Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P01178 (
oxytocin
)
15,767
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The hypothalamo-neurohypophysial system (HNS), synthesizing arginine vasopressin (AVP) and
oxytocin
(
OXT
), is well known to show structural plasticity during chronic physiological stimulation such as salt loading and lactation. In the present study, we undertook in the HNS to study localization and activity-dependent changes in the expression of matrix-degrading enzymes such as tissue plasminogen activator (tPA) and
matrix metalloprotease
-3 (MMP-3). Double labeling confocal microscopy demonstrated that the immunoreactivity of tPA was localized at AVP-positive dendrites in the supraoptic nucleus (SON) and AVP-positive terminals in the neurohypophysis (NH). The immunoreactivity of tPA was also seen at astrocytic processes in the HNS. Likewise, the immunoreactivity of MMP-3 was observed at AVP-positive dendrites and terminals. High magnification observation further revealed punctate distribution of tPA and MMP-3 immunoreactivity at dendrites and terminals, suggesting that they are localized at neurosecretory granules. Salt loading, known as the chronic stimulation to cause the structural plasticity, increased protein and mRNA levels of tPA in the SON but reduced protein levels of it in the NH. The chronic stimulation also increased protein levels of urokinase plasminogen activator in the SON, but the stimulation did not change protein levels of MMP-3 in the SON and NH. Depolarizing agent KCl released tPA from isolated neurosecretosomes, and this depolarization-dependent release was abolished by verapamil, a Ca(2+) channel blocker. These results demonstrate that tPA and MMP-3 are localized mainly at dendrites and terminals of AVP-expressing magnocellular neurons and tPA is released in an activity-dependent manner, suggesting that matrix-degrading proteases are candidate molecules to be concerned with the structural plasticity in the HNS.
...
PMID:Matrix-degrading enzymes tissue plasminogen activator and matrix metalloprotease-3 in the hypothalamo-neurohypophysial system. 1615 Apr 23
Objective To investigate the factors associated with depression, including the serum
oxytocin
(
OXT
) levels, disease activity, activities of daily living (ADLs) and quality of life (QOL), and their effects on rheumatoid arthritis (RA). Methods This study included 42-RA-patients. We measured the following variables before and after 6 months of treatment with biological disease-modifying antirheumatic drugs (bDMARDs): the baseline characteristics (including age, sex, disease duration, smoking, and body mass index), the doses of prednisolone and methotrexate, the serum level of
matrix metalloprotease
-3, the erythrocyte sedimentation rate and the C-reactive protein level. The disease activity of RA was assessed using the Simplified Disease Activity Index (SDAI), depression was assessed using the Hamilton Depression Rating Scale (HAM-D), the ADLs were assessed using the Health Assessment Questionnaire disability index and the QOL was assessed using the Short Form (SF)-36. The serum
OXT
levels were determined using an enzyme-linked immunosorbent assay. Results The HAM-D score was significantly correlated with the SDAI, and the mental component summary score of the SF-36. However, the serum
OXT
levels were not correlated with the HAM-D score. The serum
OXT
levels before and after bDMARDs treatment did not differ to a statistically significant extent, regardless of the presence of depression. Although the differences in the serum levels of
OXT
were observed prior to the initiation of treatment, there was no gender difference after treatment. Conclusion Although RA complicated by depression may be related to the following high disease activity, a poor QOL and poor ADLs, the serum
OXT
levels were not directly correlated.
...
PMID:The Relationship between the Serum Oxytocin Levels, Disease Activity, the ADLs and the QOL in Patients with Rheumatoid Arthritis. 2902 42