کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6271546 | 1614766 | 2015 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effects of angiotensin II on leptin and downstream leptin signaling in the carotid body during acute intermittent hypoxia
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کلمات کلیدی
PBSphosphorylated signal transducer and activator of transcription 3Angiotensin type-2 receptorSOCS3cAPTAT2RpSTAT3AT1ROb-RbSTAT3ACERASERK1/2 - ERK1 / 2Angiotensin II - آنژیوتانسین دوAngiotensin I converting enzyme - آنژیوتانسین من تبدیل آنزیمEDTA - اتیلن دی آمین تترا استیک اسید Ethylenediaminetetraacetic acid - اتیلینیدامین تتراستیک اسیدLos - اینAng II - دومsuppressor of cytokine signaling 3 - سرکوب سیگنالینگ سیتوکین 3Renin–angiotensin system - سیستم رنین-آنژیوتانسینlosartan - لوزارتانsignal transducer and activator of transcription 3 - مبدل سیگنال و فعال کننده رونویسی 3Phosphate-buffered saline - محلول نمک فسفات با خاصیت بافریintermittent hypoxia - هیپوکسی متناوبacute intermittent hypoxia - هیپوکسی متناوب حادcaptopril - کاپتوپریلextracellular-signal-regulated kinase 1/2 - کیناز 1/2 کنترل شده خارج سلولی سیگنالAT1 receptor - گیرنده AT1Angiotensin type-1 receptor - گیرنده آنژیوتانسین نوع-1Leptin receptors - گیرنده های لپتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Effects of angiotensin II on leptin and downstream leptin signaling in the carotid body during acute intermittent hypoxia Effects of angiotensin II on leptin and downstream leptin signaling in the carotid body during acute intermittent hypoxia](/preview/png/6271546.png)
چکیده انگلیسی
Angiotensin II (ANG II) is known to promote leptin production and secretion. Although ANG II type 1 receptors (AT1Rs) and leptin are expressed within the carotid body, it is not known whether AT1R and leptin are co-expressed in the same glomus cells nor if these peptides are affected within the carotid body by intermittent hypoxia (IH). This study was done to investigate whether ANG II modulated leptin signaling in the carotid body during IH. Rats were treated with captopril (Capt) or the AT1R blocker losartan (Los) in the drinking water for 3Â days prior to being exposed to IH (8h) or normoxia (8h). IH induced increases in plasma ANG II and leptin compared to normoxic controls. Capt treatment abolished the plasma leptin changes to IH, whereas Los treatment had no effect on the IH induced increase in plasma leptin. Additionally, carotid body glomus cells containing both leptin and the long form of the leptin receptor (OB-Rb) were found to co-express AT1R protein, and IH increased the expression of only AT1R protein within the carotid body in both Capt- and non-Capt-treated animals. On the other hand, Los treatment did not modify AT1R protein expression to IH. Additionally, Capt and Los treatment eliminated the elevated carotid body leptin protein expression, and the changes in phosphorylated signal transducer and activator of transcription three protein, the short form of the leptin receptor (OB-R100), suppressor of cytokine signaling 3, and phosphorylated extracellular-signal-regulated kinase 1/2 protein expression induced by IH. However, Capt elevated the expression of OB-Rb protein, whereas Los abolished the changes in OB-Rb protein to IH. These findings, taken together with the previous observation that ANG II modifies carotid body chemosensitivity, suggest that the increased circulating levels of ANG II and leptin induced by IH act at the carotid body to alter leptin signaling within the carotid body which in turn may influence chemoreceptor function.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 310, 3 December 2015, Pages 430-441
Journal: Neuroscience - Volume 310, 3 December 2015, Pages 430-441
نویسندگان
J.M. Moreau, S.A. Messenger, J. Ciriello,