The kinin B(1)R may contribute to keratinocyte differentiation and migration by triggering specific tyrosine signalling pathways or by interacting with the ErbB receptor family.
Kinins are key pro-inflammatory peptides that exhibit mitogenic effects in tissue-specific cellular systems. Since the life span of the keratinocyte is regulated by receptors that control proliferation and differentiation, and since both processes are affected during wound healing, we have examined the consequence of kinin B2 receptors (B2R) activation in cultured human keratinocytes. Stimulation of keratinocytes by Lys-bradykinin (LBK) induced a rapid and sustained phosphorylation of 42/44 mitogen-activated protein kinase (MAPK) that translocated to the nucleus, and decreased only after 120 min of stimulation. Kinin B1 and B2 receptor (B1R and B2R) antagonists showed that phosphorylation was mainly because of B2R activation. The GF109203X inhibitor almost completely abolished the effect of LBK, suggesting the involvement of protein kinase C in the signal cascade. MAPK phosphorylation was partially dependent on epidermal growth factor receptor transactivation as assessed by the selective inhibitor, AG1478. LBK stimulation did not result in cell proliferation, but produced a rapid c-Fos expression, nuclear translocation of nuclear factor-kappaB, and a moderated (pro)filaggrin synthesis, indicating that it may modulate cell differentiation. Our results support the view that kinins may affect the life span of human keratinocytes and highlight the importance that kinin peptides may have in the pathogenesis and/or progression of skin diseases.
Background Epicardial adipose tissue (EPI) and pericardial adipose tissue (PERI) measured using echocardiography or magnetic resonance imaging have shown to be markers of metabolic syndrome and begin to be regarded as predictors of coronary artery disease. EPI is also thought to have paracrine effects on coronary vessels and, therefore, might be more intimately linked to ischemic heart disease. Purpose We aim to study if EPI related to PERI thickness is a predictor of ischemic etiology of left ventricular (LV) systolic dysfunction among ambulatory patients. Methods We retrospectively evaluated 56 consecutive patients followed on a heart failure clinic. A cardiologist, blind to the clinical records and systolic dysfunction etiology, reviewed the echocardiographic images and measured EPI and PERI thickness on right ventricle free wall (parasternal long axis view). Cardiovascular risk factors, body mass inex (BMI), LV dimensions by echo, LV systolic dysfunction etiology (investigated by other means such as angiography or magnetic resonance) were analyzed. Results Echocardiographic image quality allowed for analyzing 55 patients (80% male, 62% hypertension, 51% diabetes, 44% dyslipidemia, BMI 28,9 ± 4,0, age 66 ± 14 years). Mean EPI thickness was 3,4 ± 2,0 mm and PERI was 5,6 ± 3,4 mm. LV ejection fraction 33 ± 10% and LV end diastolic volume 157 ± 48ml. Supplementary investigations showed an ischemic etiology of LV systolic dysfunction in 45% of patients. We found that patients with EPI thickness equal or greater than PERI were more likely to have an ischemic etiology (univariate analysis: OR 9,8 p = 0,002; adjusted for BMI and diabetes: OR 5,8 p = 0,032). Conclusions Epicardial adipose tissue thickness equal or greater than pericardial adipose tissue, parameter easily obtained using transthoracic echocardiography, may predict ischemic etiology of LV systolic dysfunction in a cohort of ambulatory patients . Future research will be necessary to confirm this finding and its possible value in every-day clinical practice as marker of coronary artery disease. ALL ISCHEMIC NON ISCHEMIC p Epicardial Adipose Tissue 3,4 ± 2,0 3,7 ± 1,6 3,1 ± 2,2 0,53 Pericardial Adipose Tissue 5,6 ± 3,4 4,6 ± 3,0 6,4 ± 3,5 0,09 Ratio EPI/PERI 0,82 ± 0,66 1,16 ± 0,83 0,55 ± 0,28 0,000 Table Adipose tissue thickness measured on paraesternal long axis (mm): mean ± SD.
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