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Nobuo Hisano

Publications and source records attributed to Nobuo Hisano.

4 recordsLinked to original sources

Sphingosine 1-phosphate breakdown in platelets.

We examined the formation of sphingolipid mediators in platelets, which abundantly store, and release extracellularly, sphingosine 1-phosphate (Sph-1-P). Challenging [(3)H]Sph-labeled platelet suspensions with thrombin or 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in a decrease in Sph-1-P formation and an increase in sphingosine (Sph), ceramide (Cer), and sphingomyelin formation. Sph conversion into Cer, and Cer conversion into sphingomyelin were not affected upon activation, suggesting that Sph-1-P dephosphorylation may initiate the formation of sphingolipid signaling molecules. In fact, Sph-1-P phosphatase (but not lyase) activity was detected in platelets, but this activity was not enhanced by thrombin or TPA. When quantified with [(3)H]acetic anhydride acetylation, followed by HPLC separation, the amounts of Sph-1-P and Sph decreased and increased, respectively, upon stimulation with thrombin or TPA, and these changes were attenuated by staurosporine. Under these TPA treatment conditions, over half of the [(3)H]Sph-1-P (formed in platelets incubated with [(3)H]Sph) was detected extracellularly, possibly due to its release from platelets, which was completely inhibited by staurosporine pretreatment. Furthermore, when TPA-induced Sph-1-P release was blocked by staurosporine after the stimulation, the extracellular [(3)H]Sph-1-P radioactivity decreased, suggesting that the Sph-1-P released may undergo dephosphorylation extracellularly. To support this, [(32)P]Sph-1-P, when added extracellularly to platelet suspensions, was rapidly degraded, possibly due to the ecto-phosphatase activity. Our results suggest the presence in anucleate platelets of a transmembrane cycling pathway starting with Sph-1-P dephosphorylation and leading to the formation of other sphingolipid mediators.

Blood Platelets↗

[A case of type 1 diabetes mellitus in an elderly patient with a history of idiopathic portal hypertension].

The patient is a 71-year-old woman who underwent splenectomy after the diagnosis of idiopathic portal hypertension (IPH) at the age of 51 years. Thirst and polyuria occurred in December 1995. In April 1996, she was hospitalized for assessment because of elevation of her blood glucose and HbA1c levels to 535 mg/dl and 14.9%, respectively. The GAD antibody level was high (256 units/ml) and tests for ICA and anti-TPO antibody were positive. Since her HLA type was A 24, B 13, B 46, CW 1, CW 3, DRB 1*[0901/0901], DQB 1*[0303/0303], and DPB 1*[0201/0201], this patient was regarded as being susceptible to type 1 diabetes mellitus. There was no evidence of portal hypertension at the time of consultation. Although there was a considerable difference in the time of onset between IPH and type I diabetes mellitus, we reported this patient as a valuable case for investigating the complications of autoimmune disease.

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