Prenatal Exposure to Delta-9-tetrahydrocannabinol (THC) Alters the Expression of miR-122-5p and Its Target Igf1r in the Adult Rat Ovary

Martínez-Peña, Annia A.; Lee, Kendrick; Pereira, Madison; Ayyash, Ahmed; Petrik, Jim; Hardy, Daniel B.; Holloway, Alison C.

doi:10.3390/ijms23148000

Cited by 4 publications

(7 citation statements)

References 90 publications

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“…The authors propose that these epigenetic modifications could contribute to addiction vulnerability later in life [56]. Prenatal THC exposure can also lead to the differential expression of micro RNA (miRNAs) [57]. In one study, prenatal THC exposure was associated with the upregulation of miR-122-5p and the resultant downregulation of insulin-like growth factor 1 receptor (Igf1r) [57].…”

Section: Cannabis-induced Epigenetic Effectsmentioning

confidence: 99%

Cannabinoids Transmogrify Cancer Metabolic Phenotype via Epigenetic Reprogramming and a Novel CBD Biased G Protein-Coupled Receptor Signaling Platform

Bunsick

Matsukubo

Szewczuk

2023

Cancers

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The concept of epigenetic reprogramming predicts long-term functional health effects. This reprogramming can be activated by exogenous or endogenous insults, leading to altered healthy and different disease states. The exogenous or endogenous changes that involve developing a roadmap of epigenetic networking, such as drug components on epigenetic imprinting and restoring epigenome patterns laid down during embryonic development, are paramount to establishing youthful cell type and health. This epigenetic landscape is considered one of the hallmarks of cancer. The initiation and progression of cancer are considered to involve epigenetic abnormalities and genetic alterations. Cancer epigenetics have shown extensive reprogramming of every component of the epigenetic machinery in cancer development, including DNA methylation, histone modifications, nucleosome positioning, non-coding RNAs, and microRNA expression. Endocannabinoids are natural lipid molecules whose levels are regulated by specific biosynthetic and degradative enzymes. They bind to and activate two primary cannabinoid receptors, type 1 (CB1) and type 2 (CB2), and together with their metabolizing enzymes, form the endocannabinoid system. This review focuses on the role of cannabinoid receptors CB1 and CB2 signaling in activating numerous receptor tyrosine kinases and Toll-like receptors in the induction of epigenetic landscape alterations in cancer cells, which might transmogrify cancer metabolism and epigenetic reprogramming to a metastatic phenotype. Strategies applied from conception could represent an innovative epigenetic target for preventing and treating human cancer. Here, we describe novel cannabinoid-biased G protein-coupled receptor signaling platforms (GPCR), highlighting putative future perspectives in this field.

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Section: Cannabis-induced Epigenetic Effectsmentioning

confidence: 99%

Cannabinoids Transmogrify Cancer Metabolic Phenotype via Epigenetic Reprogramming and a Novel CBD Biased G Protein-Coupled Receptor Signaling Platform

Bunsick

Matsukubo

Szewczuk

2023

Cancers

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“…Moreover, several studies proved that using antidepressants during gestational age would induce birth defects, especially for congenital heart disease. For example, Sun et al (2022) indicated that the use of maternal antidepressant 3 months before pregnancy and early pregnancy exposure to an antidepressant would elevate the risk of congenital heart disease among the offspring. In addition, intrauterine fluoxetine exposure was associated with several congenital malformations (RR = 1.18, 95% CI = 1.08-1.29).…”

Section: Antidepressantsmentioning

confidence: 99%

“…Indeed, poor placental function has been proven to be associated with obesity, hypertension, and diabetes in later adult life. While García-Otero et al (2022) demonstrated an observational study to identify that intrauterine exposure to HIV and antiretroviral therapy were not associated with cardiovascular changes from fetal development to infant growth, they did not measure the longterm outcomes of the cardiovascular system.…”

Section: Antiretroviral Therapymentioning

confidence: 99%

“…Exposure to cannabis-induced placental dysfunction was associated with postnatal metabolic diseases ( Lee et al, 2021 ; Lee and Hardy, 2021 ). Martínez-Peña et al (2022 ) indicated that intra-uterine THC exposure unregulated the expression of miR-122-5p, which inhibited insulin-like growth factor 1 receptor (IGF1R). IGF1R has been associated with cardiovascular diseases.…”

Section: Association Between Prenatal Drug Exposure and Programmed Ca...mentioning

confidence: 99%

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The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease

Zhou

Hua

et al. 2023

Front. Pharmacol.

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The “developmental origins of health and disease” (DOHaD) hypothesis posits that early-life environmental exposures have a lasting impact on individual’s health and permanently shape growth, structure, and metabolism. This reprogramming, which results from fetal stress, is believed to contribute to the development of adulthood cardiovascular diseases such as hypertension, coronary artery disease, heart failure, and increased susceptibility to ischemic injuries. Recent studies have shown that prenatal exposure to drugs, such as glucocorticoids, antibiotics, antidepressants, antiepileptics, and other toxins, increases the risk of adult-onset cardiovascular diseases. In addition, observational and animal experimental studies have demonstrated the association between prenatal drug exposure and the programming of cardiovascular disease in the offspring. The molecular mechanisms underlying these effects are still being explored but are thought to involve metabolism dysregulation. This review summarizes the current evidence on the relationship between prenatal drug exposure and the risk of adult cardiovascular disorders. Additionally, we present the latest insights into the molecular mechanisms that lead to programmed cardiovascular phenotypes after prenatal drug exposure.

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“…CBD alone was shown to suppress inflammation in an animal model of EAE by modulating several miRNAs [ 127 ]. It was shown that prenatal THC exposure enhanced miR-122-5p; reduced the expression of its target, insulin-like growth factor 1 receptor (Igf1r), in adult rat ovary follicular cells; and caused follicular apoptosis [ 169 ]. In another study, activation of CB 2 by a specific agonist (AM1241) was suggested to protect dopaminergic neurons in Parkinson’s disease animals.…”

Section: Regulation Of Micrornas and Cannabinoid Receptorsmentioning

confidence: 99%

Molecular Insights into Epigenetics and Cannabinoid Receptors

Basavarajappa

Subbanna²

2022

Biomolecules

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The actions of cannabis are mediated by G protein-coupled receptors that are part of an endogenous cannabinoid system (ECS). ECS consists of the naturally occurring ligands N-arachidonylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG), their biosynthetic and degradative enzymes, and the CB1 and CB2 cannabinoid receptors. Epigenetics are heritable changes that affect gene expression without changing the DNA sequence, transducing external stimuli in stable alterations of the DNA or chromatin structure. Cannabinoid receptors are crucial candidates for exploring their functions through epigenetic approaches due to their significant roles in health and diseases. Epigenetic changes usually promote alterations in the expression of genes and proteins that can be evaluated by various transcriptomic and proteomic analyses. Despite the exponential growth of new evidence on the critical functions of cannabinoid receptors, much is still unknown regarding the contribution of various genetic and epigenetic factors that regulate cannabinoid receptor gene expression. Recent studies have identified several immediate and long-lasting epigenetic changes, such as DNA methylation, DNA-associated histone proteins, and RNA regulatory networks, in cannabinoid receptor function. Thus, they can offer solutions to many cellular, molecular, and behavioral impairments found after modulation of cannabinoid receptor activities. In this review, we discuss the significant research advances in different epigenetic factors contributing to the regulation of cannabinoid receptors and their functions under both physiological and pathological conditions. Increasing our understanding of the epigenetics of cannabinoid receptors will significantly advance our knowledge and could lead to the identification of novel therapeutic targets and innovative treatment strategies for diseases associated with altered cannabinoid receptor functions.

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Prenatal Exposure to Delta-9-tetrahydrocannabinol (THC) Alters the Expression of miR-122-5p and Its Target Igf1r in the Adult Rat Ovary

Cited by 4 publications

References 90 publications

Cannabinoids Transmogrify Cancer Metabolic Phenotype via Epigenetic Reprogramming and a Novel CBD Biased G Protein-Coupled Receptor Signaling Platform

Cannabinoids Transmogrify Cancer Metabolic Phenotype via Epigenetic Reprogramming and a Novel CBD Biased G Protein-Coupled Receptor Signaling Platform

The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease

Molecular Insights into Epigenetics and Cannabinoid Receptors

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