Редактирование: CNP

2',3'-cyclic-nucleotide 3'-phosphodiesterase precursor (EC 3.1.4.37) (CNP) (CNPase)

==Publications==

{{medline-entry
|title=Environmental Enrichment Elicits a Transient Rise of Bioactive C-Type Natriuretic Peptide in Young but Not Aged Rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30072880
|abstract=Beneficial molecular and neuroplastic changes have been demonstrated in response to environmental enrichment (EE) in laboratory animals across the lifespan. Here, we investigated whether these effects extend to C-type Natriuretic Peptide ([[CNP]]), a widely expressed neuropeptide with putative involvement in neuroprotection, neuroplasticity, anxiety, and learning and memory. We determined the [[CNP]] response in 36 young (8-9 months) and 36 aged (22-23 months) male PVGc hooded rats that were rehoused with new cage mates in either standard laboratory cages or EE for periods of 14 or 28 days. Tissues were rapidly excised from four brain regions associated with memory formation (dorsal hippocampus, retrosplenial cortex, medial prefrontal cortex, and mammillary bodies) plus the occipital cortex and hypothalamus, and immediately frozen. Radioimmunoassay was used to measure bioactive [[CNP]] and the amino-terminal fragment of pro[[CNP]], NTpro[[CNP]]. Because [[CNP]] but not NTpro[[CNP]] is rapidly degraded at source, NTpro[[CNP]] reflects [[CNP]] production whereas the ratio NTpro[[CNP]]:[[CNP]] is a biomarker of [[CNP]]'s local degradation rate. EE increased [[CNP]] at 14 days in all brain regions in young, but not old rats; this effect in young rats was lost at 28 days in all regions of interest. NTpro[[CNP]]:[[CNP]] ratio, but not NTpro[[CNP]], was reduced in all regions by EE at 14 days in young rats, but not in old rats, which suggests a period of reduced degradation or receptor mediated clearance, rather than increased production of [[CNP]] in these young EE rats. Aged rats tended to show reduced NTpro[[CNP]]:[[CNP]] ratios but this did not occur in dorsal hippocampus or mammillary bodies. This is the first study demonstrating modulation of [[CNP]] protein concentrations, and the effect of age, in response to environmental stimulation. Furthermore, it is the first to show that changes in degradation rate [i]in vivo[/i] may be an important component in determining [[CNP]] bioactivity in neural tissues.

|keywords=* C-type natriuretic peptide
* aging
* environmental enrichment
* hippocampus
* medial prefrontal cortex
* retrosplenial cortex
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6060231
}}
{{medline-entry
|title=In aging, the vulnerability of rat brain mitochondria is enhanced due to reduced level of 2',3'-cyclic nucleotide-3'-phosphodiesterase ([[CNP]]) and subsequently increased permeability transition in brain mitochondria in old animals.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25277077
|abstract=Aging is accompanied by progressive dysfunction of mitochondria associated with a continuous decrease of their capacity to produce ATP. Mitochondria isolated from brain of aged animals show an increased mitochondrial permeability transition pore (mPTP) opening. We recently detected new regulators of mPTP function in brain mitochondria, the enzyme 2', 3'-cyclic nucleotide 3'-phosphodiesterase ([[CNP]]) and its substrates 2', 3'-cAMP and 2', 3'-cNADP, and the neuronal protein p42(IP4). Here, we compared parameters of mPTP opening in non-synaptic brain mitochondria isolated from young and old rats. In mitochondria from old rats (>18 months), mPTP opening occurred at a lower threshold of Ca(2 ) concentration than in mitochondria from young rats (<3 months). mPTP opening in mitochondria from old rats was accelerated by 2', 3'-cAMP, which further lowered the threshold Ca(2 ) concentration. In non-synaptic mitochondria from old rats, the [[CNP]] level was decreased by 34%. Lowering of the [[CNP]] level in non-synaptic mitochondria with aging was accompanied by decreased levels of voltage-dependent anion channel (VDAC; by 69%) and of p42(IP4) (by 59%). Thus, reduced levels of [[CNP]] in mitochondria could lead to a rise in the concentration of the mPTP promoter 2', 3'-cAMP. The level of [[CNP]] and p42(IP4) and, probably VDAC, might be essential for myelination and electrical activity of axons. We propose that in aging the reduction in the level of these proteins leads to mitochondrial dysfunction, in particular, to a decreased threshold Ca(2 ) concentration to induce mPTP opening. This might represent initial steps of age-related mitochondrial dysfunction, resulting in myelin and axonal pathology. 
|mesh-terms=* 2',3'-Cyclic Nucleotide 3'-Phosphodiesterase
* Aging
* Animals
* Brain
* Male
* Mitochondria
* Mitochondrial Membrane Transport Proteins
* Mitochondrial Permeability Transition Pore
* Rats
* Rats, Wistar
|keywords=* 2′,3′-cyclic nucleotide 3′-phosphodiesterase
* Age-dependent changes
* Aging
* Rat brain mitochondria (RBM)
* mPTP
|full-text-url=https://sci-hub.do/10.1016/j.neuint.2014.09.008
}}