The total study group consisted of 105 menopausal women: 75 AI patients [27 with nonfunctional AI (NAI) and 48 with (possible) autonomous cortisol secretion ((P)ACS)] and 30 age-, BMI-, LH- and menopause duration-matched healthy control (HC) women.
In left ventricular biopsies from patients with aortic valve stenosis (AS) and aortic valve regurgitation and from control subjects, we quantitated mRNAs for angiotensin-converting enzyme (ACE), chymase, transforming growth factor-beta1 (TGF-beta1), collagen I, collagen III and fibronectin by reverse-transcription polymerase chain reaction.
We characterized expression of (P)RR, ACE2 and Mas receptor as well as renin, prorenin and angiotensin II type 2 (AT(2)) receptors in human aortic valves, and compared normal control valves (n = 11) with valves obtained from patients with aortic regurgitation (AR, n = 14), AR with fibrosis (n = 20) and AS (n = 61).
Cardiopulmonary function and structure, remodeling and apoptosis, as well as G protein‑coupled receptor (GPCR) and β2‑AR signaling, were documented over a period of 6 weeks.
Finally beta-AR signalling is strongly regulated by members of the G-protein-coupled receptor kinase family (GRKs), the best known of which is beta-adrenergic receptor kinase 1 (beta-ARK1). beta-ARK1 mRNA, protein level and enzymatic activity is increased in heart disease, further contributing to an attenuation in beta-AR signalling.
The total study group consisted of 105 menopausal women: 75 AI patients [27 with nonfunctional AI (NAI) and 48 with (possible) autonomous cortisol secretion ((P)ACS)] and 30 age-, BMI-, LH- and menopause duration-matched healthy control (HC) women.
Studies with caffeine and <sup>6</sup>N-cyclohexyladenosine, a non-selective antagonist and a selective agonist of adenosine A1 receptor (A1AR) respectively, indicated the involvement of adenosine receptor (AR) signaling.
Cardiopulmonary function and structure, remodeling and apoptosis, as well as G protein‑coupled receptor (GPCR) and β2‑AR signaling, were documented over a period of 6 weeks.
Finally beta-AR signalling is strongly regulated by members of the G-protein-coupled receptor kinase family (GRKs), the best known of which is beta-adrenergic receptor kinase 1 (beta-ARK1). beta-ARK1 mRNA, protein level and enzymatic activity is increased in heart disease, further contributing to an attenuation in beta-AR signalling.
Finally beta-AR signalling is strongly regulated by members of the G-protein-coupled receptor kinase family (GRKs), the best known of which is beta-adrenergic receptor kinase 1 (beta-ARK1). beta-ARK1 mRNA, protein level and enzymatic activity is increased in heart disease, further contributing to an attenuation in beta-AR signalling.
Cardiopulmonary function and structure, remodeling and apoptosis, as well as G protein‑coupled receptor (GPCR) and β2‑AR signaling, were documented over a period of 6 weeks.
β2-adrenergic receptor (AR) signaling modulates Cx43 expression in myocytes via components downstream of protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac).
We found that repression of β2-AR but not β1-AR signaling selectively suppressed cell viability, induced G1-phase cell cycle arrest, caused both intrinsic and extrinsic pathways-mediated apoptosis of specific CRC cells and inhibited CRC-xenograft growth in vivo.
NCI-H292 epithelial cell line was used to determine the contribution of β2-AR signaling to CSE-induced MUC5AC production by treatment with β2-AR antagonists propranolol and ICI118551 and β2-AR-targeted small interfering RNA.
Catecholamine triggered beta2-adrenergic receptor (β2-AR) signaling is important in creating a bidirectional response in the progression of ADs due to factors including diverse expression patterns, single nucleotide polymorphisms (SNPs), biased signals, and desensitization of β2-AR, as well as different subtypes of Gα binding to β2-AR.
Argonaute 2 (AGO2) co-immunoprecipitation, reporter assays and western blot analysis demonstrate that the microRNAs directly target several components of the mitogen-activated protein kinase (MAPK) and androgen receptor (AR) signaling pathways, among those several AR coregulators and HRAS (Harvey rat sarcoma viral oncogene homolog), and repress signaling activity.
We characterized expression of (P)RR, ACE2 and Mas receptor as well as renin, prorenin and angiotensin II type 2 (AT(2)) receptors in human aortic valves, and compared normal control valves (n = 11) with valves obtained from patients with aortic regurgitation (AR, n = 14), AR with fibrosis (n = 20) and AS (n = 61).
The aim of the study was to evaluate the development of cardiac hypertrophy (CH) in response to left ventricle (LV) volume overload (VO) caused by chronic aortic valve regurgitation (AR) in male and female rats treated or not with angiotensin II receptor blocker (ARB), valsartan.
Here we investigate the effect of simultaneous inhibition of the aryl hydrocarbon receptor (AhR) and Src on androgen receptor (AR) signaling in prostate cancer cells.
Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE<sub>2</sub> - and 4-OHE<sub>2</sub> -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E<sub>2</sub> β and other β-AR signalling hormones (i.e. catecholamines).
Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE<sub>2</sub> - and 4-OHE<sub>2</sub> -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E<sub>2</sub> β and other β-AR signalling hormones (i.e. catecholamines).
In this study, we investigated a potential interaction between androgen receptor (AR) signaling and FBI-1 and demonstrated that overexpression of FBI-1 inhibited ligand-dependent AR activation.
In addition, AKR1C3 activation increases intracrine androgen synthesis and enhances androgen receptor (AR) signaling via activating AR transcriptional activity.
Zanthoxyli Fructus induces growth arrest and apoptosis of LNCaP human prostate cancer cells in vitro and in vivo in association with blockade of the AKT and AR signal pathways.