prevent secondary stroke damage, or by providing trophic support to existing cells in the infarct region [65,129] .…”

Section: Differentiation and Neurogenesismentioning

confidence: 97%

“…Despite the exciting prospects of these cells, considerable safety concerns remain regarding their potential to form teratomas. (For a more detailed review of [81] Teramoto et al, 2003 [71] Cooke et al, 2011 [135] Türeyen et al, 2005 [153] Sugiura et al, 2005 [127] Jin et al, 2004 [74] Sun et al, 2003 [154] Wang et al, 2009 [128] Zhu et al, 2008 [155] , 2009 [83] Popa-Wagner et al, 2010 [80] Kobayashi et al, 2006 [78] Guerra-Crespo et al, 2009 [85] Chou et al, 2006 [84] Wang et al, 2012 [113] Schäbitz et al, 2007 [34] Li et al, 2011 [94] Chern et al, 2012 [93] Kilic et al, 2008 [92] Wang et al, 2004 [87] Wang et al, 2012 [89] www.chinaphar.com Dibajnia P et al Acta Pharmacologica Sinica npg different stem cells, see Burns and Steinberg [43] ). Transplantation of NPCs has advantages over other cell types for a number of reasons.…”

Section: Stroke Models and Outcome Measuresmentioning

confidence: 99%

“…However, there is no evidence to date on the effects of GH on NPCs in an animal stoke model, which may be a novel therapeutic target. Some recent work has demonstrated that melatonin can also promote NPC proliferation and reduce neurological deficits that result following stroke [92,93] . Melatonin, delivered orally to mice for 29 d after MCAO, leads to improved motor coordination, as well as decreased hyperactivity and anxiety [92] .…”

Section: Proliferationmentioning

confidence: 99%

See 1 more Smart Citation

Role of neural precursor cells in promoting repair following stroke

Dibajnia

Morshead

2012

Acta Pharmacol Sin

View full text Add to dashboard Cite

Stem cell-based therapies for the treatment of stroke have received considerable attention. Two broad approaches to stem cell-based therapies have been taken: the transplantation of exogenous stem cells, and the activation of endogenous neural stem and progenitor cells (together termed neural precursors). Studies examining the transplantation of exogenous cells have demonstrated that neural stem and progenitor cells lead to the most clinically promising results. Endogenous activation of neural precursors has also been explored based on the fact that resident precursor cells have the inherent capacity to proliferate, migrate and differentiate into mature neurons in the uninjured adult brain. Studies have revealed that these neural precursor cell behaviours can be activated following stroke, whereby neural precursors will expand in number, migrate to the infarct site and differentiate into neurons. However, this innate response is insufficient to lead to functional recovery, making it necessary to enhance the activation of endogenous precursors to promote tissue repair and functional recovery. Herein we will discuss the current state of the stem cell-based approaches with a focus on endogenous repair to treat the stroke injured brain.

show abstract

“…Earlier studies underscore the functional role of MT2 during the process of cell proliferation. Chern et al [68] showed that melatonin-mediated activation of MT2 promotes cell proliferation and neurogenesis after ischemic stroke. Furthermore, a relation between MT2 and cell proliferation was shown for splenic lymphocytes when melatonin-mediated activation of MT2 enhanced proliferation of these cells in MT1 KO mice [46].…”

Section: Mt2-mediated Changes In Cell Proliferationmentioning

confidence: 99%

Differential Regulation of Cell Proliferation and Apoptosis by Melatonin Receptor Subtype-Signaling in the Adult Murine Brain

2018

View full text Add to dashboard Cite

Background/Aims: Zeitgeber time (ZT)-dependent changes in cell proliferation and apoptosis are regulated by melatonin receptor (MT)-mediated signaling in the adult hippocampus and hypothalamic-hypophyseal system. There are two G-protein-coupled MT subtypes, MT1 and MT2. Therefore, the present study examined which MT subtype is required for the regulation of ZT-dependent changes in cell proliferation and/or apoptosis in the adult murine brain and pituitary. Methods: Adult melatonin-proficient (C3H) mice with targeted deletion of MT1 (MT1 KO) or MT2 (MT2 KO) were adapted to a 12-h light/12-h dark photoperiod and sacrificed at ZT00, ZT06, ZT12, and ZT18. Immunohistochemistry for Ki67 or activated caspase-3 served to quantify proliferating and apoptotic cells in the hippocampal subgranular zone (SGZ) and granule cell layer, the hypothalamic median eminence (ME), and the hypophyseal pars tuberalis. Results: ZT-dependent changes in cell proliferation were found exclusively in the SGZ and ME of MT1 KO mice, while apoptosis showed no ZT-dependent changes in the regions analyzed, neither in MT1 nor in MT2 KO mice. Comparison with our previous studies in C3H mice with functional MTs and MT1/2 KO mice revealed that MT2-mediated signaling is required and sufficient for ZT-dependent changes in cell proliferation in the SGZ and ME, while ZT-dependent changes in apoptosis require signaling from both MT subtypes. Conclusions: Our results indicate that generation and timing of ZT-dependent changes in cell proliferation and apoptosis by melatonin require different MT subtype constellations and emphasize the importance to shed light on the specific function of each receptor subtype in different tissues and physiological conditions.

show abstract

Melatonin ameliorates neural function by promoting endogenous neurogenesis through the MT2 melatonin receptor in ischemic-stroke mice

Cited by 133 publications

References 31 publications

Melatonin promotes blood-brain barrier integrity in methamphetamine-induced inflammation in primary rat brain microvascular endothelial cells

Melatonin promotes blood-brain barrier integrity in methamphetamine-induced inflammation in primary rat brain microvascular endothelial cells

Role of neural precursor cells in promoting repair following stroke

Differential Regulation of Cell Proliferation and Apoptosis by Melatonin Receptor Subtype-Signaling in the Adult Murine Brain

Contact Info

Product

Resources

About