Heavy marijuana users show increased serum apolipoprotein C-III levels: evidence from proteomic analyses

Jayanthi, Subramaniam; S, Buie; Moore, S. S.; Herning, Ronald I.; Better, Warren; Wilson, Nicola; Contoreggi, Carlo; Cadet, Jean Lud

doi:10.1038/mp.2008.50

Cited by 21 publications

(14 citation statements)

References 66 publications

(57 reference statements)

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“…Evidence supporting marijuana as a stroke risk factor is increasing. Recent studies have shown marijuana users to have increased levels of apolipoprotein C‐III, a known cardiovascular risk factor, as well as an adjusted odds ratio of 1.76 for ischaemic stroke 23 , 24 . Amphetamines increase the risk of stroke by several mechanisms, including elevation of blood pressure, vasculitis and cerebral vasospasm, 25 and are frequently misused in Australia 22 .…”

Section: Discussionmentioning

confidence: 99%

Ischaemic stroke among young people aged 15 to 50 years in Adelaide, South Australia

Phillips

Leyden

Chong

et al. 2011

Medical Journal of Australia

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Section: Discussionmentioning

confidence: 99%

Ischaemic stroke among young people aged 15 to 50 years in Adelaide, South Australia

Phillips

Leyden

Chong

et al. 2011

Medical Journal of Australia

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“…The health risks of marijuana use are well documented: including dose‐dependent respiratory symptoms such as shortness of breath, coughing and increased sputum production (21–24). Long‐term marijuana abuse is associated with cognitive deficits, as well as with cerebrovascular disorders such as stroke (25). Isolated incidents of severe Aspergillosis fumigatus infection from contaminated marijuana have occurred in transplant recipients (26–28).…”

Section: Discussionmentioning

confidence: 99%

Marijuana Use in Potential Liver Transplant Candidates

Ranney¹,

Acker²,

Al-Holou³

et al. 2009

American Journal of Transplantation

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Concern exists that liver transplant center substance abuse policies may have an inappropriate and disproportionate impact on marijuana users. Our hypothesis is that patients with chronic liver disease who were marijuana users will have inferior survival. This is a retrospective (1999-2007) cohort study. The primary outcome measure is time-dependent, adjusted patient survival from the time of liver transplant evaluation. The primary exposure variable is a positive cannabinoid toxicology screen during the liver transplant evaluation period. Overall, 155 patients qualified as marijuana users while 1334 patients were marijuana non-users. Marijuana users were significantly (p < 0.05) younger (48.3 vs. 52.1), more likely to be male (78.1% vs. 63.0%), have hepatitis C (63.9% vs. 40.6%) and were less likely to receive a transplant (21.8% vs. 14.8%). Marijuana users were more likely to use tobacco, narcotics, benzodiazepines, amphetamines, cocaine or barbiturates (p < 0.05). Unadjusted survival rates were similar between cohorts. Upon multivariate analysis, MELD score, hepatitis C and transplantation were significantly associated with survival, while marijuana use was not (HR 1.09, 95% CI 0.78-1.54). We conclude that patients who did and did not use marijuana had similar survival rates. Current substance abuse policies do not seen to systematically expose marijuana users to additional risk of mortality.

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“…This is the first proteomic approach to the understanding of AEA pro-apoptotic activity. By the way, the first ever proteomic analysis on the effects of the cannabis-derived ⌬ 9 -tetrahydrocannabinol in chronic users (45), and in mouse cerebellum (46), appeared during the preparation of this manuscript.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the Endocannabinoid System in Human Neuronal Cells and Proteomic Analysis of Anandamide-induced Apoptosis

Pasquariello

Catanzaro

Marzano

et al. 2009

Journal of Biological Chemistry

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Anandamide (AEA) is an endogenous agonist of type 1 cannabinoid receptors (CB1R) that, along with metabolic enzymes of AEA and congeners, compose the "endocannabinoid system." Here we report the biochemical, morphological, and functional characterization of the endocannabinoid system in human neuroblastoma SH-SY5Y cells that are an experimental model for neuronal cell damage and death, as well as for major human neurodegenerative disorders. We also show that AEA dose-dependently induced apoptosis of SH-SY5Y cells. Through proteomic analysis, we further demonstrate that AEA-induced apoptosis was paralleled by an ϳ3 to ϳ5-fold up-regulation or down-regulation of five genes; IgG heavy chain-binding protein, stress-induced phosphoprotein-1, and triose-phosphate isomerase-1, which were up-regulated, are known to act as antiapoptotic agents; actin-related protein 2/3 complex subunit 5 and peptidylprolyl isomerase-like protein 3 isoform PPIL3b were down-regulated, and the first is required for actin network formation whereas the second is still function-orphan. Interestingly, only the effect of AEA on BiP was reversed by the CB1R antagonist SR141716, in SH-SY5Y cells as well as in human neuroblastoma LAN-5 cells (that express a functional CB1R) but not in SK-NBE cells (which do not express CB1R). Silencing or overexpression of BiP increased or reduced, respectively, AEA-induced apoptosis of SH-SY5Y cells. In addition, the expression of BiP and of the BiP-related apoptotic markers p53 and PUMA was increased by AEA through a CB1R-dependent pathway that engages p38 and p42/44 mitogen-activated protein kinases. Consistently, this effect of AEA was minimized by SR141716. In conclusion, we identified BiP as a key protein in neuronal apoptosis induced by AEA.Endocannabinoids bind to and activate both type 1 (CB1R) 4 and type 2 (CB2R) cannabinoid receptors and are widely recognized as important regulators of central and peripheral functions (1-3). The most studied endocannabinoids are anandamide (N-arachidonoylethanolamine, AEA) and 2-arachidonoylglycerol (2-AG) (1, 3). AEA, unlike 2-AG, binds to and activates also transient receptor potential vanilloid 1 (TRPV1), thus being considered a true "endovanilloid" (4).The "endocannabinoid system (ECS)" includes the receptors, their ligands AEA and 2-AG, and the enzymes that synthesize (N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D (NAPE-PLD) and diacylglycerol lipase (DAGL)) or degrade (fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL)) AEA and 2-AG, respectively (1-3). On the other hand, there is still controversy about the identity and even the existence of purported "endocannabinoid transporters" that have not yet been cloned, isolated, or characterized (5). A growing interest is concerned with the ability of AEA to induce apoptosis in neuronal and non-neuronal cells (for comprehensive reviews see Refs. 6 -9). Such a pro-apoptotic activity of AEA

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Heavy marijuana users show increased serum apolipoprotein C-III levels: evidence from proteomic analyses

Cited by 21 publications

References 66 publications

Ischaemic stroke among young people aged 15 to 50 years in Adelaide, South Australia

Ischaemic stroke among young people aged 15 to 50 years in Adelaide, South Australia

Marijuana Use in Potential Liver Transplant Candidates

Characterization of the Endocannabinoid System in Human Neuronal Cells and Proteomic Analysis of Anandamide-induced Apoptosis

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