Design and biological assessment of membrane-tethering neuroprotective peptides derived from the pituitary adenylate cyclase-activating polypeptide type 1 receptor

Molliens, Mathilde Poujol de; Jamadagni, Priyanka; Létourneau, Myriam; Devost, Dominic; Hébert, Terence E.; Patten, Shunmoogum A.; Fournier, Alain; Chatenet, David

doi:10.1016/j.bbagen.2019.07.007

Cited by 8 publications

(10 citation statements)

References 75 publications

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“…The zebrafish has emerged as a very powerful tool for investigating the in vivo developmental toxicity of compounds on a large scale [33][34][35]. The small size, ease of genetic manipulations, and relatively economical cost has paved the way for zebrafish to be the best organism for human disease models [36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51][52][53]. The zebrafish developmental toxicity study revealed the chronic toxicity of CM1 and CM2.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic Evaluation and Anti-Angiogenic Effects of Two Furano-Sesquiterpenoids from Commiphora myrrh Resin

et al. 2020

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Commiphora myrrh resin (Myrrh) has been used in traditional Arabic medicine to treat various inflammatory diseases. Two furano-sesquiterpenoids, 2-methoxyfuranodiene (CM1) and 2-acetoxyfuranodiene (CM2), were isolated from the chloroform fraction of the ethanolic extract of Arabic Commiphora myrrh resin. The cytotoxicity of the compounds was evaluated using human liver carcinoma, breast cancer cells (HepG2 and MCF-7, respectively) and normal human umbilical vein endothelial cells (HUVECs) cell lines. The development toxicity and anti-angiogenic activity of both compounds were also evaluated using zebrafish embryos. Cell survival assays demonstrated that both compounds were highly cytotoxic in HepG2 and MCF7 cells, with IC50 values of 3.6 and 4.4 µM, respectively. Both compounds induced apoptosis and caused cell cycle arrest in treated HepG2 cells, which was observed using flow cytometric analysis. The development toxicity in zebrafish embryos showed the chronic toxicity of both compounds. The toxicity was only seen when the embryos remained exposed to the compounds for more than three days. The compound CM2 showed a significant level of anti-angiogenic activity in transgenic zebrafish embryos at sublethal doses. Thus, we demonstrated the cytotoxic properties of both compounds, suggesting that the molecular mechanism of these compounds should be further assessed.

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Section: Discussionmentioning

confidence: 99%

Cytotoxic Evaluation and Anti-Angiogenic Effects of Two Furano-Sesquiterpenoids from Commiphora myrrh Resin

et al. 2020

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“…Evidence suggests that PACAP also helps maintain the BBB, combats neuroinflammation via secretion of neurotrophic and anti-inflammatory factors, and bears regenerative potential. Some mechanisms potentially underlying PACAP's anti-oxidative and anti-apoptotic properties include the Gαq and Gαs pathways [70,91], MAPK/ERK signaling [96], and NMDAR [41,62,63], all of which serve as potential targets for PACAP-based therapy. However, further investigation into these pathways is warranted.…”

Section: Discussionmentioning

confidence: 99%

“…PACAP's capacity to safeguard neuronal cells from glutamate excitotoxicity and 6hydroxydopamine neurotoxicity [11,34,81], as well as ameliorate oxidative injury and cell death, elucidates its restorative potential in Parkinson's Disease (PD) [70,91,92]. The G protein signaling pathways, Gas and Gaq, may play a key role in PACAP-induced cell viability in PD [91,92]. In neuroblastoma cells, PACAP23 promoted cell survival via the activation of G protein pathways, specifically Gαs and Gαq [92].…”

Section: Parkinson's Disease (Pd)mentioning

confidence: 99%

Pituitary Adenylate Cyclase-Activating Polypeptide: A Potent Therapeutic Agent in Oxidative Stress

et al. 2021

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Stroke is a life-threatening condition that is characterized by secondary cell death processes that occur after the initial disruption of blood flow to the brain. The inability of endogenous repair mechanisms to sufficiently support functional recovery in stroke patients and the inadequate treatment options available are cause for concern. The pathology behind oxidative stress in stroke is of particular interest due to its detrimental effects on the brain. The oxidative stress caused by ischemic stroke overwhelms the neutralization capacity of the body’s endogenous antioxidant system, which leads to an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and eventually results in cell death. The overproduction of ROS compromises the functional and structural integrity of brain tissue. Therefore, it is essential to investigate the mechanisms involved in oxidative stress to help obtain adequate treatment options for stroke. Here, we focus on the latest preclinical research that details the mechanisms behind secondary cell death processes that cause many central nervous system (CNS) disorders, as well as research that relates to how the neuroprotective molecular mechanisms of pituitary adenylate cyclase-activating polypeptides (PACAPs) could make these molecules an ideal candidate for the treatment of stroke.

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“…SH-SY5Y cells were treated with RA (SH-SY5Y/RA) at a concentration of 10 µM every 24 h for six days [ 48 ]. Briefly, cells were detached and plated (1 × 10 5 cells/cm 2 ) in 100 mm plates for 24 h. The day after, they were treated with 10 μM retinoic acid (RA, Sigma) for 6 days following Piras’ protocol [ 58 ].…”

Section: Methodsmentioning

confidence: 99%

“…Maasz et al, have demonstrated the neuroprotective action of PACAP in rats treated with 6-OHDA, with complications to neuronal metabolism [ 47 ]. It has been found that PAC1-R pepducins prevented the SH-SY5Y human neuroblastoma cells, treated with MPP + [ 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 ]. PACAP is a small peptide that presents low half-life in the bloodstream, representing an important concern for the treatment of neurodegenerative diseases.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of gH625-lipoPACAP in an In Vitro Fluid Dynamic Model of Parkinson’s Disease

et al. 2022

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Parkinson’s disease (PD) is an aggressive and devastating age-related disorder. Although the causes are still unclear, several factors, including genetic and environmental, are involved. Except for symptomatic drugs, there are not, to date, any real cures for PD. For this purpose, it is necessary develop a model to better study this disease. Neuroblastoma cell line, SH-SY5Y, differentiated with retinoic acid represents a good in vitro model to explore PD, since it maintains growth cells to differentiated neurons. In the present study, SH-SY5Y cells were treated with 1-methyl-4-phenylpyridinium (MPP+), a neurotoxin that induces Parkinsonism, and the neuroprotective effects of pituitary adenylate cyclase-activating polypeptide (PACAP), delivered by functionalized liposomes in a blood–brain barrier fluid dynamic model, were evaluated. We demonstrated PACAP neuroprotective effects when delivered by gH625-liposome on MPP+-damaged SH-SY5Y spheroids.

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Design and biological assessment of membrane-tethering neuroprotective peptides derived from the pituitary adenylate cyclase-activating polypeptide type 1 receptor

Cited by 8 publications

References 75 publications

Cytotoxic Evaluation and Anti-Angiogenic Effects of Two Furano-Sesquiterpenoids from Commiphora myrrh Resin

Cytotoxic Evaluation and Anti-Angiogenic Effects of Two Furano-Sesquiterpenoids from Commiphora myrrh Resin

Pituitary Adenylate Cyclase-Activating Polypeptide: A Potent Therapeutic Agent in Oxidative Stress

Neuroprotective Effects of gH625-lipoPACAP in an In Vitro Fluid Dynamic Model of Parkinson’s Disease

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