Effects of androgens and estrogens on sirtuin 1 gene expression in human aortic endothelial cells

Abstract

1 ‫السورتوين‬ ‫تعبير‬ ‫على‬ ‫واالستروجني‬ ‫األندروجينات‬ ‫تأثير‬ ‫دراسة‬ ‫األهداف:‬ .)HAECs(‫البشرية‬ ‫األبهرية‬ ‫البطانية‬ ‫اخلاليا‬ ‫في‬)SIRT1(‫مدار‬ ‫على‬ SIRT-1 ‫لتعبير‬ ‫البلمرة‬ ‫سلسلة‬ ‫تفاعل‬ ‫حتليل‬ ‫أجري‬ ‫املنهجية:‬ ،)DHEA(‫من‬ ‫مختلفة‬ ‫بتركيزات‬ ‫املعاجلة‬ HAECs ‫في‬)h(‫ساعة‬ 48 ‫االستروجني)‬ ‫(هرمون‬)E3(‫و‬)E2(،)E1(‫واالستروجني‬ ‫واألندروجني‬ ‫املرتفع‬ ‫اجللوكوز‬ ‫تأثير‬ ‫كذلك‬ ‫فحصنا‬ ‫الزمنية.‬ ‫الدورات‬ ‫اجلرعة-تبعية‬ ‫لدراسة‬ ‫واإلستروجني.‬ ‫األندروجينات‬ ‫عن‬ ‫الناجم‬ SIRT1 ‫تعبير‬ ‫على‬ ‫وهرمون‬ ‫واالستروجني،‬ ‫واألندروجني‬ ،)DHEA(‫أنتجت‬ ‫النتائج:‬ SIRT1 ‫تعبير‬ ‫في‬ ‫اجلرعة‬ ‫على‬ ‫تعتمد‬ ‫وبزيادة‬ ‫ملحوظ‬ ‫بشكل‬ ‫التستوستيرون‬ ‫ملم)‬ 40(‫املرتفع‬ ‫للجلوكوز‬ ‫كان‬ ‫02ميكروغرام/مل.‬ ‫إلى‬ 10 ‫نطاق‬ ‫في‬ ‫01ميكروغرام/‬ ‫عن‬ ‫الناجت‬ SIRT1 ‫تعبير‬ ‫على‬ ‫ملحوظ‬ ‫بشكل‬ ‫مثبطة‬ ‫تأثيرات‬ ‫زيادة‬ ‫في‬ ،E3 ‫ليس‬ ‫ولكن‬ ، E2 ‫و‬ ‫االستروجني‬ ‫تسبب‬ .)p=0.024(‫مل‬ ‫ميكروغرام/‬ 20 ‫إلى‬ 10 ‫من‬ SIRT1 ‫تعبير‬ ‫في‬ ‫اجلرعة‬ ‫على‬ ‫تعتمد‬ ‫ملحوظة‬ ‫تعبير‬ ‫كبير‬ ‫بشكل‬ ‫مينع‬ ‫لم‬ ‫اجللوكوز‬ ‫من‬ ‫ملم‬ 40 ‫أو‬ ‫ملم‬ 20 ‫مع‬ ‫العالج‬ ‫مل.‬ ‫كال‬ ‫أكد‬ ‫ذلك،‬ ‫ومع‬ ‫التحكم؛‬ ‫وسيط‬ ‫في‬ E3 ‫و‬ E1 ‫عن‬ ‫الناجم‬ SIRT1 E2 ‫عن‬ ‫الناجم‬ SIRT1 ‫تعبير‬ ‫على‬ ‫كبير‬ ‫بشكل‬ ‫للجلوكوز‬ ‫املرتفعني‬ ‫الوسطني‬ ‫التوالي.‬ ‫على‬ ،)p=0.007، p=0.005(‫التحكم‬ ‫وسط‬ ‫في‬ E1 ‫و‬ ‫واالستروجني‬ ‫األندروجني‬ ‫و‬ DHEA ‫أن‬ ‫إلى‬ ‫النتائج‬ ‫هذه‬ ‫تشير‬ ‫اخلالصة:‬ ‫اجللوكوز‬ ‫متوسط‬ ‫إن‬ .HAECs ‫في‬ SIRT1 ‫تعبير‬ ‫بالتأكيد‬ ‫ينشطون‬ E2 ‫و‬ ‫احلد‬ ‫ميكن‬ ‫ال‬ ‫فإنه‬ ، ‫ذلك‬ ‫ومع‬ ‫؛‬ ‫األساسي‬ ‫اجليني‬ ‫التعبير‬ ‫لتثبيط‬ ‫فعال‬ ‫املرتفع‬ .HAECs ‫في‬ ‫قوية‬ ‫واالستروجني‬ ‫األندروجني‬ ‫عن‬ ‫الناجم‬ SIRT1 ‫التعبير‬ ‫من‬ Objectives: To investigate the effect of androgens and estrogens on surtuin 1 (SIRT1) expression in human aortic endothelial cells (HAECs). Methods: Real-time polymerase chain reaction analysis of SIRT-1 expression over 48 hours (h) was performed in HAECs treated with various concentrations of dehydroepiandrostendione (DHEA), androstenedione and testosterone (androgens), estrone (E1), estradiol (E2), and estriol (E3) (estrogens) to investigate the dose-dependency of time courses. The influence of high glucose on SIRT1 expression induced by the androgens and estrogens was also examined. Results: Dehydroepiandrostendione, androstenedione, and testosterone remarkably Original Article produced a dose-dependent increase in SIRT1 expression in the range of 10 to 20 µg/ml. High glucose (40mM) medium had significantly inhibitory effects on 10 µg/ml DHEA-induced SIRT1 expression (p=0.024). Estrone and E2, but not E3, caused a marked dose-dependent increase in SIRT1 expression from 10 to 20 µg/ml. Treatment with 20 mM or 40 mM glucose medium did not significantly inhibit E1and E3-induced SIRT1 expression in control medium; however, both high glucose mediums significantly emphasized E2-induced SIRT1 expression in control medium (p=0.007, p=0.005). Conclusion: These results suggest that DHEA, androstenedione, testosterone, E1, and E2 definitely activate SIRT1 expression in HAECs. A high glucose medium is potent to inhibit the basa...

Evaluation of potential aging biomarkers in healthy individuals: telomerase, AGEs, GDF11/15, sirtuin 1, NAD+, NLRP3, DNA/RNA damage, and klotho

“…Thus, sirtuin 1 levels seem to be more affected in women, most likely by sex hormones and their fluctuations. Tsuchyia et al demonstrated that DHEA, androstenedione, testosterone, estrone, and estradiol induce the expression of sirtuin 1 (Tsuchiya et al 2020 ).…”

Sexual Dimorphism in Cardiometabolic Diseases: The Role of AMPK

“…This, in turn, increases the activity of LKB1 [38]. It was shown that E1 and E2, but not E3, increase expression of Sirt1 via active ERs cellular translocation and binding to ERE located in the Sirt1 promotor region [104].…”

Estradiol as the Trigger of Sirtuin-1-Dependent Cell Signaling with a Potential Utility in Anti-Aging Therapies

“…The relationship between estradiol and SIRT1 expression has so far been identified in several types of cells, tissues, and organs. Estradiol has been shown to affect the expression of SIRT1 mRNA and/or proteins in the brain (both in experimental rodents [ 36 , 37 , 38 ] and in vitro in the SH-SY54 (neuroblastoma cell line)) [ 36 ]; heart (in experimental animals in vivo) [ 39 , 40 ]; skeletal muscles (in vivo in animal models and in the C2C12 myoblast cell line) [ 41 ]; aorta (in vivo in animal models) [ 42 ]; vascular smooth muscle (isolated from diabetic rats) [ 43 ]; vascular endothelium (in human umbilical vein endothelial cell (HUEVEC) and human aortic endothelial cell (HAEC) cell lines) [ 44 , 45 ]; in vitro, in systems using Hep3B (hepatoma cell line) and HEK293 (human embryonic kidney cell) cell lines [ 46 , 47 ], and in vivo, in mice liver [ 48 ]; lung cancer cells (A549 and H14350 (lung cancer cell lines)) [ 49 ]; cervical cancer cells (HeLa cell line) [ 50 ] and mammary gland cancer cells using different cell lines, like MCF-7, T47D, MDA-MB-231, and SkBr3 [ 51 , 52 ]; peripheral mononuclear blood cells isolated from [ 53 ] mouse bone marrow [ 54 ]; and chondrocytes (ATDC5 cell line) [ 55 ]. As can be seen, few tissues appear to exhibit any relationship between estradiol and SIRT1 expression and the quite short list of tissues tested to this date suggests that this field is in the initial phase of investigations.…”

“…Estradiol can increase the expression of the SIRT1 protein in many types of cells, including the brain in animal models and in vitro cultured cell lines [ 36 , 37 , 38 ], heart [ 39 , 40 ] and skeletal muscles cultured in vitro [ 41 ], aorta in vivo in an animal models [ 42 ], vascular smooth muscles isolated from animals and treated in vitro [ 43 ] and vascular endothelium in vitro [ 44 , 45 ], hepatocytes in vivo in animal models [ 48 ], lung cancer cells [ 49 ], cervical cancer cells (HeLa cell line) [ 50 ] and mammary gland cancer cells (different cell lines mentioned throughout the review) [ 51 , 52 ], bone marrow in mouse animal models [ 54 ], and chondrocytes (ATDC5 cell line) [ 55 ].…”