Редактирование: AGER

Advanced glycosylation end product-specific receptor precursor (Receptor for advanced glycosylation end products) [RAGE]

==Publications==

{{medline-entry
|title=Vitamin D3 regulates apoptosis and proliferation in the testis of D-galactose-induced aged rat model.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31575929
|abstract=The age-associated imbalances between proliferation and apoptosis lead to impaired spermatogenesis and infertility. The age-associated decline in vitamin D3 levels has been reported and suggested the anti-aging potential of vitamin D3. However, the age-associated decline levels of vitamin D3 has not been studied in relation to the testicular activity. Thus, we investigated the effect of vitamin D3 on the expression of testicular proliferation markers, apoptotic markers, antioxidants system and oxidative stress in a D-gal-induced aged rat model. The present study investigated the levels of vitamin D3 and AGE in serum and testes along with the expression of the AGE-receptor ([[AGER]]) in the testis. Vitamin D3 treatment significantly increases cell proliferation and decreases apoptosis in a D-gal-induced aged rat testis. Furthermore, vitamin D3 significantly decreases oxidative stress in aged rat testis by improving the antioxidant defense systems. The expression of [[AGER]] was down-regulated by vitamin D3 treatment in aged testis. The circulating and intra-testicular AGE was higher in aged groups, however, only circulating vitamin D3 levels decreased in aged groups. The immunolocalization of [[VDR]] showed increased immunostaining in the testis by vitamin D3 treatment. Thus, it can be concluded that vitamin D3 delays testicular senescence by regulating proliferation and apoptosis.
|mesh-terms=* Aging
* Animals
* Antioxidants
* Apoptosis
* Cell Proliferation
* Cholecalciferol
* Down-Regulation
* Galactose
* Male
* Oxidative Stress
* Rats
* Spermatogenesis
* Testis

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6773724
}}
{{medline-entry
|title=Vitamin D3 treatment regulates apoptosis, antioxidant defense system, and DNA integrity in the epididymal sperm of an aged rat model.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31566824
|abstract=The present study aimed to investigate the effects of vitamin D3 in the epididymal sperm cells of D-gal-induced aged rats. It is well known that during aging sperm quality and quantity declines and leads to age-related infertility problems in males. The results of the present study showed that there were elevated levels of oxidative stress and poor DNA integrity of sperm of aged rats. The expression of [[BCL2]] also showed a significant decline in the sperm of aged rats, however, the expression of [[BAX]] and active caspase-3 did not show significant change compared with the control group. The treatment of vitamin D3 at lower doses to aged rats showed increased expression of [[BAX]] and active caspase-3 in the sperm, this finding suggests that increased apoptosis may be responsible for removal of poor quality sperm during aging. Vitamin D3 treatment at both doses showed improvement in the oxidative stress and DNA integrity in the sperm of aged rats. We also investigated the expression of [[AGER]], visfatin, and [[HSPA1A]] in the epididymal sperm. It has been found that expression of [[AGER]], visfatin, and [[HSPA1A]] increased in the sperm aged rats and vitamin D3 treatments at both doses decreased its expression. Thus, it might be suggested that during aging vitamin D3 treatment would be important for managing the sperm quality by regulating the apoptosis, antioxidant system and DNA integrity via modulation of visfatin and [[HSPA1A]].
|mesh-terms=* Aging
* Animals
* Antioxidants
* Apoptosis
* Cholecalciferol
* Epididymis
* Male
* Rats
* Rats, Wistar
* Spermatozoa
|keywords=* aging
* apoptosis
* oxidative stress
* sperm
|full-text-url=https://sci-hub.do/10.1002/mrd.23280
}}
{{medline-entry
|title=Long-lived rodents reveal signatures of positive selection in genes associated with lifespan.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29570707
|abstract=The genetics of lifespan determination is poorly understood. Most research has been done on short-lived animals and it is unclear if these insights can be transferred to long-lived mammals like humans. Some African mole-rats (Bathyergidae) have life expectancies that are multiple times higher than similar sized and phylogenetically closely related rodents. To gain new insights into genetic mechanisms determining mammalian lifespans, we obtained genomic and transcriptomic data from 17 rodent species and scanned eleven evolutionary branches associated with the evolution of enhanced longevity for positively selected genes (PSGs). Indicating relevance for aging, the set of 250 identified PSGs showed in liver of long-lived naked mole-rats and short-lived rats an expression pattern that fits the antagonistic pleiotropy theory of aging. Moreover, we found the PSGs to be enriched for genes known to be related to aging. Among these enrichments were "cellular respiration" and "metal ion homeostasis", as well as functional terms associated with processes regulated by the mTOR pathway: translation, autophagy and inflammation. Remarkably, among PSGs are [[RHEB]], a regulator of mTOR, and [[IGF1]], both central components of aging-relevant pathways, as well as genes yet unknown to be aging-associated but representing convincing functional candidates, e.g. [[RHEB]]L1, [[AMHR2]], [[PSMG1]] and [[AGER]]. Exemplary protein homology modeling suggests functional consequences for amino acid changes under positive selection. Therefore, we conclude that our results provide a meaningful resource for follow-up studies to mechanistically link identified genes and amino acids under positive selection to aging and lifespan determination.
|mesh-terms=* Animals
* Genome
* Homeostasis
* Ion Transport
* Longevity
* Oxidative Stress
* Rodentia
* Selection, Genetic
* Species Specificity
* Transcriptome

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884551
}}
{{medline-entry
|title=Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24194717
|abstract=Harboring the behavioral and histopathological signatures of Alzheimer's disease (AD), senescence accelerated mouse-prone 8 (SAMP8) mice are currently considered a robust model for studying AD. However, the underlying mechanisms, prioritized pathways and genes in SAMP8 mice linked to AD remain unclear. In this study, we provide a biological interpretation of the molecular underpinnings of SAMP8 mice. Our results were derived from differentially expressed genes in the hippocampus and cerebral cortex of SAMP8 mice compared to age-matched SAMR1 mice at 2, 6, and 12 months of age using cDNA microarray analysis. On the basis of PPI, MetaCore and the co-expression network, we constructed a distinct genetic sub-network in the brains of SAMP8 mice. Next, we determined that the regulation of synaptic transmission and apoptosis were disrupted in the brains of SAMP8 mice. We found abnormal gene expression of [[RAF1]], [[MAPT]], [[PTGS2]], [[[[CDKN2A]]]], [[CAMK2A]], [[NTRK2]], [[AGER]], ADRBK1, [[MCM3AP]], and [[STUB1]], which may have initiated the dysfunction of biological processes in the brains of SAMP8 mice. Specifically, we found microRNAs, including miR-20a, miR-17, miR-34a, miR-155, miR-18a, miR-22, miR-26a, miR-101, miR-106b, and miR-125b, that might regulate the expression of nodes in the sub-network. Taken together, these results provide new insights into the biological and genetic mechanisms of SAMP8 mice and add an important dimension to our understanding of the neuro-pathogenesis in SAMP8 mice from a systems perspective. 

|keywords=* Alzheimer's disease
* apoptosis
* cerebral cortex
* differential expressed genes
* hippocampus
* molecular network
* senescence accelerated mouse prone 8
* synaptic transmission
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810591
}}