Disease relevance of C-FOS

• Verification that the CRH neurons could express cFos when adequately stimulated was made by exposing an additional group of four preterm animals (125 days gestational age) to hypoxemia; the six untreated fetuses served as controls [1].
• In many neurodegenerative diseases, activation of the p38 pathway and of the immediate-early gene termed c-Fos appears to be required for the initiation of apoptosis [2].

Psychiatry related information on C-FOS

• Expression of c-fos protein was examined in the brains of sheep (n = 2 per treatment) subjected to physical stress in a transport simulator, the psychological stress of isolation, insulin-induced hypoglycaemia or intracerebroventricular (I.C.V.) injection of ovine corticotrophin-releasing hormone (CRH) [3].

High impact information on C-FOS

• Transcriptional start site analysis using reverse transcription-PCR verified that the transcriptional initiation of the -215-bp deletion construct, with or without cotransfected c-Jun/c-Fos, was the same as that observed in vivo [4].
• Site-directed mutagenesis of the -120 and -83 sites showed that each element was required for stimulation by c-Jun and c-Fos proteins as well as 12-O-tetradecanoyl phorbol-13-acetate in transient transfection assays [4].
• Activation of the CRH neurons by hypoxemia produced a rapid induction of cFos in CRH neurons, with approximately 50% of the cells strongly expressing cFos protein 1 h after exposure to hypoxia [1].
• The brains of nine fetuses (removed by ceasarian section under anesthesia at gestational ages of 125-145 days) and four newborn sheep were perfused and stained for cFos and CRH [1].
• The present study tested the hypothesis that activation (evidenced by expression of the oncogene product cFos) of a specific population of PVN neurons containing CRH accompanies labor in sheep [1].

Biological context of C-FOS

• Activation of cFos in ovine fetal corticotropin-releasing hormone neurons at the time of parturition [1].
• At the time uterine contractions were first detected, 70% of CRH neurons expressed cFos, and cFos immunoreactivity persisted until just after birth. cFos staining declined rapidly, reaching prelabor levels in some animals by 2-3 h after birth [1].
• Changes in c-jun mRNA levels, in general, paralleled changes in GnRH-R mRNA concentrations, being highest on the day before estrus and declining thereafter. c-Fos mRNA followed a different time course than c-jun mRNA, remaining elevated from Day 8 prior to estrus until the onset of estrus.(ABSTRACT TRUNCATED AT 250 WORDS)[5]
• Our study suggests that the increase in c-Fos levels may play a role in the neuronal apoptosis observed in scrapie-infected mice [2].
• The presence of the immediate early gene product, c-Fos, a marker for cellular activation, was also investigated using immunocytochemistry and in situ hybridization [6].

Anatomical context of C-FOS

• Immunoreactivity of c-Fos was also observed in astrocytes in many brain areas of scrapie-infected mice, particularly in the hippocampus and cortex [2].
• Differential c-Fos expression in the newborn lamb nucleus tractus solitarius and area postrema following ingestion of colostrum or saline [7].
• In late gestation, challenges to fetal homeostasis are accompanied by increases in adrenocorticotropin (ACTH) concentrations in fetal peripheral plasma and Fos (c-fos protein) activation in corticotropin-releasing hormone (CRH) neurons of the fetal hypothalamic paraventricular nucleus (PVN) [8].
• After 15 days of distraction, when bone trabeculae start to form distally and proximally in the distracted regeneration tissue, mostly preosteoblasts and osteoblasts retained c-Fos and c-Jun immunoreactivity, similar to bone-associated cells in control non-distracted fracture repair tissue [9].
• Immunostaining for c-Fos was present in the endometrium at days 0-3 of the oestrous cycle, and some scattered immunopositive nuclei were present in prepubertal animals. c-Fos immunoreactivity was also found in the myometrium and in blood vessels at all other stages examined [6].

Associations of C-FOS with chemical compounds

• Brain C-FOS expression and pressor responses after I.V. or I.C.V. angiotensin in the near-term ovine fetus [10].
• Melatonin was able to significantly inhibit forskolin-stimulated induction of c-fos and jun B mRNA whilst forskolin had no effect upon c-jun or jun D. Induction of c-Fos translation by forskolin was also inhibited by melatonin [11].

Analytical, diagnostic and therapeutic context of C-FOS

• Sheep maxillary bone was distracted daily for 15 days. c-Jun and c-Fos were evaluated by Northern blotting analysis and immunohistochemistry in biopsy specimens removed at 8 and 15 days and were compared with post-osteotomy but not distracted repair tissue [9].

References