cyclic-gmp has been researched along with davunetide* in 2 studies
2 other study(ies) available for cyclic-gmp and davunetide
| Article | Year |
|---|---|
NAP mechanisms of neuroprotection.
An 8-amino-acid peptide, NAPVSIPQ (NAP), was identified as the smallest active element of activity-dependent neuroprotective protein that exhibits potent neuroprotective action. Potential signal transduction pathways include cGMP production and interference with inflammatory mechanisms, tumor necrosis factor-alpha, and MAC1-related changes. Because of its intrinsic structure, NAP might interact with extracellular proteins and also transverse membranes. NAP-associated protection against oxidative stress, glucose deprivation, and apoptotic mechanisms suggests interference with fundamental processes. This paper identifies p53, a key regulator of cellular apoptosis, as an intracellular target for NAP's activity. Topics: Alzheimer Disease; Animals; Apoptosis; Brain; Brain Ischemia; Cyclic GMP; Down-Regulation; Encephalitis; Macrophage-1 Antigen; Neuroprotective Agents; Oligopeptides; Oxidative Stress; PC12 Cells; Rats; Tumor Necrosis Factor-alpha; Tumor Suppressor Protein p53 | 2004 |
Vasoactive intestinal peptide and related molecules induce nitrite accumulation in the extracellular milieu of rat cerebral cortical cultures.
Nanomolar concentrations of vasoactive intestinal peptide (VIP), picomolar concentrations of stearyl-norleucine17-VIP (SNV) and femtomolar concentrations of NAPVSIPQ (NAP), an 8-amino-acid peptide derived from the VIP-responsive activity-dependent neuroprotective protein, provide broad neuroprotection. In rat cerebral cortical cultures, 10(-16)-10(-7) M NAP increased intracellular cyclic guanosine monophosphate (cGMP) (2.5-4-fold) and 10(-10) M NAP increased extracellular nitric oxide (NO) by 60%. In the same culture system, VIP and SNV (at micromolar concentrations) increased extracellular NO by 45-55%. The NAP dose required for cGMP increases correlated with the dose providing neuroprotection. However, the concentrations of NAP, SNV and VIP affecting NO production did not match the neuro-protective doses. Thus, NO may mediate part of the cell-cell interaction and natural maintenance activity of VIP/SNV/NAP, while cGMP may mediate neuroprotection. Topics: Animals; Animals, Newborn; Cells, Cultured; Cerebral Cortex; Cyclic GMP; Dose-Response Relationship, Drug; Extracellular Space; Neuroglia; Neurons; Neuroprotective Agents; Nitric Oxide; Nitrites; Oligopeptides; Rats; Vasoactive Intestinal Peptide | 2001 |