Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

Xu, Wei; Hu, Xiao; Xi, Qi; Zhu, Rui; Li, Chen; Zhu, Yanjing; Yin, Shuai; Cheng, Liming; Zhu, Rongrong

doi:10.1159/000496164

Cited by 16 publications

(9 citation statements)

References 37 publications

(34 reference statements)

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“…HO-1 deletion in myeloid cells promotes the polarization of proinflammatory M1 macrophages both in vivo and ex vivo, while transgenic overexpression of HO-1 favors an M2 anti-inflammatory phenotype [57], revealing a regulatory role of HO-1 in macrophage inflammation and atherogenesis. Additionally, activation of PPARγ has been shown to reduce proinflammatory cytokine secretion by upregulating HO-1 expression in multiple cell types [58,59]. The present study demonstrated that knockdown of PPARγ, LXRα, and HO-1 with siRNAs abolished the inhibitory effect of BCA on TNF-α, IL-1β, and IL-6 secretion from THP-1 macrophage-derived foam cells.…”

Section: Discussionsupporting

confidence: 56%

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response

Chen

Deng

et al. 2020

Oxidative Medicine and Cellular Longevity

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Biochanin A (BCA), a dietary isoflavone extracted from red clover and cabbage, has been shown to antagonize hypertension and myocardial ischemia/reperfusion injury. However, very little is known about its role in atherogenesis. The aim of this study was to observe the effects of BCA on atherosclerosis and explore the underlying mechanisms. Our results showed that administration of BCA promoted reverse cholesterol transport (RCT), improved plasma lipid profile, and decreased serum proinflammatory cytokine levels and atherosclerotic lesion area in apoE-/- mice fed a Western diet. In THP-1 macrophage-derived foam cells, treatment with BCA upregulated ATP-binding cassette (ABC) transporter A1 (ABCA1) and ABCG1 expression and facilitated subsequent cholesterol efflux and diminished intracellular cholesterol contents by activating the peroxisome proliferator-activated receptor γ (PPARγ)/liver X receptor α (LXRα) and PPARγ/heme oxygenase 1 (HO-1) pathways. BCA also activated these two signaling pathways to inhibit the secretion of proinflammatory cytokines. Taken together, these findings suggest that BCA is protective against atherosclerosis by inhibiting lipid accumulation and inflammatory response through the PPARγ/LXRα and PPARγ/HO-1 pathways. BCA may be an attractive drug for the prevention and treatment of atherosclerotic cardiovascular disease.

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Section: Discussionsupporting

confidence: 56%

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response

Chen

Deng

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Wei Xu et al studied the effect of vitamin D on endothelial progenitor cells (EPCs) pretreated with AngII. Their study demonstrated that vitamin D reversed AngII-induced oxidative stress injury by the peroxisome proliferator-activated receptor-γ (PPAR-γ) pathway [108]. PPAR-γ lowers the production of superoxide and enhances the repair capacity of EPCs [109].…”

Section: Role Of Vitamin D In the Endothelial Cell Activationmentioning

confidence: 99%

Emerging Role of Vitamin D and its Associated Molecules in Pathways Related to Pathogenesis of Thrombosis

2019

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Vitamin D, besides having an essential role in calcium and bone metabolism, also acts as a mediator of many non-calcemic effects through modulations of several biological responses. Vitamin D exists in its two major forms, vitamin D 2 , or commonly known as ergocalciferol, and vitamin D 3 , or commonly known as cholecalciferol. Both of these forms bind to vitamin D-binding protein to get transported to all vital target organs, where it serves as a natural ligand to vitamin D receptors for enabling their biological actions. Clinical reports corroborating vitamin D deficiency with an increase in thrombotic episodes implicate the role of vitamin D and its associated molecule in the regulation of thrombosis-related pathways. Thrombosis is the formation and propagation of a blood clot, known as thrombus. It can occur either in the arterial or the venous system resulting in many severe complications, including myocardial infarction, stroke, ischemia, and venous thromboembolism. Vitamin D, directly or indirectly, controls the expression of several genes responsible for the regulation of cellular proliferation, differentiation, apoptosis, and angiogenesis. All of these are the processes of potential relevance to thrombotic disorders. This review, thus, discussed the effects of vitamin D on pathways involved in thrombosis, such as hemostatic process, inflammatory pathway, and endothelial cell activation, with a focus on the molecular mechanisms associated with them.

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“…[1] The partial agonist of PPAR-γ has been extensively studied in some angiotensin type 1 receptor (ATR1) blockers. [3][4][5] Studies have shown that Telmisartan induces PPAR-γ activity despite ATR1 being absent, making it more evident that its stimulation occurs despite ATR1 blockade. Studies are showing the evidence of the relationship between some angiotensin receptor blockers (ARBs) with PPAR-γ by their binding to the PPAR-γ receptor.…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effects of azilsartan compared with that of telmisartan on an in vivo model of myocardial ischemia‐reperfusion injury

Garg

Khan

Malhotra

et al. 2021

J Biochem & Molecular Tox

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Azilsartan is found to be more potent than other angiotensin receptor blockers in reducing blood pressure. However, its effect on the heart following myocardial infarction remains to be established. For the first time, we investigated the peroxisome proliferator-activated receptor-γ (PPAR-γ) agonistic and cardioprotective properties of azilsartan. Computational modeling studies of interactions between azilsartan and PPAR-γ revealed azilsartan as an agonist of PPAR-γ and showed the mechanism of azilsartan in cardioprotection. Our study compared the cardioprotective potential of telmisartan to that of azilsartan in a murine model of myocardial ischemia-reperfusion injury by comparing their antioxidant, ant apoptotic, antiinflammatory, mitogen-activated protein kinase (MAPK)-modulating ability, and PPAR-γ agonistic activity. Male Wistar rats were grouped into four to receive vehicle (dimethyl sulfoxide [0.05%] 2 ml/kg) telmisartan (10 mg/kg p.o.), azilsartan (10 mg/kg p.o.) or azilsartan with specific PPAR-γ blocker, GW 9662 for 28 days.Ischemia was induced for 45 min on the 29th day followed by 60 min of reperfusion.Telmisartan and azilsartan pretreatment significantly nearly normalized cardiac parameters and preserved structural changes. Both drugs inhibited oxidative burst, inflammation, as well as cell death by modulating apoptotic protein expression along with reduction in 4′,6-diamidino-2-phenylindole/terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. An increment in pro-survival kinase ERK paralleled with a reduction in p38 and JNK was also revealed by MAPK pathway studies, after administration of these drugs. Interestingly, the aforementioned changes induced by both drugs were reversed by administration of the specific PPAR-γ antagonist, GW9662. However, we found that azilsartan upregulated PPAR-γ to a lesser extent as compared to telmisartan and the latter may be preferred in hypertensive patients at risk of myocardial infarction.

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Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

Cited by 16 publications

References 37 publications

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response

Emerging Role of Vitamin D and its Associated Molecules in Pathways Related to Pathogenesis of Thrombosis

Cardioprotective effects of azilsartan compared with that of telmisartan on an in vivo model of myocardial ischemia‐reperfusion injury

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