Transient Receptor Potential Vanilloid 1 Expression Mediates Capsaicin-Induced Cell Death

Ramírez-Barrantes, Ricardo; Córdova, Claudio; Gatica, Sebastián; Rodríguez, Belén; Lozano, Carlo; Marchant, Ivanny; Echeverría, César; Simón, Felipe; Olivero, Pablo

doi:10.3389/fphys.2018.00682

Cited by 32 publications

(30 citation statements)

References 49 publications

(63 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, similar results have been reported for CAP without TRPV1 participation, suggesting both dependent and independent effects of this vanilloid (MacHo et al, 2000). Our explanation is that the amount of CAP is able to modify the amount of calcium entry and release from inner cell stores (Ramírez-Barrantes et al, 2018).…”

Section: Introductionsupporting

confidence: 87%

“…Actually, TRPV1 channels control the mitochondrial integrity through regulation of mitochondrial membrane depolarization in neurons (Medvedeva et al, 2008;Ramírez-Barrantes et al, 2018). For example, low doses of capsaicin in dorsal root ganglion trigger a transitory calcium signaling by TRPV1, which, in turn, activates calcium uptake by mitochondria and slow release (10-20 min later) to prolong glutamate release from these sensory neurons (Medvedeva et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…High concentrations of activators or sustained activation of the channel might induce toxicity by deregulation of mitochondrial function. If TRPV1 is overactivated, a loss of transience of the signal is accompanied by dysfunction of mitochondria, calcium overload and cell death (Ramírez-Barrantes et al, 2018). It is likely that the physiological mechanism of action of TRPV1 (Pegorini et al, 2005;Huang et al, 2017) consists in, sequentially: activation, transient raise in intracellular calcium and consequent calcium-mediated desensitization.…”

Section: Discussionmentioning

confidence: 99%

“…To evaluate the role of TRPV1 in estrogen protection against oxidative stress-induced cell death, we utilized as inductor hydrogen peroxide (H 2 O 2 ) and recorded simultaneously the mitochondrial function and plasma membrane integrity by flow cytometry applying the AVD model analysis (Ramírez- Barrantes et al, 2018). We performed a dose-response curve of H 2 O 2 in both cell types and measured cell viability ( Figure 1C).…”

Section: Specificity Of 17β-estradiol-induced Cell Death Protectionmentioning

confidence: 99%

See 3 more Smart Citations

TRPV1-Estradiol Stereospecific Relationship Underlies Cell Survival in Oxidative Cell Death

et al. 2020

Self Cite

View full text Add to dashboard Cite

Ramírez-Barrantes et al. TRPV1 Contribution in 17β-Estradiol Cell Protection GRAPHICAL ABSTRACT | TRPV1 is sufficient condition for 17β-estradiol resistance against oxidative stress-induced cell death. The cell death induced by oxidative stress could be characterized by a kinetic model of three state: alive, vulnerable and dead. In particular, the transition from alive to vulnerable state involves the depolarization of mitochondrial membrane potential, and the evolution to cell death the activation of caspases. Only in TRPV1 expressing cells, the initial application of 17β-estradiol protects against the irreversible damage triggered by oxidative stress, by inhibition of the transition from alive to vulnerable state. This mechanism includes blocking oxidative stress-dependent mitochondrial depolarization and the activation of caspases 3/7. Furthermore, 17β-estradiol potentiates TRPV1 activity associated with an increased open probability. Despite the relationship between the activation of TRPV1 and the maintenance of the mitochondrial membrane potential should be clarified, it could include the increase of the calcium buffer capacity of the mitochondria and/or the overexpression of anti-apoptotic proteins such as the Bcl-2 family as previously reported. Finally, the 17β-estradiol cell protection was independent of estrogen receptors, and was membrane started and stereospecific. These results support the role of TRPV1 as a 17β-estradiol ionotropic receptor being critical to cell survival.

show abstract

Section: Introductionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Specificity Of 17β-estradiol-induced Cell Death Protectionmentioning

confidence: 99%

See 2 more Smart Citations

TRPV1-Estradiol Stereospecific Relationship Underlies Cell Survival in Oxidative Cell Death

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

“…It could be envisaged that chronic TRPV1 activation could lead to an aberrant increase in [Ca 2+ ] i , thereby inducing to Ca 2+ -dependent cell death [148]. This hypothesis is supported by the notion that capsaicin-induced prolonged Ca 2+ entry promotes apoptosis in prostate cancer cells [128], breast cancer cells [149], and cervical tumor cells [150]. On the other hand, TRPV1 activation was shown to reduce the ischemia/reperfusion (IR) injury in several organs, including the heart, brain, lungs, and kidney [151].…”

Section: Stimulating Trpv1 To Promote Angiogenesismentioning

confidence: 96%

Endothelial TRPV1 as an Emerging Molecular Target to Promote Therapeutic Angiogenesis

Negri

Faris

Rosti

et al. 2020

Cells

View full text Add to dashboard Cite

Therapeutic angiogenesis represents an emerging strategy to treat ischemic diseases by stimulating blood vessel growth to rescue local blood perfusion. Therefore, injured microvasculature may be repaired by stimulating resident endothelial cells or circulating endothelial colony forming cells (ECFCs) or by autologous cell-based therapy. Endothelial Ca2+ signals represent a crucial player in angiogenesis and vasculogenesis; indeed, several angiogenic stimuli induce neovessel formation through an increase in intracellular Ca2+ concentration. Several members of the Transient Receptor Potential (TRP) channel superfamily are expressed and mediate Ca2+-dependent functions in vascular endothelial cells and in ECFCs, the only known truly endothelial precursor. TRP Vanilloid 1 (TRPV1), a polymodal cation channel, is emerging as an important player in endothelial cell migration, proliferation, and tubulogenesis, through the integration of several chemical stimuli. Herein, we first summarize TRPV1 structure and gating mechanisms. Next, we illustrate the physiological roles of TRPV1 in vascular endothelium, focusing our attention on how endothelial TRPV1 promotes angiogenesis. In particular, we describe a recent strategy to stimulate TRPV1-mediated pro-angiogenic activity in ECFCs, in the presence of a photosensitive conjugated polymer. Taken together, these observations suggest that TRPV1 represents a useful target in the treatment of ischemic diseases.

show abstract

Intracellular and extracellular targets as mechanisms of cancer therapy by nanomaterials in relation to their physicochemical properties

Gulumian

2020

WIREs Nanomed Nanobiotechnol

View full text Add to dashboard Cite

Cancer nanomedicine has evolved in recent years and is only expected to increase due to the ease with which nanomaterials (NMs) may be manipulated to the advantage of the cancer patient. The success of nanomedicine is dependent on the cell death mechanism, which in turn is dependent on the organelle initially targeted. The success of cancer nanomedicine is also dependent on other cellular mechanisms such as the induction of autophagy dysfunction, manipulation of the tumor microenvironment (TME) and secretome or induction of host immune responses. Current cancer phototherapies for example, photothermal‐ or photodynamic therapies as well as radio enhancement also form a major part of cancer nanomedicine. In general, cancer nanomedicine may be grouped into those NMs exhibiting inherent anti‐cancer properties that is, self‐therapeutic NMs (Group 1), NMs leading to localization of phototherapies or radio‐enhancement (Group 2), and NMs as nanocarriers in the absence or presence of external radiation (Group 3). The recent advances of these three groups, together with their advantages and disadvantages as well as their cellular mechanisms and ultimate outcomes are summarized in this review. By exploiting these different intracellular mechanisms involved in initiating cell death pathways, it is possible to synthesize NMs that may have the desirable characteristics to maximize their efficacy in cancer therapy. Therefore, a summary of these important physicochemical characteristics is also presented that need to be considered for optimal cancer cell targeting and initiation of mechanisms that will lead to cancerous cell death. This article is categorized under: Therapeutic Approaches and Drug Discovery > Nanomedicine for Oncologic Disease Toxicology and Regulatory Issues in Nanomedicine > Toxicology of Nanomaterials Toxicology and Regulatory Issues in Nanomedicine > Regulatory and Policy Issues in Nanomedicine

show abstract

Transient Receptor Potential Vanilloid 1 Expression Mediates Capsaicin-Induced Cell Death

Cited by 32 publications

References 49 publications

TRPV1-Estradiol Stereospecific Relationship Underlies Cell Survival in Oxidative Cell Death

TRPV1-Estradiol Stereospecific Relationship Underlies Cell Survival in Oxidative Cell Death

Endothelial TRPV1 as an Emerging Molecular Target to Promote Therapeutic Angiogenesis

Intracellular and extracellular targets as mechanisms of cancer therapy by nanomaterials in relation to their physicochemical properties

Contact Info

Product

Resources

About