GDF11 activated both smad1/5/8 and smad2/3 signals in HUVECs but showed no significant effect on endothelial cell proliferation and migration.
Does GDF11 improve proliferation and migration in human umbilical vein endothelial cells and primary rat aortic endothelial cells?
GDF11 activates smad signaling but does not significantly affect endothelial cell proliferation or migration, challenging its proposed role as a vascular rejuvenation factor.
// Yong-Hui Zhang 1 , Feng Cheng 1 , Xue-Ting Du 1 , Jin-Lai Gao 1 , Xiao-Lin Xiao 1 , Na Li 1 , Shan-Liang Li 1 and De-Li Dong 1 1 Department of Pharmacology (The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), Translational Medicine Research and Cooperation Center of Northern China, Heilongjiang Academy of Medical Sciences, Harbin Medical University, Harbin, P.R.China Correspondence to: De-Li Dong, email: // Keywords : bone morphogenetic protein 11, growth differentiation factor 11, smad2/3, smad1/5/8, endothelial cells, Pathology Section Received : November 07, 2015 Accepted : February 09, 2016 Published : February 23, 2016 Abstract GDF11/BMP11, a member of TGF-β superfamily, was reported to rejuvenate heart, skeletal muscle and blood vessel architecture in aged mice. However, the rejuvenative effects of GDF11 were questioned recently. Here, we investigated the effects of GDF11 on smad and non-smad signals in human umbilical vein endothelial cells (HUVECs) and the effects of GDF11 on proliferation and migration of HUVECs and primary rat aortic endothelial cells (RAECs). GDF11 factor purchased from two different companies (PeproTech and R&D Systems) was comparatively studied. Western blot was used to detect the protein expressions. The cell viability and migration were examined by using MTT and wound healing assays. Results showed that GDF11 activated both smad1/5/8 and smad2/3 signals in HUVECs. GDF11 increased protein expression of NADPH oxidase 4(NOX4) in HUVECs. GDF11 showed no significant effect on the protein level of p38, p-p38, ERK, p-ERK, Akt, p-Akt (Ser473) and p-Akt(Thr308), but increased the protein level of p-JNK and p-AMPK in HUVECs, and these increases were inhibited by antioxidant mitoTEMPO treatment. GDF11 slightly increased cell viability after short-term treatment and slightly decreased cell viability after long-term treatment. GDF11 showed no significant effect on cell proliferation and migration. These data indicated that the notion of GDF11 as a rejuvenation-related factor for endothelial cells needs to be cautious.
Zhang et al. (Tue,) conducted a other in Endothelial cell function. GDF11/BMP11 was evaluated on Proliferation and migration of HUVECs and RAECs, and smad signaling activation. GDF11 activated both smad1/5/8 and smad2/3 signals in HUVECs but showed no significant effect on endothelial cell proliferation and migration.
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