Gap Junctions (GJs) and Glaucoma

GJs Can Offer Neuroprotection
This study references use of our GFAP Antibody,

Gap junctions (GJs), intercellular channels composed of subunit connexins, can play a major role in secondary cell death by forming conduits through which toxic molecules from dying cells pass to and injure coupled neighbors. Secondary cells like glia and astrocytes are involved in this process though the precise mechanisms have yet to be defined: Abram Akopian, Sandeep Kumar, Hariharasubramanian Ramakrishnan, Kaushambi Roy, Suresh Viswanathan, and Stewart A. Bloomfield. Targeting neuronal gap junctions in mouse retina offers neuroprotection in glaucoma. J Clin Invest. doi:10.1172/JCI91948. Copyright © 2017, The American Society for Clinical Investigation. ...anti-GFAP (1:1,000, RA22101; Neuromics)...

Figure: Reactive gliosis in retinas of microbead-injected mice is significantly reduced by GJ blockade/ablation. (A) Confocal images of retinal layers stained for GFAP, SMI32, and DAPI in control and glaucomatous retinas. Scale bar: 50 μm in all panels. Z-stack: 7 sections, 3-μm steps. (B) GFAP expression in the retinal layers of CxWT and Cx36–/– mouse retinas under different conditions (n = 6 retinas per group). (C) GFAP labeling in retinal sections from control and microbead-injected CxWT (n = 5 retinas), Cx36–/– (n = 5 retinas), and Cx36–/– Cx45–/– mice (n = 3 retinas). GFAP expression is presented as percentage of immunolabeling per area.

Our Neuron/Synapse, Astrocytes, Glia, Microglia, Oligodendrocytes, Progenitors and Schwann Cell Markers are frequently referenced and I will continue to post new developments.

Connective-Tissue Growth Factor (CTGF/CCN2) Induces Astrogenesis

SOX-2 Proves a Marker For Astrogenesis

This proved  surprising to the authors of a recent publication referencing use of our Monoclonal SOX-2 Antibody. We have added our SOX-2 abs to our Glial-Astrocyte Markers. See: Fabio A. Mendes , Juliana M. Coelho Aguiar , Suzana A. Kahn, Alice H. Reis, Luiz Gustavo Dubois, Luciana Ferreira Romão, Lais S. S. Ferreira, Hervé Chneiweiss, Vivaldo Moura Neto, José G. Abreu. Connective-Tissue Growth Factor (CTGF/CCN2) Induces Astrogenesis and Fibronectin Expression of Embryonic Neural Cells In Vitro. Published: August 4, 2015DOI: 10.1371/journal.pone.0133689...monoclonal anti-Sox2 (Neuromics, Acris, Germany) in blocking solution were incubated with the membranes overnight at 4°C, followed by incubation with Peroxidase-conjugated anti-rabbit IgG and peroxidase-conjugated anti-mouse IgG secondary antibodies...

Figure: Exogenous CTGF protein increases the number of Sox2-positive cells of a neural progenitor culture. Immunostaining showing Sox2 (A and D) expression of untreated and CTGF-treated cells. C and F show merged pictures of Sox2 immunostaining together with nuclei-DAPI staining. Scale bars 10 μm. G shows the percentage of cells that were positive for Sox2. doi:10.1371/journal.pone.0133689.g002

Neuromics have a significant catalog of potent and proven Asytoglial, Neuronal, Schwann Cell and Oligodendrocyte Markers.

GFAP and Mouse Myenteric Plexus

Our Neuronal-Glial Markers are important tools for our customers investigating expression in the CNS and PNS. I have posted images showing staining of mouse retinal astrocytes and in the ventral horn, funiculus of adult rat spinal cord and mouse medulloblastoma stem cells using our GFAP antibodies.

I wanted to share an excellent image generated by Dr. Kate Ellacott's lab at Vanderbilt University.

GFAP (Chicken-Cat#: CH22102) staining in of enteric glia in the myenteric plexus of the mouse gastrointestinal tract. Staining was performed in methanol/acetone fixed frozen sections using 1:1000 dilution of the antibody followed by 1:500 anti-chicken Alexa 594.

Related Reagents:

• GFAP (Chicken-Cat#: CH23011)
• GFAP (Mouse-Cat#; MO15052)
• GFAP (Rabbit-Cat#:RA19063)
• Neuronal-Glial Markers -Astrocytes, Glia, Microglia, Olidogodendrocytes, Progenitors and Schwann Cell.

Nestin as a Marker for Astrocytomas

I recently highlighted the growing parade of pubs referencing use of our reagents for Cancer Research.

I would like to add a new one. Angogenesis of Astrocytomas show stem like properties. This makes our Nestin Antibodies excellent markers.

J H Tchaicha, A K Mobley, M G Hossain, K D Aldape and J H McCarty. A mosaic mouse model of astrocytoma identifies αvβ8 integrin as a negative regulator of tumor angiogenesis. Oncogene , (7 June 2010) doi:10.1038/onc.2010.199...chicken anti-Nestin IgY (Neuromics, Edina, MN, USA)...

Abstract: Angiogenesis involves a complex set of cell–cell and cell–extracellular matrix (ECM) interactions that coordinately promote and inhibit blood vessel growth and sprouting. Although many factors that promote angiogenesis have been characterized, the identities and mechanisms of action of endogenous inhibitors of angiogenesis remain unclear. Furthermore, little is known about how cancer cells selectively circumvent the actions of these inhibitors to promote pathological angiogenesis, a requisite event for tumor progression. Using mosaic mouse models of the malignant brain cancer, astrocytoma, we report that tumor cells induce pathological angiogenesis by suppressing expression of the ECM protein receptor αvβ8 integrin. Diminished integrin expression in astrocytoma cells leads to reduced activation of latent TGFβs, resulting in impaired TGFβ receptor signaling in tumor-associated endothelial cells. These data reveal that astrocytoma cells manipulate their angiogenic balance by selectively suppressing αvβ8 integrin expression and function. Finally, these results show that an adhesion and signaling axis normally involved in developmental brain angiogenesis is pathologically exploited in adult brain tumors.

Related Reagents:

Nestin Mouse Monoclonal-Cat#:MO15012
Nestin-Mouse Monoclonal-Cat#:MO15056
Nestin-Goat Polyclonal
Stem Cell Research Reagents

New Mouse Monoclonal GFAP Antibody

Check it out!

GFAP Antibody

Excelent marker for human astrocyte intermediate filaments in the central nervous system. It has also been detected in the glial cells of the enteric nervous system and some Schwann cells in the peripheral nervous systems.

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Ischemia, Inflammatory Response and Umbilical Stem Cells

We would like to send Kudos to Dr. Yan Xu and his colleagues at University of Pittburgh for their findings on inflammatory response in Golbal Ischemia. Their work was recently published:

Aaron Hirko, Renee Dallasen, Sachiko Jomura, Yan Xu. Modulation of Inflammatory Responses after Global Ischemia by Transplanted Umbilical-Cord Matrix Stem Cells. Stem Cells First published online August 21, 2008; doi:doi:10.1634/stemcells.2008-0075

Secondary to Cardiac Arrest is Brain Damage do to lack of blood flow. This is marked by a delayed loss of Neurons in CA1 hippocampus region of the brain due to inflammatory response.

The story timeline of this response is good then bad with interesting twists. The delay in neuronal loss is linked to initial inflammation. It involves both reactive astrocytes (astrocytosis) and glia. Delaying the loss is, of course, good.

...But then, the reactive astrocytosis and related glial scarring cause a physical and biochemical barrier to regeneration of neurons...a bad thing. Protecting the microglia is a good thing, because they these cells serve as scavengers for clearing the cellular debris. They can also secrete a variety of cytotoxic and protective chemicals.

The wow factor in this research is that implanted rat umbilical-cord matrix (RUCM) cells can provide partial protection against neuronal injury in rat brains. Rats treated with RUCM cells three days prior to an 8-min CA had only 25-32% neuronal loss in the hippocampal CA1 region compared to the typical 50-68% neuronal loss observed in the untreated or the vehicle-treated animals. This could be due to to the favaorable modulation of the "good-bad" inflammatory response.

The good news in the search for therapies for stroke and cardiac arrest victims is combined, stem-cell-like RUCM cells offer protection against neuronal injury after global cerebral ischemia by enhancing the survivability of the astroglia in the selectively vulnerable regions.

We are pleased that the research team used our GFAP antibody as an marker for astrotytic in their studies.