Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats with bilateral lateral hypothalamic lesions die of starvation in approximately 7 days after surgery. Rats that were treated with alpha-methyl-p-tyrosine for 3 days prior to lateral hypothalamic surgery spontaneously eat, drink, and gain weight after surgery. These data suggest that recovery of function after lateral hypothalamic damage involves denervation supersensitivity.
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PMID:Facilitation of recovery by -methyl-p-tyrosine after lateral hypothalamic damage. 505 Apr 88

The discovery that mammalian cells can survive late-stage apoptosis challenges the general assumption that active caspases are markers of impending death. However, tools have not been available to track healthy cells that have experienced caspase activity at any time in the past. Therefore, to determine if cells in whole animals can undergo reversal of apoptosis, known as anastasis, we developed a dual color CaspaseTracker system for Drosophila to identify cells with ongoing or past caspase activity. Transient exposure of healthy females to environmental stresses such as cold shock or starvation activated the CaspaseTracker coincident with caspase activity and apoptotic morphologies in multiple cell types of developing egg chambers. Importantly, when stressed flies were returned to normal conditions, morphologically healthy egg chambers and new progeny flies were labeled by the biosensor, suggesting functional recovery from apoptotic caspase activation. In striking contrast to developing egg chambers, which lack basal caspase biosensor activation under normal conditions, many adult tissues of normal healthy flies exhibit robust caspase biosensor activity in a portion of cells, including neurons. The widespread persistence of CaspaseTracker-positivity implies that healthy cells utilize active caspases for non-apoptotic physiological functions during and after normal development.
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PMID:In vivo CaspaseTracker biosensor system for detecting anastasis and non-apoptotic caspase activity. 2575 39

Glial scar formation derived from astrocyte proliferation and migration influences the functional recovery after spinal cord injury. Cyclin-dependent kinase inhibitor p27(kip1), whose activity is closely related to its phosphorylation state, reportedly regulates astrocyte proliferation and migration. In this study, we reported that p27(Kip1) undergoes O-GlcNAc modification at Ser 2, Ser 110 and Thr 197. Inhibiting O-GlcNAcylation on Ser 2 by gene mutation (S2A) attenuated the phosphorylation of Ser 10, and vice versa. Interestingly, compared with wild type p27(Kip1), S2A p27(Kip1) displayed a decreased interaction with CRM1 and reduced nuclear export following serum starvation and release. In addition, the interaction between stathmin and S2A p27(Kip1) was also decreased. Cytoskeletal proteins microtubules appeared high density in astrocytes transfected with S2A p27(Kip1) especially at the leading edge of the scratch wound. Accordingly, scratch-wound assay revealed that the motility of astrocytes transfected with S2A p27(Kip1) was faster than that of control. Finally, we injected lentiviral vectors immediately after spinal cord contusion, and found the lesion volume of the rat injected with S2A p27(Kip1) was smaller than that of rat injected with wild type p27(Kip1). Besides, the BBB and CBS behavioral tests showed greater functional recovery in S2A p27(Kip1) treated rats. Taken together, our findings revealed a novel function of O-GlcNAc modification of p27(Kip1) in mediating astrocytes migration and functional recovery after spinal cord contusion.
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PMID:O-GlcNAc glycosylation of p27(kip1) promotes astrocyte migration and functional recovery after spinal cord contusion. 2656 63

Transplantation with mesenchymal stem cells (MSCs) has shown beneficial effects in treating spinal cord injury. Autophagy is an evolutionarily conserved process of degradation and recycling of cellular components that plays an important role in tissue homeostasis and cellular survival. Whether regulating autophagy in MSCs may affect their therapeutic potential in spinal cord injury repair has not yet been determined. In this study, autophagy was inhibited in MSCs with lentiviruses expressing short hairpin RNA (shRNA) to knock down Becn-1 expression, and autophagy was upregulated in MSCs under nutrient starvation. These MSCs were then labelled with Hoechst and applied to spinal cord-injured rats to evaluate their therapeutic effects. After transplanting MSCs into rats with spinal cord injuries, functional recovery, immunohistochemistry, and remyelination analyses were performed. After inducing autophagy, the MSCs exhibited an accumulation of LC3-positive autophagosomes in the cytoplasm. The expression levels of neurotrophic factors, including vascular endothelial growth factor and brain derived neurotrophic factor, were significantly higher in autophagic MSCs than normal MSCs. The in vivo study showed that more labelled MSCs migrated to the lesion site after induction of autophagy. Inducing autophagy in MSCs promoted functional recovery after spinal cord injury, whereas functional recovery was weak after inhibiting autophagy in MSCs. In contrast to the autophagy inhibition group, transplanting autophagic MSCs exhibited a greater positive impact on axon regeneration, growth of serotonergic fibers, blood vessel regeneration, and myelination, indicating a multifactorial contribution to spinal cord injury repair. These results suggest that autophagy plays important roles in MSCs during spinal cord injury repair. Regulation of autophagy in MSCs before in vivo transplantation may be a potential therapeutic interventional strategy for spinal cord injury.
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PMID:Regulation of autophagy in mesenchymal stem cells modulates therapeutic effects on spinal cord injury. 3127 35