Immunohistochemical localization of calcium-binding proteins in the brainstem vestibular nuclei of the jaundiced Gunn rat

Global changes in gene regulation demonstrate that unconjugated bilirubin is able to upregulate and activate select components of the endoplasmic reticulum stress response pathway

“…Literature reports document that UCB has the ability to alter the intracellular redox state [11,24], alter the expression of a number of major calcium handling proteins [25,26], as well as to perturb energy metabolism. In this study, we also show that the transcripts of three proteins of the S100a family of Ca 2+ -binding proteins, S100a4, S100a8, and S100a10 are significantly downregulated following treatment with UCB (50 μM; Table 1).…”

“…If ER stress is prolonged and cells are unable to alleviate the accumulation of unfolded proteins, the cell may be committed to apoptosis, a process thought to be initiated via activation of the initiator caspase, caspase-12 [21,22]. Interestingly, UCB has been shown to alter intracellular redox state [11,23,24], alter the expression of a number of major calcium-handling proteins [25,26], and to perturb energy metabolism [27]. Despite the fact that the ER is exposed to concentrated UCB because this is the site for its glucuronidation, very little is known about the effect of UCB on ER function or its ability to elicit ER stress.…”

Quantification of gait in dystonic Gunn rats

“…On postnatal day 15 (baseline) and again on postnatal day 31, dystonia was rated subjectively using a Kernicterus Clinical Rating Scale (KCRS) (Shaia et al, 2002) based on Schutta and Johnson (1969) and Rose and Wisniewski (1979) as follows: 0, normal; 1, slight limb dystonia and gait abnormality; 2, mild limb dystonia and gait abnormality, and impaired righting reflex; 3, moderate limb dystonia and gait abnormality with prolonged righting reflex; 4, severe failure of ambulation, general lack of spontaneous movement with occasional bursts of hyperactivity, and no righting reflex; 5, moribund, including seizures and agonal respiration. An additional 0.5 was added to the score of animals appearing to be midway between one category and the next higher one.…”

The molecular basis of bilirubin encephalopathy and toxicity: Report of an EASL Single Topic Conference, Trieste, Italy, 1–2 October, 2004

“…Developmental expression of CaM kinase II activity is impaired in jaundiced Gunn rats [65], and there is a selective decrease in expression of the calcium binding proteins, calbindin and parvalbumin, in the CNS of jaundiced Gunn rats treated with sulfonamide to acutely displace UCB from albumin [66,67].…”