Involvement of profilin-1 in angiotensin II-induced vascular smooth muscle cell proliferation

Cheng, Jinfang; Ni, Guohua; Chen, Mei‐Fang; Li, Yuan‐Jian; Wang, Yongjin; Wang, Changlu; Yuan, Qiong; Shi, Ruizheng; Hu, Chang-Ping; Yang, Tianlun

doi:10.1016/j.vph.2011.04.003

Cited by 28 publications

(26 citation statements)

References 28 publications

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“…This pathway can be reversed by F-actin inhibitor, cytochalasin D or profilin-I mutant, 88R/L. Consistent with our finding, very recent studies showed increased profilin-I expression in hypertrophic thoracic aorta and mesenteric arteries of spontaneously hypertensive rats with subsequent elevation in both P-ERK and P-JNK, suggesting that profilin-I may contribute to the vascular remodeling in these rats (Cheng et al, 2011;Zhong et al, 2011). In this context, previous studies suggested that mechanical stretch is closely related to JNK and ERK1/2 activation (Hu et al, 1997;Pyles et al, 1997).…”

Section: Role Of Profilin In Vascular Remodeling and Hypertensionsupporting

confidence: 92%

“…The same study indicated that profilin-induced VSMCs migration is dependent on PI3K activity (Caglayan et al, 2010). Moreover, Cheng et al, (2011) found that profilin-I plays a key role in Angiotensin (Ang) II-induced VSMCs proliferation. They also suggested that Ang-II increases profilin-I expression and promotes VSMCs proliferation via activating AT1 receptor/JAK2/STAT3 pathway (Cheng et al, 2011).…”

Section: Fig 7 Inner Lining Of Normal Arterymentioning

confidence: 92%

“…On the contrary, other studies described the involvement of phospho-extracellular signal-regulated kinase1/2 (P-ERK1/2) and phospho-c-Jun NH2-terminal kinase (P-JNK) in Ang-II-induced profilin-I expression (Zhong et al, 2011), and that PI3-kinase, Src, and, to a lesser extent, P-ERK1/2 are required for profilin-I-dependent VSMCs proliferation (Caglayan et al, 2010). Consequently, Cheng et al, (2011) proposed that the interaction of these signaling pathways mediating the role of profilin-I in VSMCs proliferation requires further investigation. Consistent with these data, we observed that the treatment of mouse aortic VSMCs with Ang-II (100 nM/10 min) resulted in increased profilin-I expression (Hassanain HH, unpublished)…”

Section: Fig 7 Inner Lining Of Normal Arterymentioning

confidence: 97%

“…Moreover, Cheng et al, (2011) found that profilin-I plays a key role in Angiotensin (Ang) II-induced VSMCs proliferation. They also suggested that Ang-II increases profilin-I expression and promotes VSMCs proliferation via activating AT1 receptor/JAK2/STAT3 pathway (Cheng et al, 2011). On the contrary, other studies described the involvement of phospho-extracellular signal-regulated kinase1/2 (P-ERK1/2) and phospho-c-Jun NH2-terminal kinase (P-JNK) in Ang-II-induced profilin-I expression (Zhong et al, 2011), and that PI3-kinase, Src, and, to a lesser extent, P-ERK1/2 are required for profilin-I-dependent VSMCs proliferation (Caglayan et al, 2010).…”

Section: Fig 7 Inner Lining Of Normal Arterymentioning

confidence: 99%

“…Mehta & Griendling, 2007). Interestingly, it has been recently reported that profilin-I is a key component in the Ang-II-induced vascular remodeling (Cheng et al, 2011;Zhong et al, 2011).…”

Section: Role Of Profilin In Vascular Remodeling and Hypertensionmentioning

confidence: 99%

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Profilin, and Vascular Diseases

Elnakish¹,

Hassanain²

2012

Biochemistry

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Section: Role Of Profilin In Vascular Remodeling and Hypertensionsupporting

confidence: 92%

Section: Fig 7 Inner Lining Of Normal Arterymentioning

confidence: 92%

Section: Fig 7 Inner Lining Of Normal Arterymentioning

confidence: 97%

Section: Fig 7 Inner Lining Of Normal Arterymentioning

confidence: 99%

“…Mehta & Griendling, 2007). Interestingly, it has been recently reported that profilin-I is a key component in the Ang-II-induced vascular remodeling (Cheng et al, 2011;Zhong et al, 2011).…”

Section: Role Of Profilin In Vascular Remodeling and Hypertensionmentioning

confidence: 99%

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Profilin, and Vascular Diseases

Elnakish¹,

Hassanain²

2012

Biochemistry

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Effect of profilin‐1 on the asymmetric dimethylarginine‐induced vascular lesion‐associated hypertension

Cheng²,

et al. 2021

The Kaohsiung J of Med Scie

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Previous studies have demonstrated that the levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthesis, are strongly associated with hypertension, diabetes, and cardiovascular diseases. Profilin‐1, an actin‐binding protein, has been documented to be involved in endothelial injury and in the proliferation of vascular smooth muscle cells resulting from hypertension. However, the role of profilin‐1 in ADMA‐induced vascular injury in hypertension remains largely unknown. Forty healthy subjects and forty‐two matched patients with essential hypertension were enrolled, and the related indexes of vascular injury in plasma were detected. Rat aortic smooth muscle cells (RASMCs) were treated with different concentrations of ADMA for different periods of time and transfected with profilin‐1 small hairpin RNA to interrupt the expression of profilin‐1. To determine the role of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway, RASMCs were pretreated with AG490 or rapamycin. The expression of profilin‐1 was tested using real‐time polymerase chain reaction (PCR) and western blot analysis. Cell proliferation was measured by flow cytometry and 3‐(4,5‐dimethylthiazol‐2yl)‐2,5‐diphenyltetrazoliumbromide assays. Compared with healthy subjects, the levels of ADMA and profilin‐1 were markedly elevated in hypertensive individuals, while the levels of NO were significantly decreased (p < 0.05). In vitro, studies showed ADMA‐induced profilin‐1 expression in a concentration‐ and time‐dependent manner in RASMCs (p < 0.05), concomitantly with promoting the proliferation of RASMCs. Furthermore, ADMA‐mediated proliferation of RASMCs and upregulation expression of profilin‐1 were inhibited by blockade of the JAK2/STAT3 pathway or knockdown of profilin‐1. Profilin‐1 implicated in the ADMA‐mediated vascular lesions in hypertension.

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Monocyte chemoattractant protein-1 mediates angiotensin II-induced vascular smooth muscle cell proliferation via SAPK/JNK and ERK1/2

Yao

Gao

et al. 2012

Mol Cell Biochem

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Abnormal vascular smooth muscle cells proliferation is the pathophysiological basis of cardiovascular diseases, such as hypertension, atherosclerosis, and restenosis after angioplasty. Angiotensin II can induce abnormal proliferation of vascular smooth muscle cells, but the molecular mechanisms of this process remain unclear. Here, we explored the role and molecular mechanism of monocyte chemotactic protein-1, which mediated angiotensin II-induced proliferation of rat aortic smooth muscle cells. 1,000 nM angiotensin II could stimulate rat aortic smooth muscle cells' proliferation by angiotensin II type 1 receptor (AT(1)R). Simultaneously, angiotensin II increased monocyte chemotactic protein-1 expression and secretion in a dose-and time-dependent manner through activation of its receptor AT(1)R. Then, monocyte chemotactic protein-1 contributed to angiotensin II-induced cells proliferation by CCR2. Furthermore, we found that intracellular ERK and JNK signaling molecules were implicated in angiotensin II-stimulated monocyte chemotactic protein-1 expression and proliferation mediated by monocyte chemotactic protein-1. These results contribute to a better understanding effect on angiotensin II-induced proliferation of rat smooth muscle cells.

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Involvement of profilin-1 in angiotensin II-induced vascular smooth muscle cell proliferation

Cited by 28 publications

References 28 publications

Profilin, and Vascular Diseases

Profilin, and Vascular Diseases

Effect of profilin‐1 on the asymmetric dimethylarginine‐induced vascular lesion‐associated hypertension

Monocyte chemoattractant protein-1 mediates angiotensin II-induced vascular smooth muscle cell proliferation via SAPK/JNK and ERK1/2

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