Monday, August 27, 2012

Nucleostemin and Liver Regeneration

Our Nucleostemin Stem Cell/Cell Regeneration Marker is widely used and published. I have multiple posting highlighting results of the marker in action. This includes use for staining Tendon Progenitors/Stem Cells (TSCs).

Here researchers use the antibody as a marker for injury induced liver regeneration: Haruhiko Shugo, Takako Ooshio, Masako Naito, Kazuhito Naka, Takayuki Hoshii, Yuko Tadokoro, Teruyuki Muraguchi, Akira Tamase, Noriyuki Uema, Taro Yamashita, Yasunari Nakamoto, Toshio Suda, Shuichi Kaneko, and Atsushi Hirao.Nucleostemin in Injury-Induced Liver Regeneration. Stem Cells and Development. -Not available-, ahead of print. doi:10.1089/scd.2011.0725...Membranes were then incubated with a goat anti-NS antibody (1:1,000; Neuromics, Edina, MN)...

Abstract: The high regenerative capacity of liver contributes to the maintenance of its size and function when injury occurs. Partial hepatectomy induces division of mature hepatocytes to maintain liver function, whereas severe injury stimulates expansion of undifferentiated hepatic precursor cells, which supply mature cells. Although several factors reportedly function in liver regeneration, the precise mechanisms underlying regeneration remain unclear. In this study, we analyzed expression of nucleostemin (NS) during development and in injured liver by using transgenic green fluorescent protein reporter (NS-GFP Tg) mice. In neonatal liver, the hepatic precursor cells that give rise to mature hepatocytes were enriched in a cell population expressing high levels of NS. In adult liver, NS was abundantly expressed in mature hepatocytes and rapidly upregulated by partial hepatectomy. Severe liver injury promoted by a diet containing 3,5-diethoxycarbonyl-1,4-dihydrocollidine induced the emergence of NS-expressing ductal epithelial cells as hepatic precursor cells. NS knockdown inhibited both hepatic colony formation in vitro and proliferation of hepatocytes in vivo. These data strongly suggest that NS plays a critical role in regeneration of both hepatic precursor cells and hepatocytes in response to liver injury.

Check out Neuromics' Stem Cell Research Reagents.

Friday, August 17, 2012

Vagal Nerve Stimulation and Mechanisms for Treating Depression

How does VNS work?

Vagal Nerve Stimulation (VNS) has proven effective in treating severe, intractable depression. It is a procedure that sends electrical impulses into your brain in an effort to improve depression symptoms. Side effects with VNS Therapy include temporary hoarseness or a slight change in voice tone, increased coughing, shortness of breath upon physical exertion, and a tickling in the throat (Rush AJ, Sackeim HA, Marangell LB, et al.).

I wanted to post highlights of a recent study that for the first time shows that VNS increases brain-derived neurotrophic factor (BDNF) in brain or activate, via phosphorylation, its receptor, TrkB: Havan Furmaga, Flavia Regina Carreno, and Alan Frazer. Vagal Nerve Stimulation Rapidly Activates Brain-Derived Neurotrophic Factor Receptor TrkB in Rat Brain. PLoS One. 2012; 7(5): e34844. Published online 2012 May 1. doi: 10.1371/journal.pone.0034844.

Images: Vagal nerve stimulation (VNS) rapidly induces TrkB activation in rat hippocampus. Effects of acute (2 hr) VNS, desipramine (DMI, 10 mg/kg, i.p) or fluoxetine (15 mg/kg, i.p) on TrkB phosphorylation at different tyrosine residues in rat hippocampus.Phospho-TrkB values are normalized against total-TrkB values. One-way MANOVA, Student's Newman-Keuls post-hoc test, *P<0 .05=".05" br="br" group.="group." n="4−8" per="per">

It is this phosphorylation of TrkB that could make VNS a distinct and effective treatment. This VNS induced mechanism is distinct from the effect of standard antidepressant drugs.

Further understanding could result in therapies that are less intrusive, less costly and more effective for treating severe depressive disorders. I will continue to post new findings here.

Wednesday, August 15, 2012

Mu Opioid Receptor, Aging and Immune Response

Mu Opioid Receptors (MOR) play an integral role in modulating perception of pain. Our Opioid Receptor and Opioid Neuropeptide Antibodies have been widely used and extensively published by Pain Researchers.

Here researchers determine a pivotal role of synaptic IGF-1R/Fyn signaling controlled by MOR downstream signaling cascades were crucial for the age-dependent neuroimmune modulation following traumatic stress: Hui Zhao, Xiaocong Zhao, Xiaoding Cao and Gencheng Wu. Age-Dependent Neuroimmune Modulation of IGF-1R in the Traumatic Mice. Immunity & Ageing 2012, 9:12 doi:10.1186/1742-4933-9-12.

Highlights: Fyn activity, as well as its molecular connection with IGF-1R was dependent on MOR, on account of that their coupling was obviously not able to be observed when lack of MOR, accordingly, there was not improvement from the immuno-suppression mediated by traumatic stress in MOR (−/−) mice. Likewise, there was not remarkable change in MOR expression, as well as the association of MOR with IGF-1R or Fyn in the synaptic zone. Then, it is plausible that a characteristic feature of IGF-1R was probably due to age-dependent Fyn activation that was triggered by MOR signaling cascades, this specialized process was mainly concentrated within synaptic zone and might contribute to the recovery from traumatic stress mediated immuno-suppression.

Images: MOR expression during traumatic stress. 2-month and 1-year mice were killed 1 and 3 days after traumatic stress (n = 5 for each group), synaptoneurosome from frontal cortex was prepared, Western blot analysis was used to detect MOR expression (A). Immunoprecipitation was used to analyze alterations of MOR and IGF-1R/Fyn interaction. The immunoprecipitation antibody was anti-Fyn (B) or anti-IGF-1R (D) and the immunoblotting antibody was anti-MOR. Panel C and E depict quantitative analysis of B and D respectively. Data are presented as percentage of control, values represent mean ± SD for 3 independent experiments. Con: control; T3: 3 days after trauma.

I will continue to post new applications for our MOR antibodies.