Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of the collapse response mediator protein CRMP5 in the prenatal mouse is largely unknown. Evidence suggests that CRMP family members play important roles in neurite outgrowth, and CRMP5 is known to modulate outgrowth of processes in oligodendrocytes through signalling via neuropilin-1 and SemaA. Furthermore, CRMP family members function in axon regeneration after injury and are implicated in the early stages of Alzheimer's disease. Despite these findings relatively little is known about the specific roles these proteins play. The aim of the present study was to evaluate CRMP5 expression in the developing mouse forebrain using in situ hybridisation. Serial coronal sections of brain from E12.5 to E18.5 were analysed. We found highly specific patterns of expression which were restricted to the post-mitotic layers of both the ganglionic eminence and neocortex, and an additional domain of strong expression in the pyramidal layers of the hippocampus in all prenatal ages. Our results are therefore consistent with a role for CRMP5 in process extension. Interestingly, our results also revealed a temporal switch in high-expression levels from the ganglionic eminence to the cortex at a critical time during tangential cell migration. However, the pattern of expression appeared more representative of a general permissiveness for neurite outgrowth rather than one which is restricted to a particular cell subset or cell class. Additionally, expression was also found during periods predominated by neurogenesis and not neurite extension. We conclude that expression of CRMP5 is consistent with a dynamic implicit role in forebrain development.
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PMID:Localization of CRMP5 mRNA by in situ hybridisation during development of the mouse forebrain. 1821 65

Mammalian eye development requires vitamin A (retinol, ROL). The role of vitamin A at specific times during eye development was studied in rat fetuses made vitamin A deficient (VAD) after embryonic day (E) 10.5 (late VAD). The optic fissure does not close in late VAD embryos, and severe folding and collapse of the retina is observed at E18.5. Pitx2, a gene required for normal optic fissure closure, is dramatically downregulated in the periocular mesenchyme in late VAD embryos, and dissolution of the basal lamina does not occur at the optic fissure margin. The addition of ROL to late VAD embryos by E12.5 restores Pitx2 expression, supports dissolution of the basal lamina, and prevents coloboma, whereas supplementation at E13.5 does not. Surprisingly, ROL given as late as E13.5 completely prevents folding of the retina despite the presence of an open fetal fissure, showing that coloboma and retinal folding represent distinct VAD-dependent defects. Retinal folding due to VAD is preceded by an overall reduction in the percentage of cyclin D1 positive cells in the developing retina, (initially resulting in retinal thinning), as well as a dramatic reduction in the cell adhesion-related molecules, N-cadherin and beta-catenin. Reduction of retinal cell number combined with a loss of the normal cell-cell adhesion proteins may contribute to the collapse and folding of the retina that occurs in late VAD fetuses.
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PMID:The temporal requirement for vitamin A in the developing eye: mechanism of action in optic fissure closure and new roles for the vitamin in regulating cell proliferation and adhesion in the embryonic retina. 1895 41

Maternal hyperglycemia can inhibit morphogenesis of ureteric bud branching, Glial cell line-derived neurotrophilic factor (GDNF) is a key regulator of the initiation of ureteric branching. Early growth response gene-1 (EGR-1) is an immediate early gene. Preliminary study found EGR-1 persistently expressed with GDNF in hyperglycemic environment. To evaluate the potential relationship of hyperglycemia-GDNF-EGR-1 pathway, in vitro human renal proximal tubular epithelial (HRPTE) cells as target and in vivo streptozotocin-induced mice model were used. Our in vivo microarray, real time-PCR and confocal morphological observation confirmed apoptosis in hyperglycemia-induced fetal nephropathy via activation of the GDNF/MAPK/EGR-1 pathway at E12-E15. Detachment between ureteric branch and metanephrons, coupled with decreasing number and collapse of nephrons on Day 1 newborn mice indicate hyperglycemic environment suppress ureteric bud to invade metanephric rudiment. In vitro evidence proved that high glucose suppressed HRPTE cell migration and enhanced GDNF-EGR-1 pathway, inducing HRPTE cell apoptosis. Knockdown of EGR-1 by siRNA negated hyperglycemic suppressed GDNF-induced HRPTE cells. EGR-1 siRNA also reduced GDNF/EGR-1-induced cRaf/MEK/ERK phosphorylation by 80%. Our findings reveal a novel mechanism of GDNF/MAPK/EGR-1 activation playing a critical role in HRPTE cell migration, apoptosis and fetal hyperglycemic nephropathy.
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PMID:Hyperglycemia: GDNF-EGR1 pathway target renal epithelial cell migration and apoptosis in diabetic renal embryopathy. 2346 76