Role of nifedipine and hydrochlorothiazide in MAPK activation and vascular smooth muscle cell proliferation and apoptosis

Wang, J; Liu, K; Wang, H; Li, Z; Li, Y; Ping, Suning; Bardeesi, Adham Sameer A.; Guo, Ying; Zhou, Yunjiao; Tu, Pei Chi; Dai, Lie; Sheng, Puyi; Liu, S; Li, C

doi:10.1007/s00059-016-4489-2

Cited by 10 publications

(8 citation statements)

References 48 publications

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“…In vitro, various stimuli, including oxidized lipoproteins, alter mechanical stress, and free radicals can induce SMC apoptosis [ 70 ]. Studies that exposed mouse SMCs cultured on gelatin to physiological stretching (< 10%) for less than 24 h have reported increased apoptosis compared to static controls [ 71 , 72 , 73 ]. The increased apoptosis seen in these studies was accompanied by increased proliferation.…”

Section: Cyclic Mechanical Stretchmentioning

confidence: 99%

The Phenotypic Responses of Vascular Smooth Muscle Cells Exposed to Mechanical Cues

Jensen

Bentzon

Albarrán-Juárez

2021

Cells

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During the development of atherosclerosis and other vascular diseases, vascular smooth muscle cells (SMCs) located in the intima and media of blood vessels shift from a contractile state towards other phenotypes that differ substantially from differentiated SMCs. In addition, these cells acquire new functions, such as the production of alternative extracellular matrix (ECM) proteins and signal molecules. A similar shift in cell phenotype is observed when SMCs are removed from their native environment and placed in a culture, presumably due to the absence of the physiological signals that maintain and regulate the SMC phenotype in the vasculature. The far majority of studies describing SMC functions have been performed under standard culture conditions in which cells adhere to a rigid and static plastic plate. While these studies have contributed to discovering key molecular pathways regulating SMCs, they have a significant limitation: the ECM microenvironment and the mechanical forces transmitted through the matrix to SMCs are generally not considered. Here, we review and discuss the recent literature on how the mechanical forces and derived biochemical signals have been shown to modulate the vascular SMC phenotype and provide new perspectives about their importance.

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Section: Cyclic Mechanical Stretchmentioning

confidence: 99%

The Phenotypic Responses of Vascular Smooth Muscle Cells Exposed to Mechanical Cues

Jensen

Bentzon

Albarrán-Juárez

2021

Cells

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“…To explore the correlation between VSMC death and AAD/aneurysm rupture, numerous studies have investigated the effects of CMS on VSMC activity and gene expression using in vitro technologies, wherein CMS is applied to cultured cells or tissues to mimic in vivo wall distension [ 20 , 21 , 22 , 23 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 ]. The majority of such experiments available in the literature have used rats [ 20 , 21 , 23 , 46 , 47 , 48 , 49 , 50 , 51 ], mice [ 21 , 52 , 53 , 54 , 55 , 56 ], and human SMCs [ 21 , 22 , 57 , 58 ], while a few of them have employed porcine SMCs [ 59 ]. It has been reported that applying ≥10% stretching to mouse/rat SMCs cultured on collagen for 4–24 h resulted in enhanced apoptosis in comparison to static controls [ 20 , 23 , 46 , 47 , 48 , 49 , 51 , 56 ].…”

Section: Cms-induced Cell Death (Including Apoptosis) and Proliferati...mentioning

confidence: 99%

“…In addition to normal physiological stretching, multiple studies evaluated the effects of hypertension-associated stretching (>10%) on the proliferation of human, mouse, and rat aortic SMCs. Mouse SMCs subjected to 10% stretching for 1 h have been reported to exhibit increased apoptosis and proliferation [ 52 , 53 , 54 , 55 ]. Exposing human aortic SMCs to >10% stretching for 12–24 h has been reported to result in enhanced apoptosis and proliferation in comparison to static cells (control) [ 57 , 58 ].…”

Section: Cms-induced Cell Death (Including Apoptosis) and Proliferati...mentioning

confidence: 99%

A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures

Zhao,

Yoshizumi

2024

IJMS

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Acute aortic dissection (AAD) and associated ruptures are the leading causes of death in cardiovascular diseases (CVDs). Hypertension is a prime risk factor for AAD. However, the molecular mechanisms underlying AAD remain poorly understood. We previously reported that cyclic mechanical stretch (CMS) leads to the death of rat aortic smooth muscle cells (RASMCs). This review focuses on the mechanisms of CMS-induced vascular smooth muscle cell (VSMC) death. Moreover, we have also discussed the potential therapeutics for preventing AAD and aneurysm ruptures.

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“…Further research found that both SS and AGEs alone were able to induce different levels of MAPKs (including ERK, JNK and P38MAPK) activation and simultaneous increases in the proliferation and apoptosis of VSMCs (Ping et al 2015; Wang et al 2017), while the combination of both had a synergistic effect (Ping et al 2015). The transformation of the VSMC subtypes is closely related to the pathophysiology of vascular disorders.…”

Section: Simultaneous Increases In Proliferation and Apoptosis Of Vsm...mentioning

confidence: 99%

Biomechanical signal communication in vascular smooth muscle cells

Zhou

Liu

2020

J. Cell Commun. Signal.

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Biomechanical stresses are closely associated with cardiovascular development and diseases. In vivo, vascular smooth muscle cells are constantly stimulated by biomechanical factors caused by increased blood pressure leading to the non‐specific activation of cell transmembrane proteins. Thus, various intracellular signal molecules are simultaneously activated via signaling cascades, which are closely related to alterations in the differentiation, phenotype, inflammation, migration, pyroptosis, calcification, proliferation, and apoptosis of vascular smooth muscle cells. Meanwhile, mechanical stress‐induced miRNAs and epigenetics modification on vascular smooth muscle cells play critical roles as well. Eventually, the overall pathophysiology of the cells is altered, resulting in the development of many major clinical diseases, including hypertension, atherosclerosis, grafted venous atherosclerosis, and aneurysm, among others. In this paper, important advances in mechanical signal communication in vascular smooth muscle cells are reviewed.

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Role of nifedipine and hydrochlorothiazide in MAPK activation and vascular smooth muscle cell proliferation and apoptosis

Abstract: Nifedipine and hydrochlorothiazide have opposing functions in the increased phosphorylation of MAPK and in the proliferation and apoptosis of VSMCs induced by stretch stress. The former plays a role as an inhibitor, while the latter functions as a promoter.

Cited by 10 publications

References 48 publications

The Phenotypic Responses of Vascular Smooth Muscle Cells Exposed to Mechanical Cues

The Phenotypic Responses of Vascular Smooth Muscle Cells Exposed to Mechanical Cues

A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures

Biomechanical signal communication in vascular smooth muscle cells

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