Редактирование: EDN1 (раздел)

==Publications==

{{medline-entry
|title=Dexamethasone downregulates [[SIRT1]] and [[IL6]] and upregulates [[EDN1]] genes in stem cells derived from gingivae via the AGE/RAGE pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29302812
|abstract=To evaluate the effects of dexamethasone on the aging of mesenchymal stem cells from human gingiva using next-generation sequencing. Four mRNAs were upregulated and 12 were downregulated when the results of dexamethasone at 24 h were compared with the control at 24 h. Expressions of [[SIRT1]] and [[IL6]] were decreased in dexamethasone at 24 h but expression of [[EDN1]] was increased. Application of dexamethasone reduced the expression of [[SIRT1]] and [[IL6]] but enhanced the expression of [[EDN1]] of stem cells.
|mesh-terms=* Cells, Cultured
* Cellular Senescence
* Dexamethasone
* Endothelin-1
* Gene Expression Profiling
* Gene Expression Regulation
* Gingiva
* Humans
* Interleukin-6
* Mesenchymal Stem Cells
* RNA, Messenger
* Signal Transduction
* Sirtuin 1
|keywords=* Aging
* Dexamethasone
* Gingiva
* Messenger RNA
* Stem cells
|full-text-url=https://sci-hub.do/10.1007/s10529-017-2493-0
}}
{{medline-entry
|title=Variation in genes in the endothelin pathway and endothelium-dependent and endothelium-independent vasodilation in an elderly population.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23336501
|abstract=Indirect evidences by blockade of the endothelin receptors have suggested a role of endothelin in endothelium-dependent vasodilation. This study aimed to investigate whether circulating levels of endotehlin-1 or genetic variations in genes in the endothelin pathway were related to endothelium-dependent vasodilation. In 1016 seventy-year-old participants of the population-based Prospective Study of the Vasculature in Uppsala Seniors (PIVUS) study (52% women), we measured endothelium-dependent vasodilation using the invasive forearm technique with acetylcholine given in the brachial artery (EDV) and the brachial artery ultrasound technique with measurement of flow-mediated dilatation (FMD). Plasma endothelin-1 levels were measured and 60 SNPs in genes in the endothelin pathway (ECE1, [[EDN1]], [[EDNRA]], [[EDNRB]]) were genotyped. No significant associations were found between circulating endothelin levels and EDV or FMD. No single genotype was related to EDV or FMD following adjustment for multiple testing, but a genotype score for 3 SNPs (rs11618266 in [[EDNRB]], rs17675063 in [[EDNRA]], rs3026868 in ECE1) was significantly related to EDV (beta coefficient 0.070, 95% CI 0.025-0.12, P = 0.002) when adjusting for gender, systolic blood pressure, HDL and LDL cholesterol, serum triglycerides, BMI, diabetes, smoking, antihypertensive medication or statins and [[CRP]]. This score was also related to nitroprusside-induced vasodilation in the forearm. A combination of genotypes in the endothelin pathway was related to both endothelium-dependent and endothelium-independent vasodilation in forearm resistance vessels, but not in the brachial artery in an elderly population, giving evidence for a role of the endothelin system in resistance vessel reactivity independent of major cardiovascular risk factors.
|mesh-terms=* Age Factors
* Aged
* Aging
* Aspartic Acid Endopeptidases
* Brachial Artery
* Endothelin-1
* Endothelin-Converting Enzymes
* Endothelium, Vascular
* Female
* Forearm
* Genotype
* Humans
* Infusions, Intra-Arterial
* Linear Models
* Male
* Metalloendopeptidases
* Phenotype
* Polymorphism, Single Nucleotide
* Prospective Studies
* Receptor, Endothelin A
* Receptor, Endothelin B
* Regional Blood Flow
* Sweden
* Ultrasonography
* Vasodilation
* Vasodilator Agents

|full-text-url=https://sci-hub.do/10.1111/apha.12068
}}
{{medline-entry
|title=Endothelin-1 is a transcriptional target of p53 in epidermal keratinocytes and regulates ultraviolet-induced melanocyte homeostasis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23279852
|abstract=Keratinocytes contribute to melanocyte activity by influencing their microenvironment, in part, through secretion of paracrine factors. Here, we discovered that p53 directly regulates Edn1 expression in epidermal keratinocytes and controls UV-induced melanocyte homeostasis. Selective ablation of endothelin-1 ([[EDN1]]) in murine epidermis ([[EDN1]](ep-/-) ) does not alter melanocyte homeostasis in newborn skin but decreases dermal melanocytes in adult skin. Results showed that keratinocytic [[EDN1]] in a non-cell autonomous manner controls melanocyte proliferation, migration, DNA damage, and apoptosis after ultraviolet B (UVB) irradiation. Expression of other keratinocyte-derived paracrine factors did not compensate for the loss of [[EDN1]]. Topical treatment with [[EDN1]] receptor (EDNRB) antagonist BQ788 abrogated UV-induced melanocyte activation and recapitulated the phenotype seen in [[EDN1]](ep-/-)  mice. Altogether, the present studies establish an essential role of [[EDN1]] in epidermal keratinocytes to mediate UV-induced melanocyte homeostasis in vivo.
|mesh-terms=* Aging
* Animals
* Apoptosis
* Cell Proliferation
* DNA Damage
* DNA Repair
* Endothelin-1
* Epidermal Cells
* Gene Deletion
* Gene Expression Regulation
* Homeostasis
* Immunohistochemistry
* Keratinocytes
* MAP Kinase Signaling System
* Melanocytes
* Mice
* Organ Specificity
* Phenotype
* Protein Kinase C
* Receptor, Endothelin B
* Transcription, Genetic
* Tumor Suppressor Protein p53
* Ultraviolet Rays

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3663331
}}