17β-estradiol suppresses H2O2-induced senescence in human umbilical vein endothelial cells by inducing autophagy through the PVT1/miR-31/SIRT3 axis

The Impact of Long Noncoding RNAs in Tissue Regeneration and Senescence

“…The 17β-estradiol hormone could inhibit H 2 O 2 -induced senescence in human umbilical vein endothelial cells (HUVECs). It functioned by increasing the levels of plasmacytoma variant translocation 1 (PVT1), an anti-senescence lncRNA that could be upregulated through 17β-estradiol [73]. Decreased levels of ENSMUST00000218874 lncRNA were found in the aortas and vascular smooth muscle cells of aged mice, which could show an anti-senescence role for this lncRNA, which was confirmed through its knockdown in cells [74].…”

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 ].…”

The Current State of Research on Sirtuin-Mediated Autophagy in Cardiovascular Diseases

“…In individuals with diabetes, SIRT3 upregulates mitochondrial autophagy in the heart solely by inhibiting macrophage stimulating 1 (Mst1), and inhibiting SIRT3 expression impairs mitochondrial autophagy in myocardial cells, thereby exacerbating type 1 DCM [ 60 ]. In human umbilical vein endothelial cells (HUVECs), the upregulation of lncRNA PVT1 expression by 17beta-estradiol inhibits miR-31, activates the SIRT3 promoter, and upregulates SIRT3 expression, thereby promoting autophagy and inhibiting H 2 O 2 -induced HUVEC aging [ 61 , 62 ]. In addition, the regulation of autophagy involves the dynamic communication between the Beclin1-TLR9-SIRT3 complex [ 63 ].…”