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ABSTRACT: Lysophosphatidic acid (LPA) is a lipid mediator that is involved in many biological responses, such as, in the stimulation/inhibition
of proliferation, in cell migration, antiapoptosis, tumor cell invasion, platelet aggregation, vascular remodeling, and neurotransmitter
release. In addition, LPA indirectly enhances the contractility of smooth muscle. Furthermore, electric field stimulation
(EFS) causes contractions of isolated cat esophageal smooth muscle and relaxations of isolated cat lower esophageal sphincter
(LES). To test whether or not LPA enhances postsynaptically-mediated contraction in cat esophageal smooth muscle and LES,
both types of muscle strips were stimulated with muscarinic agonists. However, no significant effects were observed, and therefore,
to investigate whether LPA is involved in presynaptic signal transduction, cat esophageal smooth muscle and LES were pretreated
with LPA and stimulated using EFS. LPA had no effect on EFS-induced contraction in esophageal smooth muscle but the EFSinduced
LES relaxation was dose-dependently inhibited by LPA. To identify the LPA receptor subtype that inhibits EFS-induced LES relaxation,
we used the specific LPA1/LPA3 antagonist Ki16425 and the LPA3 agonist OMPT. Ki16425 significantly blocked the inhibitory effect of LPA on EFS-induced relaxation, but OMPT did not enhance
the effect of LPA. These results suggest that LPA inhibits EFS-induced relaxation in LES via LPA1 receptor-mediated signaling. It is well known that EFS-induced LES relaxation is related to the release of neurotransmitters,
such as, nitric oxide, vasoactive intestinal polypeptide, and calcitonin gene-related peptide. We then investigated whether
LPA selectively blocks NO-mediated signaling. Sodium nitroprusside-induced LES relaxation was found to be inhibited in the
same manner as EFS-induced LES relaxation by LPA. This result suggests that LPA partially blocks NO uptake by presynaptic
pathways, and thus, inhibits LES relaxation.
Key wordsSmooth muscle–Contraction–Lysophosphatidic acid receptor–Nitric oxide–Lower esophageal sphincter
Archives of Pharmacal Research 04/2012; 34(1):169-176. · 1.59 Impact Factor
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ABSTRACT: Parturition increases the risk of strokes of various types, including postpartum cerebral angiopathy (PCA), which is characterized by reversible multifocal vasoconstriction of the cerebral arteries. We describe an unusual presentation of PCA associated with postpartum non-aneurysmal subarachnoid hemorrhage (SAH). A 31-year-old multiparous woman complained of sudden headache 3 hours after an uncomplicated vaginal delivery. She had no history of pregnancy-induced hypertension. SAH was found over the bilateral frontoparietal convexities with multifocal vasculopathy. Her symptoms resolved completely within 1 week. The findings of a follow-up neurological examination, cerebral angiography, and brain MRI were normal after 2 months. PCA syndrome may be associated with postpartum non-aneurysmal SAH.
Journal of Clinical Neuroscience 09/2011; 18(9):1269-71. · 1.25 Impact Factor
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ABSTRACT: Lysophosphatidic acid (LPA) is a lipid mediator that is involved in many biological responses, such as, in the stimulation/inhibition of proliferation, in cell migration, antiapoptosis, tumor cell invasion, platelet aggregation, vascular remodeling, and neurotransmitter release. In addition, LPA indirectly enhances the contractility of smooth muscle. Furthermore, electric field stimulation (EFS) causes contractions of isolated cat esophageal smooth muscle and relaxations of isolated cat lower esophageal sphincter (LES). To test whether or not LPA enhances postsynaptically-mediated contraction in cat esophageal smooth muscle and LES, both types of muscle strips were stimulated with muscarinic agonists. However, no significant effects were observed, and therefore, to investigate whether LPA is involved in presynaptic signal transduction, cat esophageal smooth muscle and LES were pretreated with LPA and stimulated using EFS. LPA had no effect on EFS-induced contraction in esophageal smooth muscle but the EFS-induced LES relaxation was dose-dependently inhibited by LPA. To identify the LPA receptor subtype that inhibits EFS-induced LES relaxation, we used the specific LPA(1)/LPA(3) antagonist Ki16425 and the LPA(3) agonist OMPT. Ki16425 significantly blocked the inhibitory effect of LPA on EFS-induced relaxation, but OMPT did not enhance the effect of LPA. These results suggest that LPA inhibits EFS-induced relaxation in LES via LPA(1) receptor-mediated signaling. It is well known that EFS-induced LES relaxation is related to the release of neurotransmitters, such as, nitric oxide, vasoactive intestinal polypeptide, and calcitonin gene-related peptide. We then investigated whether LPA selectively blocks NO-mediated signaling. Sodium nitroprusside-induced LES relaxation was found to be inhibited in the same manner as EFS-induced LES relaxation by LPA. This result suggests that LPA partially blocks NO uptake by presynaptic pathways, and thus, inhibits LES relaxation.
Archives of Pharmacal Research 01/2011; 34(1):169-76. · 1.59 Impact Factor
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ABSTRACT: To investigate the intestinal absorption of a fibrinolytic and proteolytic lumbrokinase extracted from Eisenia andrei, we used rat everted gut sacs and an in situ closed-loop recirculation method. We extracted lumbrokinase from Eisenia andrei, and then raised polyclonal antibody against lumbrokinase. Fibrinolytic activity and proteolytic activity in the serosal side of rat everted gut sacs incubated with lumbrokinase showed dose- and time-dependent patterns. Immunological results obtained by western blotting serosal side solution using rat everted gut sacs method showed that lumbrokinase proteins between 33.6 and 54.7 kDa are absorbed mostly by the intestinal epithelium. Furthermore, MALDI-TOF mass spectrometric analysis of plasma fractions obtained by in situ recirculation method confirmed that lumbrokinase F1 is absorbed into blood. These results support the notion that lumbrokinase can be absorbed from mucosal lumen into blood by oral administration.
Korean Journal of Physiology and Pharmacology 04/2010; 14(2):71-5. · 0.96 Impact Factor
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Journal of Clinical Neuroscience 08/2008; 15(11):1311-2. · 1.25 Impact Factor
