Downregulating osteopontin reduces angiotensin II-induced inflammatory activation in vascular smooth muscle cells

Yin, Bangqi; Hao, Haibo; Wang, Y. Y.; Jiang, Yafeng; Xue, Song

doi:10.1007/s00011-009-8034-0

Cited by 19 publications

(14 citation statements)

References 30 publications

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“…It meant that an OPN-dependent pathway was necessary in nicotine-induced inflammation. It accorded with our previous report in Ang II-mediated inflammation [16], and the study in PDA also obtained approximate results [13]. Therefore, our data, collectively, indicated that NFκB/OPN amplification loop existed in this pro-inflammatory process.…”

Section: Discussionsupporting

confidence: 92%

“…Both these studies suggest nicotine playing a synergetic role in Ang II-induced vascular disease. We reported that OPN played a central role in Ang IImediated inflammation in VSMC [16], and we found that nicotine induced OPN mRNA expression and protein release obviously in this study. Therefore, the role of OPN in nicotine-induced inflammatory response was evaluated.…”

Section: Discussionsupporting

confidence: 68%

“…The experiment was conducted according to the manner described previously [16]. Briefly, after various disposals, a Qiagen RNeasy minikit (Qiagen, Valencia, CA) was used to extract RNA, and then the reverse transcription real-time PCR was conducted.…”

Section: Rna Extraction and Reverse Transcription Real-timementioning

confidence: 99%

“…The method described previously was adopted [16]. Briefly, the targeted sequence resides within the open reading frame of the human OPN gene (accession no.…”

Section: Rna Extraction and Reverse Transcription Real-timementioning

confidence: 99%

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Nicotine Induces Pro-inflammatory Response in Aortic Vascular Smooth Muscle Cells Through a NFκB/Osteopontin Amplification Loop-Dependent Pathway

et al. 2011

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Nicotine has anti- and pro-inflammatory properties in various cells. Its role in aortic vascular smooth muscle cells (VSMC) was explored. Human aortic VSMC were cultured. After nicotine (1.0 μM) and/or pyrrolidinedithiocarbamic acid (PDTC, 50 μM) treatment, the activation of nuclear factor κB (NFκB) was investigated. The levels of pro-inflammatory cytokines, osteopontin (OPN), interleukin-6 (IL-6), and monocyte chemoattractant protein 1 (MCP-1) were also assessed. After OPN was downregulated by small interfering RNA (siRNA) transfection, the pro-inflammatory effect was reassessed. We found that NFκB was activated after nicotine administration. Nicotine upregulated OPN, IL-6, and MCP-1 expressions, and this effect attenuated after PDTC pretreatment. RNAi knocked down the OPN expression in nicotine-treated cells and abolished its pro-inflammatory effects. We concluded that nicotine induces a pro-inflammatory response in VSMC through a NFκB/osteopontin amplification loop-dependent pathway.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 68%

Section: Rna Extraction and Reverse Transcription Real-timementioning

confidence: 99%

“…The method described previously was adopted [16]. Briefly, the targeted sequence resides within the open reading frame of the human OPN gene (accession no.…”

Section: Rna Extraction and Reverse Transcription Real-timementioning

confidence: 99%

See 2 more Smart Citations

Nicotine Induces Pro-inflammatory Response in Aortic Vascular Smooth Muscle Cells Through a NFκB/Osteopontin Amplification Loop-Dependent Pathway

et al. 2011

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“…TNF ␣ and IL-1 ␤ both stimulate SMC FN expression [67] , and attachment to FN stimulates transient activation of NF-B [68] . Osteopontin deposition is enhanced in the atherosclerotic plaque, and osteopontin siRNA reduces Ang II-dependent secretion of IL-6 through an NF-B-and AP-1-dependent mechanism [69] . Matrix-specific cellular responses are thought to occur through the integrin family of matrix receptors.…”

Section: Matrix Composition In the Smc Inflammatory Phenotypementioning

confidence: 99%

Complex Regulation and Function of the Inflammatory Smooth Muscle Cell Phenotype in Atherosclerosis

et al. 2009

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Role of osteokines in atherosclerosis

Liu,

Tian,

Chen

et al. 2024

Cell Biochemistry & Function

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Despite their diverse physiologies and roles, the heart, skeletal muscles, and smooth muscles all derive from a common embryonic source as bones. Moreover, bone tissue, skeletal and smooth muscles, and the heart share conserved signaling pathways. The maintenance of skeletal health is precisely regulated by osteocytes, osteoblasts, and osteoclasts through coordinated secretion of bone‐derived factors known as osteokines. Increasing evidence suggests the involvement of osteokines in regulating atherosclerotic vascular disease. Therefore, this review aims to examine the evidence for the role of osteokines in atherosclerosis development and progression comprehensively. Specifically discussed are extensively studied osteokines in atherosclerosis such as osteocalcin, osteopontin, osteoprotegerin, and fibroblast growth factor 23. Additionally, we highlighted the effects of exercise on modulating these key regulators derived from bone tissue metabolism. We believe that gaining an enhanced understanding of how osteocalcin contributes to the process of atherosclerosis will enable us to develop targeted and comprehensive therapeutic strategies against diseases associated with its progression.

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Downregulating osteopontin reduces angiotensin II-induced inflammatory activation in vascular smooth muscle cells

Abstract: This result suggested that OPN plays an important role in Ang II-induced inflammatory activation in VSMCs. The finding further supports OPN as a potential target for atherosclerotic therapy.

Cited by 19 publications

References 30 publications

Nicotine Induces Pro-inflammatory Response in Aortic Vascular Smooth Muscle Cells Through a NFκB/Osteopontin Amplification Loop-Dependent Pathway

Nicotine Induces Pro-inflammatory Response in Aortic Vascular Smooth Muscle Cells Through a NFκB/Osteopontin Amplification Loop-Dependent Pathway

Complex Regulation and Function of the Inflammatory Smooth Muscle Cell Phenotype in Atherosclerosis

Role of osteokines in atherosclerosis

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