Biomedical subjects

Shigeto Hayashi

Publications and source records attributed to Shigeto Hayashi.

4 recordsLinked to original sources

PubMed2005

Involvement of gamma protein kinase C in estrogen-induced neuroprotection against focal brain ischemia through G protein-coupled estrogen receptor.

The neuroprotective effects of estrogen were studied in the ischemic model mice by 90 min transient unilateral middle cerebral artery occlusion (MCAO) followed by 22.5 h reperfusion. The total infarct size in C57BL/6 female mice after MCAO and reperfusion was significantly smaller than that in male mice. Intraperitoneal injection of estrogen after the start of reperfusion significantly reduced the infarct volume in the male mice. However, no significant gender difference was found in total infarct size in gamma protein kinase C (PKC)-knockout mice, suggesting that the neuroprotective effects of estrogen are due to the activation of a specific subtype of PKC, gammaPKC, a neuron-specific PKC subtype, in the brain. We demonstrated that exogenous estrogen-induced neuroprotection was attenuated in gammaPKC-knockout mice. Immunocytochemical study showed that gammaPKC was translocated to nerve fiber-like structures when observed shortly after MCAO and reperfusion. We also visualized the rapid and reversible translocation of gammaPKC-GFP (green fluorescent protein) by estrogen stimulation in living CHO-K1 cells. These results suggest that the activation of gammaPKC through the G-protein-coupled estrogen receptors on the plasma membrane is involved in the estrogen-induced neuroprotection against focal brain ischemia.

Animals↗

PubMed2004

Superoxide production at phagosomal cup/phagosome through beta I protein kinase C during Fc gamma R-mediated phagocytosis in microglia.

Protein kinase C (PKC) plays a prominent role in immune signaling. To elucidate the signal transduction in a respiratory burst and isoform-specific function of PKC during FcgammaR-mediated phagocytosis, we used live, digital fluorescence imaging of mouse microglial cells expressing GFP-tagged molecules. betaI PKC, epsilonPKC, and diacylglycerol kinase (DGK) beta dynamically and transiently accumulated around IgG-opsonized beads (BIgG). Moreover, the accumulation of p47(phox), an essential cytosolic component of NADPH oxidase and a substrate for betaI PKC, at the phagosomal cup/phagosome was apparent during BIgG ingestion. Superoxide (O(2)(-)) production was profoundly inhibited by Gö6976, a cPKC inhibitor, and dramatically increased by the DGK inhibitor, R59949. Ultrastructural analysis revealed that BIgG induced O(2)(-) production at the phagosome but not at the intracellular granules. We conclude that activation/accumulation of betaI PKC is involved in O(2)(-) production, and that O(2)(-) production is primarily initiated at the phagosomal cup/phagosome. This study also suggests that DGKbeta plays a prominent role in regulation of O(2)(-) production during FcgammaR-mediated phagocytosis.

Animals↗

PubMed2004

In vivo transgene expression using an adenoviral tetracycline-regulated system with neuron-specific enolase promoter.

A recombinant adenoviral tetracycline-regulated system with neuron-specific enolase (NSE) promoter was injected stereotaxically into the striatum of rat brains. The efficiency of in vivo transfection was quantified by counting the number of green fluorescent protein (GFP)-positive cells at 3 days, 1 week, and 4 weeks after injection. NeuN immunohistochemistry demonstrated that expression of gammaPKC-GFP was dominant (20-99%) in neuron and expression of gammaPKC-GFP in neuron was significantly higher in pups than adult rats. These results indicate that tetracycline-inhibitable transcription factor (tTA) can drive tetracycline-responsive promoter (TetOp) under the control of NSE promoter, thereby efficiently and selectively expressing gammaPKC-GFP in neurons in vivo.

Adenoviridae↗

PubMed2003

Congenital cavernous angioma exhibits a progressive decrease in size after birth.

CASE REPORT: We report a case of congenital intracranial cavernous angioma, which was initially found at a gestational age of 34 weeks in utero as a mass lesion associated with hydrocephalus. After birth, the patient was treated for hydrocephalus first by external drainage and then by ventricular peritoneal shunt. The natural course of the mass lesion was observed until the age of 8 months when the histopathological diagnosis confirmed the cavernous angioma after tissue was obtained by surgery. CT scans repeated monthly during this period demonstrated that the angioma continuously decreased in size. There was no evidence of hemorrhage in the angioma on serial CT scans. The histopathology revealed thrombosis of cavernous vessels with hyaloid changes in the angioma. DISCUSSION: The mechanisms of the decreasing size of the cavernous angioma have often been discussed in relation to spontaneous hemorrhages and resolution. The present case suggests a mechanism in which the spontaneous formation of a thrombus might be the dominant factor for the decrease in size. Thrombus formation may result from low perfusion due to the large size of the angioma.

Brain Neoplasms↗