Disease relevance of PCBD1

• Inappropriate, dopamine-induced activation of PCD might have a role in nigral neuronal degeneration in Parkinson's disease [1].
• Broilers from three consecutive hatches were exposed to cool temperatures to amplify the incidence of pulmonary hypertension syndrome (PHS, ascites) [2].
• Lower levels of furosemide significantly reduced PHS mortality without reducing body weights [3].
• The differences observed between normal and preascitic broilers demonstrate that systemic hypotension can trigger renal mechanisms contributing to fluid and solute retention during development of PHS [4].
• Neither body weight on Day 1 or 21 nor net weight gain from Days 1 to 21 determined susceptibility to PHS during the subsequent grower and finisher intervals in either experiment.(ABSTRACT TRUNCATED AT 250 WORDS)[5]

High impact information on PCBD1

• The highest levels of cDcoHalpha mRNA were found in the kidney, liver, heart and ovarian follicles, while the major tissues expressing cDcoH were hypothalamus, kidney and liver. cDcoH and cDcoHalpha probes did not cross-hybridize to human hepatocyte mRNA [6].
• This technique resulted in the cloning of a novel counterpart of the previously cloned chicken dimerization cofactor of hepatocyte nuclear factor (HNF)-1 (cDcoH), which was identified as cDcoHalpha [6].
• Here we report on the isolation, nucleotide sequence and genomic structure of the chicken and rat DCoH genes [7].
• We recently reported that the neurotransmitter DA can trigger apoptosis (programmed cell death; PCD) in cultured, postmitotic chick embryo sympathetic neurons, suggesting a role for apoptosis in degenerative processes such as Parkinson's disease (PD) [8].
• We report that exposure of cultured, postmitotic chick-embryo sympathetic neurons, to physiological concentrations of dopamine (0.1-1 mM) for 24 h initiates a cellular death process characteristic of apoptosis (= programmed-cell-death, PCD) [1].

Chemical compound and disease context of PCBD1

• The capacity of the pulmonary vasculature in the ARGININE group to accommodate an increased BF at a normal PAP accounts for the previously reported lower incidence of pulmonary hypertension syndrome (PHS, ascites) in cold-stressed broilers fed supplemental dietary arginine [9].
• Previous studies have suggested cardiac taurine is released into the plasma in response to hypoxemia (low blood oxygen levels) during the pathogenesis of pulmonary hypertension syndrome (PHS, ascites) [10].
• Previous studies demonstrated that bacterial lipopolysaccharide (LPS, endotoxin) triggers pulmonary vasoconstriction leading to pulmonary hypertension (PHS, ascites) in broilers [11].
• The combined results indicate the presence of a site-specific defect at either Complex II, ubiquinone, or both in liver mitochondria obtained from broilers with PHS that may be responsible for the oxidative stress and mitochondrial dysfunction observed in this costly metabolic disease [12].

Biological context of PCBD1

• These observations demonstrate for the first time that PHS (ascites) can be directly induced by a primary increase in pulmonary vascular resistance [13].
• Respiration studies of PHS liver mitochondria also revealed disease-associated decreases in the respiratory control ratio (RCR, an index of electron transport chain coupling) [12].
• Lower levels of the primary antioxidants, alpha- and beta-tocopherol, and glutathione (GSH) in PHS mitochondria confirmed the presence of oxidative stress [12].
• The inherent capacity for flow-dependent pulmonary vasodilation may reduce the susceptibility of Giant Jungle Fowl to PHS by reducing the increment in pulmonary arterial pressure required to propel an elevated blood flow through the lungs [14].
• These results demonstrate that broiler breeders capable of thriving after having their entire cardiac output forced to flow through one lung, subsequently produced male and female progeny with substantially improved resistance to the onset of PHS induced by fast growth and exposure to cool environmental temperatures [15].

Anatomical context of PCBD1

• The present study was conducted to determine whether a more prolonged period of bronchus occlusion causes PHS similar to that induced by clamping one pulmonary artery [16].
• In a second experiment, similar improvements in functional indices following sequential additions of ADP and responses to respiratory chain inhibitors were observed in liver mitochondria isolated from Single Comb White Leghorn (SCWL) males (resistant to PHS) similar to that observed in control broiler mitochondria in Experiment 1 [12].
• Accordingly, the maximum increment in PAP attainable by the right ventricle during acute increases in PVR apparently was inadequate to propel the entire CO through the pulmonary vasculature, setting the stage for the congestive right-sided pooling of blood routinely associated with PHS in broilers [9].
• During the pathophysiological progression of pulmonary hypertension syndrome (PHS; ascites), broilers concurrently develop systemic hypotension (low mean systemic arterial pressure) that may initiate renal retention of water and solute, contributing to fluid accumulation in the abdominal cavity (ascites) [4].

Associations of PCBD1 with chemical compounds

• Cumulative PHS mortality was significantly reduced by 1% L-arginine HCl on Days 34 to 46 in Experiment 1 [5].
• Neither the incidence of PHS nor specific predictors of PHS susceptibility (electrocardiogram Lead II S-wave amplitude, % saturation of hemoglobin with oxygen, heart rate, right to total ventricular weight ratio) were affected by taurine or beta-alanine supplementation [10].
• Cumulative PHS mortality was significantly reduced by furosemide in both experiments [3].

Analytical, diagnostic and therapeutic context of PCBD1

• Characterization of the chicken and rat DCoH gene domains using an improved ligation-mediated PCR method [7].
• Ascitic birds in all treatment groups had higher RV:TV ratios and more negative ECG Lead II S-wave amplitudes than nonascitic birds, reflecting the right ventricular hypertrophy and generalized ventricular dilation typically associated with PHS [16].

References