ArticleJournal of cellular and molecular medicine2013
Akt-mediated anti-apoptotic effects of substance P in Anti-Fas-induced apoptosis of human tenocytes.
Article in Journal of cellular and molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Anticancer Mechanism ofPharmaceuticals (Basel, Switzerland) · 2024Review
- Investigation of the mechanism of the anti-cancer effects ofFrontiers in pharmacology · 2022Article
- Prognostic Significance of Substance P/Neurokinin 1 Receptor and Its Association with Hormonal Receptors in Breast Carcinoma.BioMed research international · 2021Article
- Sensory Neuropeptides and their Receptors Participate in Mechano-Regulation of Murine Macrophages.International journal of molecular sciences · 2019Article
- Substance P modulates bone remodeling properties of murine osteoblasts and osteoclasts.Scientific reports · 2018Article
- Substance P increases CCN2 dependent on TGF-beta yet Collagen Type I via TGF-beta1 dependent and independent pathways in tenocytes.Connective tissue research · 2018Article
- β-Arrestin 1 has an essential role in neurokinin-1 receptor-mediated glioblastoma cell proliferation and GThe Journal of biological chemistry · 2017Article
- Transforming Growth Factor Beta 1 Modulates the Functional Expression of the Neurokinin-1 Receptor in Human Keratocytes.Current eye research · 2016Article
- Role of VEGF, Nitric Oxide, and Sympathetic Neurotransmitters in the Pathogenesis of Tendinopathy: A Review of the Current Evidences.Frontiers in aging neuroscience · 2016Review
- Article
- Substance P induces cardioprotection in ischemia-reperfusion via activation of AKT.American journal of physiology. Heart and circulatory physiology · 2015Article
- The effects of substance p on tendinopathy are dose-dependent: an in vitro and in vivo model study.The journal of nutrition, health & aging · 2015Article
- Gelatin nanoparticle-mediated intranasal delivery of substance P protects against 6-hydroxydopamine-induced apoptosis: an in vitro and in vivo study.Drug design, development and therapy · 2015Article
- Substance P reduces TNF-α-induced apoptosis in human tenocytes through NK-1 receptor stimulation.British journal of sports medicine · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substance P (SP) and its receptor, the neurokinin-1 receptor (NK-1 R), are expressed by human tenocytes, and they are both up-regulated in cases of tendinosis, a condition associated with excessive apoptosis. It is known that SP can phosphorylate/activate the protein kinase Akt, which has anti-apoptotic effects. This mechanism has not been studied for tenocytes. The aims of this study were to investigate if Anti-Fas treatment is a good apoptosis model for human tenocytes in vitro, if SP protects from Anti-Fas-induced apoptosis, and by which mechanisms SP mediates an anti-apoptotic response. Anti-Fas treatment resulted in a time- and dose-dependent release of lactate dehydrogenase (LDH), i.e. induction of cell death, and SP dose-dependently reduced the Anti-Fas-induced cell death through a NK-1 R specific pathway. The same trend was seen for the TUNEL assay, i.e. SP reduced Anti-Fas-induced apoptosis via NK-1 R. In addition, it was shown that SP reduces Anti-Fas-induced decrease in cell viability as shown with crystal violet assay. Protein analysis using Western blot confirmed that Anti-Fas induces cleavage/activation of caspase-3 and cleavage of PARP; both of which were inhibited by SP via NK-1 R. Finally, SP treatment resulted in phosphorylation/activation of Akt as shown with Western blot, and it was confirmed that the anti-apoptotic effect of SP was, at least partly, induced through the Akt-dependent pathway. In conclusion, we show that SP reduces Anti-Fas-induced apoptosis in human tenocytes and that this anti-apoptotic effect of SP is mediated through NK-1 R and Akt-specific pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.