Angiotensin II promotes differentiation of mouse embryonic stem cells to smooth muscle cells through PI3-kinase signaling pathway and NF-κB

Zheng, Xiaodong; Wu, Yutao; Zhu, Liangfeng; Chen, Qishan; Zhou, Yunyun; Yan, Hui; Chen, Ting; Xiao, Qingzhong; Zhu, Jianhua; Zhang, Li

doi:10.1016/j.diff.2012.11.003

Cited by 25 publications

(18 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We also confirmed that phosphorylation level of Akt in the RVLM was upregulated in SHR compared with WKY rats. Recently, a recent study reported that upregulation of PI3K-Akt-NFkB signaling pathway in the RVLM from SHR involved in the pathogenesis of hypertension [44]. In this work, we demonstrated that central infusion of moxonidine in SHR significantly reduced expression of PI3K/Akt signaling in the RVLM.…”

Section: Discussionmentioning

confidence: 62%

Centrally acting drug moxonidine decreases reactive oxygen species via inactivation of the phosphoinositide-3 kinase signaling in the rostral ventrolateral medulla in hypertensive rats

Wang

Tan

et al. 2016

Journal of Hypertension

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 62%

Centrally acting drug moxonidine decreases reactive oxygen species via inactivation of the phosphoinositide-3 kinase signaling in the rostral ventrolateral medulla in hypertensive rats

Wang

Tan

et al. 2016

Journal of Hypertension

View full text Add to dashboard Cite

show abstract

“…48 On the other hand, Ang II is also reported to activate PI3K/Akt signaling via AT1R in various cells. 43,49 Thus, PI3K/Akt signaling is considered to be one of speculated pathways between Ang II and Runx2. Further study to investigate Ang II-induced PI3K/Akt signaling in chondrocytes is needed.…”

Section: Discussionmentioning

confidence: 99%

Continuous infusion of angiotensin II modulates hypertrophic differentiation and apoptosis of chondrocytes in cartilage formation in a fracture model mouse

et al. 2015

View full text Add to dashboard Cite

Although components of the renin-angiotensin system (RAS) are reported to be expressed in cultured chondrocytes and cartilage, little is known about the precise function of Angiotensin II (Ang II) in chondrocytes. In this study, we employed a rib fracture model mouse to investigate the effect of Ang II on chondrocytes. Ang II type 1 receptor (AT1R) was expressed in chondrocytes in the growth plate of mouse tibia. Continuous infusion of Ang II to rib-fractured mice resulted in a significant increase in the volume of cartilage, suggesting Ang II-induced hypertrophic differentiation of chondrocytes. It was also confirmed by a significant increase in the mRNA expression of Sox9 and runt-related transcription factor 2 (Runx2), which are genes related to chondrocyte differentiation, and type X collagen, matrix metalloproteinase (MMP)-13 and Indian hedgehog (Ihh), which are hypertrophic chondrocyte-specific molecular markers. Chondrocyte hypertrophy with upregulation of these genes was attenuated by administration of olmesartan, an AT1R blocker, but not by hydralazine. Moreover, Ang II infusion significantly suppressed apoptosis of chondrocytes, accompanied by significant induction of mRNA expression of bcl-2 and bcl-xL. Olmesartan, but not hydralazine, significantly attenuated the reduction of apoptotic cells and the increase in anti-apoptotic genes induced by Ang II infusion. Overall, the present study demonstrated that Ang II promoted hypertrophic differentiation of chondrocytes and reduced apoptosis of hypertrophic chondrocytes independently of high blood pressure. The present data indicate the role of Ang II in cartilage, and might provide a new concept for treatment of cartilage diseases.

show abstract

“…Its family includes extracellular signal-related kinases, c-Jun N-terminal kinases and p38 (32). A recent study demonstrated that high levels of glucose-protein kinase C pathways, glycation end products, oxidative stress, growth factor, osmotic pressure and stretches under diabetic conditions may activate MAPK families, increase the activity of transcription factors and lead to chronic diabetic complications (33). Blocking MAPK trans-pass may be an effective novel direction for the treatment of chronic diabetic complications (33).…”

Section: Discussionmentioning

confidence: 99%

“…A recent study demonstrated that high levels of glucose-protein kinase C pathways, glycation end products, oxidative stress, growth factor, osmotic pressure and stretches under diabetic conditions may activate MAPK families, increase the activity of transcription factors and lead to chronic diabetic complications (33). Blocking MAPK trans-pass may be an effective novel direction for the treatment of chronic diabetic complications (33). The present study illustrated that resveratrol administration is able to significantly suppress the expression of p-p38 in rats with STZ-DRMI.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of resveratrol improve cardiovascular function in rats with diabetes

Yan

Sun

2017

Exp Ther Med

View full text Add to dashboard Cite

Abstract.Resveratrol is a flavonoid with a stilbene structure that is able to suppress acute pulmonary thromboembolism-induced pulmonary artery hypertension. Furthermore, it possesses anti-cancer and antioxidant properties, is able to regulate blood lipids and increase life expectancy. In the present study, it was evaluated whether the protective effect of resveratrol was able to improve cardiovascular function in rats with diabetes. The effects of resveratrol on blood glucose, body weight, heart/body weight ratio, plasma triglyceride levels, heart rate, aspartate transaminase (AST)/alanine transaminase (ALT) ratio and total plasma insulin were evaluated. Levels of inflammation and oxidative stress were also evaluated using ELISA kits, and the expressions of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and phosphorylated (p)-p38 protein were evaluated via western blot analysis. The results demonstrated that administration of resveratrol in rats with diabetes-related myocardial infarction (DRMI) significantly reduced blood glucose, body weight, plasma triglyceride levels, heart rate and AST/ALT ratio (all P<0.01) and significantly increased total plasma insulin (P<0.01). Furthermore, resveratrol significantly reduced levels of inflammation factors (P<0.01) and malondialdehyde, a marker for oxidative stress, in rats with DRMI (P<0.01). Resveratrol significantly increased the expression of eNOS (P<0.01) and suppressed the expression of VEGF and p-p38 (both P<0.01) in rats with DRMI. These results suggest that treatment with resveratrol is able to improve cardiovascular function via inhibition of eNOS and VEGF, and suppression of p38 phosphorylation in rats with DRMI.

show abstract

Angiotensin II promotes differentiation of mouse embryonic stem cells to smooth muscle cells through PI3-kinase signaling pathway and NF-κB

Cited by 25 publications

References 66 publications

Centrally acting drug moxonidine decreases reactive oxygen species via inactivation of the phosphoinositide-3 kinase signaling in the rostral ventrolateral medulla in hypertensive rats

Centrally acting drug moxonidine decreases reactive oxygen species via inactivation of the phosphoinositide-3 kinase signaling in the rostral ventrolateral medulla in hypertensive rats

Continuous infusion of angiotensin II modulates hypertrophic differentiation and apoptosis of chondrocytes in cartilage formation in a fracture model mouse

Protective effects of resveratrol improve cardiovascular function in rats with diabetes

Contact Info

Product

Resources

About