Редактирование: CRHR2

Corticotropin-releasing factor receptor 2 (CRF-R-2) (CRF-R2) (CRFR-2) (Corticotropin-releasing hormone receptor 2) (CRH-R-2) (CRH-R2) [CRF2R] [CRH2R]

==Publications==

{{medline-entry
|title=Aging-related changes in cutaneous corticotropin-releasing hormone system reflect a defective neuroendocrine-stress response in aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22533365
|abstract=Skin, being a mirror of the body, is a major target for aging research. Aging is a complex process that involves the decline of function or dysfunction of many systems. The corticotropin-releasing hormone ([[CRH]]) system is involved in skin inflammation. In addition, [[CRH]] has a suggested role in age-associated conditions and in animal aging models. However, a consistent logic interaction between the different [[CRH]] system components and the aging process has, to our knowledge, never been examined before. The expression of [[CRH]], [[CRH]]-binding protein ([[[[CRH]]BP]]), [[CRH]] receptor 1 ([[CRH]]R1), and [[CRH]] receptor 2 ([[[[CRH]]R2]]) in healthy skin samples of 42 patients of different ages (18-92 years) was evaluated by immunohistochemistry, and the age-related changes were assessed. Compared with young skin, the aged skin displayed an upregulation of [[CRH]] in sebaceous glands and [[CRH]]R1 in hair follicles and the epidermis. Moreover, age-associated downregulation of [[[[CRH]]BP]] in the sebaceous and sweat glands was detected, whereas the [[[[CRH]]R2]] showed no age-related changes. Our findings suggest that the age-associated changes in the expression of [[CRH]] system components reflect an exaggerated stress response reaction, putting the aged skin continuously in a stress-like situation.
|mesh-terms=* Adult
* Aged
* Aging
* Carrier Proteins
* Corticotropin-Releasing Hormone
* Female
* Humans
* Male
* Middle Aged
* Receptors, Corticotropin-Releasing Hormone
* Sebaceous Glands
* Skin
* Stress, Physiological
* Young Adult

|full-text-url=https://sci-hub.do/10.1089/rej.2011.1294
}}
{{medline-entry
|title=Corticotropin-releasing hormone receptor-1 in cerebral microvessels changes during development and influences urocortin transport across the blood-brain barrier.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/20032050
|abstract=In this study we tested the hypothesis that receptor-mediated transport of urocortin across the blood-brain barrier (BBB) undergoes developmental changes. Urocortin is a peptide produced by both selective brain regions and peripheral organs, and it is involved in feeding, memory, mood, cardiovascular functions, and immune regulation. In BBB studies with multiple-time regression analysis, we found that neonatal mice had a significant influx of (125)I-urocortin. By contrast, adult mice did not transport urocortin across the BBB. Quantitative RT-PCR showed that corticotropin-releasing hormone receptor ([[CRH]]R)-1 was developmentally regulated in enriched cerebral microvessels as well as hypothalamus, being significantly higher in neonatal than adult mice. This change was less dramatic in agouti viable yellow mice, a strain that develops adult-onset obesity. The level of expression of [[CRH]]R1 mRNA was 33-fold higher in the microvessels than in hypothalamic homogenates. The mRNA for [[[[CRH]]R2]] was less abundant in both regions and less prone to changes with development or the agouti viable yellow mutation. Supported by previous findings of receptor-mediated endocytosis of urocortin, these results suggest that permeation of urocortin across the BBB is dependent on the level of [[CRH]]R1 expression in cerebral microvessels. These novel findings of differential regulation of [[CRH]] receptor subtypes help elucidate developmental processes in the brain, particularly for the urocortin system.
|mesh-terms=* Aging
* Animals
* Animals, Newborn
* Blood-Brain Barrier
* Female
* Hypothalamus
* Iodine Radioisotopes
* Male
* Mice
* Mice, Inbred C57BL
* Microvessels
* Protein Isoforms
* Receptors, Corticotropin-Releasing Hormone
* Urocortins

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840693
}}