Serotonin inhibits apoptosis of pulmonary artery smooth muscle cell by pERK1/2 and PDK through 5-HT1B receptors and 5-HT transporters

Liu, Ya; Tian, Hong Yan; Yan, Xiu-Tian; Fan, Fen Ling; Wang, Wen Ping; Han, Jun; Zhang, Junbo; Ma, Qiang; Meng, Yan; Feng, Wei

doi:10.1016/j.carpath.2013.03.003

Cited by 18 publications

(20 citation statements)

References 34 publications

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“…Apoptosis is another key factor in vascular remodeling characteristic of PAH, as such, it has been previously shown that serotonin inhibits PASMC apoptosis through 5-HT 1B R or SERT. 38 It would be interesting to understand the role of serotonin and the 5-HT 1B R in other vascular cell components, such as human PA endothelial cells, primary cultures of such cells are not readily available from control subjects and patients with PAH, and therefore are difficult to study in relation to the human disease.…”

Section: Discussionmentioning

confidence: 99%

Serotonin Signaling Through the 5-HT _1B Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension

Hood

Mair

Harvey

et al. 2017

ATVB

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Section: Discussionmentioning

confidence: 99%

Serotonin Signaling Through the 5-HT _1B Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension

Hood

Mair

Harvey

et al. 2017

ATVB

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“…It was suggested that 5-HT, as the ligand of HTR3A, may decrease apoptosis rate through 5-HT1B receptors and 5-HT transporters in pulmonary artery smooth muscle cells (33). Concurrently, 5-HT1B receptor antagonists exerted anti-mitogenic and apoptotic effects on the CRC HT29 cell line (34).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of 5‑hydroxytryptamine receptor�3A expression exerts an anticancer activity against cell growth in colorectal carcinoma cells in�vitro

et al. 2018

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5-hydroxytryptamine receptor 3A (HTR3A) is an important member of the 5-HT family, which has been suggested to contribute to human tumor development. However, the functions of HTR3A in human cancer, particularly in colorectal carcinoma (CRC) have not been well-characterized. Reverse transcription quantitative polymerase was performed to detect endogenous HTR3A expression in 6 CRC cell lines. HTR3A was then knocked down via a lentivirus-mediated shRNA system to detect the effect of HTR3A silencing on cell proliferation and apoptosis by MTT, colony formation, flow cytometry and western blotting assays in CRC. HTR3A was expressed at different levels in the 6 CRC cell lines. In addition, HTR3A knockdown inhibited CRC cell proliferation and colony formation, resulting in cell cycle arrest and the promotion of cell apoptosis. Additionally, the expression levels of apoptosis-associated proteins including BAD and BAX were increased, while Bcl-2 expression was decreased following HTR3A knockdown. In summary, the data of the present study indicated that HTR3A serves an important role in colon carcinogenesis, but in-depth studies of the mechanisms underlying these data are required to demonstrate whether it may be used as a novel target for CRC therapy.

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“…EMERGING THERAPEUTICS IN PH hydroxylase (TPH1) and acts at the 5-HT (1B and 2A) receptor and the serotonin receptor transporter (SERT or 5-HTT) to mediate constriction and proliferation of vascular smooth muscle cells (84,94).…”

Section: L771mentioning

confidence: 99%

“…Additionally, RP5063, a multimodal dopamine (DA) and 5-HT modulator with high affinity for DA2/3/4 and 5-HT2A/2B/7 receptors and moderate affinity for SERT, has been recently reported to prevent MCT and SuHx models of PAH (10,11). Moreover, supplementation with 5-HT 1B antagonists and 5-HTT antagonist, alone or in combination, increases apoptosis and reduces proliferation of PASMCs through downregulation of extracellular signal-regulated kinase-1/2 and pyruvate dehydrogenase kinase (PDK) signaling pathways (84). Although a recent study by De Raaf et al (32) demonstrated that serotonin transporter is not required for the development of severe PH in SERT knockout (KO) rats exposed to SuHx, serotonin-targeting strategies remain a promising therapeutic option for the treatment of PAH.…”

Section: L771mentioning

confidence: 99%

Emerging therapeutics in pulmonary hypertension

Hensley

Levine

Lai

2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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Pulmonary hypertension (PH) is a progressive and often fatal illness presenting with nonspecific symptoms of dyspnea, lower extremity edema, and exercise intolerance. Pathologically, endothelial dysfunction leads to abnormal intimal and smooth muscle proliferation along with reduced apoptosis, resulting in increased pulmonary vascular resistance and elevated pulmonary pressures. PH is subdivided into five World Health Organization groups based on the disease pathology and specific cause. While there are Food and Drug Administration-approved medications for the treatment of pulmonary arterial hypertension (PAH; Group 1 PH), as well as for chronic thromboembolic PH (Group 4 PH), the morbidity and mortality remain high. Moreover, there are no approved therapies for other forms of PH (Groups 2, 3, and 5) at present. New research has identified molecular targets that mediate vasodilation, anti-inflammatory, and antifibrotic changes within the pulmonary vasculature. Given that PAH is the most commonly studied form of PH worldwide and because recent studies have led to better mechanistic understanding of this devastating disease, in this review we attempt to provide an updated overview of new therapeutic approaches under investigation for the treatment of PH, with a particular focus on PAH, as well as to offer guidelines for future investigations.

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Serotonin inhibits apoptosis of pulmonary artery smooth muscle cell by pERK1/2 and PDK through 5-HT1B receptors and 5-HT transporters

Cited by 18 publications

References 34 publications

Serotonin Signaling Through the 5-HT _1B Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension

Serotonin Signaling Through the 5-HT _1B Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension

Downregulation of 5‑hydroxytryptamine receptor�3A expression exerts an anticancer activity against cell growth in colorectal carcinoma cells in�vitro

Emerging therapeutics in pulmonary hypertension

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Serotonin inhibits apoptosis of pulmonary artery smooth muscle cell by pERK1/2 and PDK through 5-HT1B receptors and 5-HT transporters

Cited by 18 publications

References 34 publications

Serotonin Signaling Through the 5-HT 1B Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension

Serotonin Signaling Through the 5-HT 1B Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension

Downregulation of 5‑hydroxytryptamine receptor�3A expression exerts an anticancer activity against cell growth in colorectal carcinoma cells in�vitro

Emerging therapeutics in pulmonary hypertension

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Serotonin Signaling Through the 5-HT _1B Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension

Serotonin Signaling Through the 5-HT _1B Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension