دورية أكاديمية

Morphine-mediated alteration of hypertension-related gene expression in human white blood cells and multilineage progenitor cells.

التفاصيل البيبلوغرافية
العنوان: Morphine-mediated alteration of hypertension-related gene expression in human white blood cells and multilineage progenitor cells.
المؤلفون: Banach M; Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Lodz, Poland., Casares FM, Kream RM, Gluba A, Rysz J, Stefano GB
المصدر: Journal of human hypertension [J Hum Hypertens] 2010 Nov; Vol. 24 (11), pp. 713-20. Date of Electronic Publication: 2010 Jul 08.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8811625 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5527 (Electronic) Linking ISSN: 09509240 NLM ISO Abbreviation: J Hum Hypertens Subsets: MEDLINE
أسماء مطبوعة: Publication: <2003->: London : Nature Publishing Group
Original Publication: Houndmills, Basingstoke, Hampshire, UK : Scientific & Medical, Macmillan Press, c1987-
مواضيع طبية MeSH: Cell Lineage*, Gene Expression Regulation/*drug effects , Hypertension/*genetics , Leukocytes/*drug effects , Morphine/*pharmacology , Stem Cells/*drug effects, Cells, Cultured ; G-Protein-Coupled Receptor Kinase 3/genetics ; Gene Expression Profiling/methods ; Humans ; Hypertension/blood ; Hypertension/physiopathology ; Hypertension/prevention & control ; Intracellular Signaling Peptides and Proteins ; Leukocytes/metabolism ; Minor Histocompatibility Antigens ; Nitric Oxide/metabolism ; Oligonucleotide Array Sequence Analysis ; Opioid Peptides/metabolism ; Protein Serine-Threonine Kinases/genetics ; RNA, Messenger/blood ; Receptors, Adrenergic, beta-3/genetics ; Stem Cells/metabolism ; Time Factors ; WNK Lysine-Deficient Protein Kinase 1
مستخلص: It has been shown that vascular endothelial cells functionally express a local circuit autocrine-paracrine regulatory pathway driven by endogenously expressed chemically authentic morphine, its cognate opiate alkaloid-selective mu3 and mu4 receptors, and constitutive nitric oxide (NO). Accordingly, the aim of the study was to examine morphine-mediated changes in hypertension-associated gene expression in two independent cell models: primary cultures of human white blood cells (WBCs) and human multilineage progenitor cells (MLPCs). In separate incubations, primary cultures of human WBC and MLPC were treated with morphine at a final concentration of 1  μM morphine for 2-4  h. After RNA extraction and reverse transcription, Human Genome Survey Arrays were used to construct and differentially analyze by strict statistical criteria transcriptional/gene expression profiles of WBC and undifferentiated human MLPC in three independent experiments. The Applied Biosystems Human Genome Survey Array contains 31,700 60-mer oligonucleotide probes representing a set of 27,868 individual human genes and >1000 control probes. After DNA microarray analyses, a variety of hypertension-associated genes from both cell types were observed to be significantly downregulated. The only genes expressed in both cell types were β-adrenergic receptor kinase 2 (ADRBK2) and coding protein kinase WNK1 (PRKWNK1); however, only PRKWNK1 showed downregulation of its expression after morphine exposure. Only two genes were observed to be significantly upregulated after morphine treatment: ADRBK2 in stem cells and β3-adrenergic receptor in WBC. Morphine administration to primary cultures of human WBC and MLPC altered the expression profile of 16 candidate hypertension-associated genes. The majority of relevant genes was observed to be downregulated, suggesting ongoing homeostatic regulation by endogenous morphine coupled to NO production and release. In sum, these data suggest a predominantly antihypertensive role for endogenous morphine/NO signaling events.
التعليقات: Comment in: J Hum Hypertens. 2010 Nov;24(11):711-2. (PMID: 20631741)
المشرفين على المادة: 0 (Intracellular Signaling Peptides and Proteins)
0 (Minor Histocompatibility Antigens)
0 (Opioid Peptides)
0 (RNA, Messenger)
0 (Receptors, Adrenergic, beta-3)
31C4KY9ESH (Nitric Oxide)
76I7G6D29C (Morphine)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
EC 2.7.11.1 (WNK Lysine-Deficient Protein Kinase 1)
EC 2.7.11.1 (WNK1 protein, human)
EC 2.7.11.15 (G-Protein-Coupled Receptor Kinase 3)
EC 2.7.11.15 (GRK3 protein, human)
تواريخ الأحداث: Date Created: 20100709 Date Completed: 20110209 Latest Revision: 20220330
رمز التحديث: 20240829
DOI: 10.1038/jhh.2010.69
PMID: 20613782
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5527
DOI:10.1038/jhh.2010.69