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The molecular and cellular mechanisms behind glycogen metabolism and the energy metabolite translocation between mammal neurons and astrocytes have been well studied. A similar mechanism is proposed for rapid mobilization of local energy stores to support energy-dependent transepithelial ion transport in gills of the Mozambique tilapia (Oreochromis mossarnbicus). A novel gill glycogen phosphorylase isoform (tGPGG), which catalyzes the initial degradation of glycogen, was identified in branchial epithelial cells of O. mossambicus. Double in situ hybridization and immunocytochemistry demonstrated that tGPGG mRNA and glycogen were colocalized in glycogen-rich cells (GRCs), which surround ionocytes (labeled with a [Na.sup.+] - [K.sup.+]-ATPase antiserum) in gill epithelia. Concanavalin-A (a marker for the apical membrane) labeling indicated that GRCs and mitochondria-rich cells share the same apical opening. Quantitative real-time PCR analyses showed that tGPGG mRNA expression levels specifically responded to environmental salinity changes. Indeed, the glycogen content, glycogen phosphorylase (GP) protein level and total activity, and the density of tGPGG-expressing cells (i.e., GRCs) in fish acclimated to seawater (SW) were significantly higher than those in freshwater controls. Short-term acclimation to SW caused an evident depletion in the glycogen content of GRCs. Taken altogether, tGPGG expression in GRCs is stimulated by hyperosmotic challenge, and this may catalyze initial glycogen degradation to provide the adjacent ionocytes with energy to carry out iono- and osmoregulatory functions. osmoregulation; [Na.sup.+]-[K.sup.+]-ATPase; salinity; ionocytes doi: 10.1152/ajpregu.00681.2006

Examination of the chain of events in the anti-inflammatory phase due to intratracheal injection of lipopolysaccharide (LPS) reveals that LPS injection stimulates endogenous leukemia inhibitory factor (LIF) secretion into the bronchoalveolar space. LIF inhibits the LPS-induced acute neutrophilic inflammation through inhibition of tumor necrosis factor expression and enhancement of interleukin-6 expression.

Based on the protein kinase A (PKA)/GSK3β interaction protein (GSKIP)/glycogen synthase kinase 3β (GSK3β) axis, we hypothesized that these might play a role in Tau phosphorylation. Here, we report that the phosphorylation of Tau Ser409 in SHSY5Y cells was increased by overexpression of GSKIP WT more than by PKA- and GSK3β-binding defective mutants (V41/L45 and L130, respectively). We conducted in vitro assays of various kinase combinations to show that a combination of GSK3β with PKA but not Ca2+/calmodulin-dependent protein kinase II (CaMK II) might provide a conformational shelter to harbor Tau Ser409. Cerebrospinal fluid (CSF) was evaluated to extend the clinical significance of Tau phosphorylation status in Alzheimer's disease (AD), neurological disorders (NAD), and mild cognitive impairment (MCI). We found higher levels of different PKA–Tau phosphorylation sites (Ser214, Ser262, and Ser409) in AD than in NAD, MCI, and normal groups. Moreover, we used the CRISPR/Cas9 system to produce amyloid precursor protein (APPWT/D678H) isogenic mutants. These results demonstrated an enhanced level of phosphorylation by PKA but not by the control. This study is the first to demonstrate a transient increase in phosphor-Tau caused by PKA, but not GSK3β, in the CSF and induced pluripotent stem cells (iPSCs) of AD, implying that both GSKIP and GSK3β function as anchoring proteins to strengthen the cAMP/PKA/Tau axis signaling during AD pathogenesis. [ABSTRACT FROM AUTHOR]

Purpose: Vitronectin is a secreted glycoprotein present in blood plasma and is present in the extracellular matrix of many tissues. It was found in the retinal cDNA library that contains genes whose expression is upregulated after optic nerve injury in a previous study. The purpose of this study was to assess the temporal and spatial changes in expression of vitronectin and integrin alphav in the retina following optic nerve injury., Methods: Adult Balb/c mice underwent crush of the optic nerve in one eye only. RT-PCR was used to determine the temporal expression of vitronectin mRNA in the retina after injury. In addition, expression at the protein level in the retina and the optic nerve of vitronectin and its major receptor subunit, integrin alphav, was analyzed by immunohistochemistry., Results: Upregulation of vitronectin mRNA in the retina was detected at one day after injury, peaking at three days, and maintained up to one week. An elevated expression of vitronectin protein was also observed in the inner retina, optic nerve head, and the optic nerve after nerve crush. In the inner retina, the increased expression of vitronectin was found in retinal ganglion cells (RGCs) and its surrounding extracellular matrix. Expression of integrin alphav was also increased in the RGC layer and in the glial cells of the nerve head and the crush site., Conclusions: As vitronectin is an extracellular protein that can support cell attachment and promote neurite extension, elevated expression of vitronectin and its receptor may facilitate axonal regeneration following injury. We propose that treatment sustaining secretion of endogenous vitronectin or direct application of exogenous vitronectin may be a method to augment regeneration of the severed optic axons.

The purpose of the present study was to search for changes in gene expression patterns in the retina following optic nerve injury. We conducted a subtractive hybridization for comparison of the mRNAs in those retinas receiving optic nerve crush injury and those receiving sham operation. Both forward and reverse subtractions were carried out for 8-h and 24-h time points postoperatively. Resultant subtractive cDNA for each group was re-amplified and cloned to a plasmid. After DNA sequencing, the identity of subtractive cDNA was analyzed by blasting sequences to the Nonredundant gene database, Unigene database, and dbest database at NCBI. Thirty-four known genes and 32 EST were found in the forward subtractions. Forty-two known genes and 46 EST were found in reverse subtractions. Identities of the rest could not been found in the databases. To verify the subtractive results, RT-PCR was performed to test expression patterns of eight known genes found in the above analysis. Among these eight genes, seven demonstrated a statistically significant difference between the crushed eyes and the control eyes by quantitative image analysis. Together, our data show that expression of fatso, ephrin B2, NonO, Zfx, vitronectin, and XLRS increased after optic nerve injury, and expression of stathmin exhibited reduction after injury.