Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen status is known to affect the incidence of cardiovascular disease. Experiments were designed to prove the influences of in vivo estrogen manipulations on vascular hyperpolarization and relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF), and to explore the possible mechanism contributing to the altered EDHF responses in estrogen-deficient states. Mesenteric arteries with intact endothelium were isolated from sham-operated (control), ovariectomized (OVX), or OVX with 17beta-estradiol replacement (OVX + E ) female rats. In the presence of apamin and charybdotoxin, there was no difference between groups in relaxations to the Ca ionophore A23187 and the endoplasmic reticulum Ca -adenosine triphosphatase inhibitor cyclopiazonic acid (CPA). However, N -nitro-L-arginine produced a marked decrease in A23187- and CPA-induced relaxations in OVX compared with control and OVX + E arteries. In control arteries, A23187 and CPA elicited membrane hyperpolarization in a sustained manner. In contrast, A23187 produced only a small and transient hyperpolarizing effect in OVX arteries. OVX also greatly attenuated the sustained pattern of hyperpolarization to CPA. Such changes in hyperpolarizations were not seen in OVX + E arteries. The EDHF-mediated relaxant and hyperpolarizing responses of control arteries to A23187 and CPA were significantly inhibited by the gap junction inhibitor 18 alpha-glycyrrhetinic acid. Immunohistochemical examination for connexin-43 showed that the expression was abundant along the endothelial layer in control and OVX + E arteries, while being much less in OVX arteries. It was concluded that estrogen deficiency specifically impairs EDHF-mediated vascular actions. This may be partly explained by the reduced expression of connexin-43, a protein molecule that could form myoendothelial gap junction channels.
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PMID:Ovariectomy attenuates hyperpolarization and relaxation mediated by endothelium-derived hyperpolarizing factor in female rat mesenteric artery: a concomitant decrease in connexin-43 expression. 1245 28

Cochlear fibrocytes are the crucial component of the inner ear homeostasis and its defect by various causes; GJB2 (connexin [Cx] 26) mutation, for example, leads to hearing loss. In the present study, we investigated the potential use of human amniotic epithelial cells, proposed to possess pluripotential properties, as a source of transplantation therapy in inner ear disease. The mRNA of the gap junction protein Cx26 and Na-K-adenosine triphosphatase, the immunohistologic expression of these proteins, and the cells' intercellular communication capacity were detected in vitro. Their transplantation into the guinea pig cochlea revealed the survival and expression of the proteins even 3 weeks after transplantation. Transplanted human amniotic epithelial cells were localized at the site where the proteins function, strongly indicating their cooperation in the regional potassium ion recycling. This technology suggests the therapeutic potential for the treatment of hearing loss.
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PMID:Transplanted human amniotic epithelial cells express connexin 26 and Na-K-adenosine triphosphatase in the inner ear. 1516 5