Concurrence of autophagy with apoptosis in alveolar epithelial cells contributes to chronic pulmonary toxicity induced by methamphetamine

Wang, Yun; Gu, Yijun; Liang, Li-Ye; Liu, Ming; Jiang, Bin; Zhu, Mei-Jia; Wang, Xin; Shi, Lin

doi:10.1111/cpr.12476

Cited by 17 publications

(19 citation statements)

References 46 publications

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“…METH-induced apoptosis of alveolar epithelium cells is mediated by endoplasmic reticulum stress 30 , resulting in the reduction of pulmonary alveoli. Concurrence of autophagy with apoptosis in alveolar epithelial cells contributes to chronic pulmonary toxicity induced by chronic METH use 31 . Also, we previously demonstrated that pharmacological levels of METH in human blood and organs are cytotoxic to ∼ 20% of the phagocytes 32 .…”

Section: Discussionmentioning

confidence: 99%

Methamphetamine facilitates pulmonary and splenic tissue injury and reduces T cell infiltration in C57BL/6 mice after antigenic challenge

Hernandez-Santini

Mitha

Chow

et al. 2021

Sci Rep

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Methamphetamine (METH) is a strong addictive central nervous system stimulant. METH abuse can alter biological processes and immune functions necessary for host defense. The acquisition and transmission of HIV, hepatitis, and other communicable diseases are possible serious infectious consequences of METH use. METH also accumulates extensively in major organs. Despite METH being a major public health and safety problem globally, there are limited studies addressing the impact of this popular recreational psychostimulant on tissue adaptive immune responses after exposure to T cell dependent [ovalbumin (OVA)] and independent [lipopolysaccharide (LPS)] antigens. We hypothesized that METH administration causes pulmonary and splenic tissue alterations and reduces T cell responses to OVA and LPS in vivo, suggesting the increased susceptibility of users to infection. Using a murine model of METH administration, we showed that METH causes tissue injury, apoptosis, and alters helper and cytotoxic T cell recruitment in antigen challenged mice. METH also reduces the expression and distribution of CD3 and CD28 molecules on the surface of human Jurkat T cells. In addition, METH decreases the production of IL-2 in these T-like cells, suggesting a negative impact on T lymphocyte activation and proliferation. Our findings demonstrate the pleotropic effects of METH on cell-mediated immunity. These alterations have notable implications on tissue homeostasis and the capacity of the host to respond to infection.

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Section: Discussionmentioning

confidence: 99%

Methamphetamine facilitates pulmonary and splenic tissue injury and reduces T cell infiltration in C57BL/6 mice after antigenic challenge

Hernandez-Santini

Mitha

Chow

et al. 2021

Sci Rep

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“…The autophagy protein microtubule-associated protein 1 light-chain 3 (LC3) exists in two forms during activation of autophagy (Fu et al, 2016). After LC3 is cleaved to LC3 I by Atg4 in the cytoplasm, phosphatidylethanolamine (PE) and LC3 I form a LC3-II-PE complex, which participates in autophagic membrane extension and is distributed on the membranes of autophagic vacuoles (Yun et al, 2018). Integration of the LC3-II-PE complex and SQSTM1(p62) transfers the wasted substance, which is degraded by autolysosomes, into autophagosomes (Katsuragi et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Diosbulbin B-Induced Mitochondria-Dependent Apoptosis in L-02 Hepatocytes is Regulated by Reactive Oxygen Species-Mediated Autophagy

Xue

Liu

et al. 2019

Front. Pharmacol.

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Aim: Diosbulbin B (DB) is a major diterpenoid compound found in Dioscorea bulbifera L, a traditional medicinal herb in China. Clinical reports have confirmed that Dioscorea bulbifera L. can induce significant hepatotoxicity. In this study, we showed that DB can induce mitochondria-dependent apoptosis and investigated the role of autophagy in DB-induced hepatotoxicity in L-02 hepatocytes. Methods: L-02 hepatocytes were treated with different concentrations of DB for 48 h, after which indicators of autophagy and apoptosis were measured. 3-Methyladenine (3-MA) and rapamycin (Rapa) were used as inhibitor and agonist of autophagy, respectively. Furthermore, the reactive oxygen species (ROS) scavenger N-acetyl-l-cysteine (NAC) was used in combination with DB to evaluate the relationship between ROS and autophagy. Results: L-02 cell viability was significantly decreased after treatment with DB for 48 h. Additionally, DB induced concentration-dependent apoptosis and autophagy and increased the activities of caspase-3, caspase-9, alanine aminotransferase (ALT), and aspartate transaminase (AST), and induced excessive leakage of lactate dehydrogenase (LDH). Inhibition of autophagy by 3-MA increased DB-induced apoptosis, resulting in aggravation of hepatotoxicity. Conversely, treatment with Rapa increased malondialdehyde (MDA) content and reduced superoxide dismutase (SOD) activity. Moreover, we found that DB treatment increased the level of intracellular ROS, decreased the mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) production, and caused abnormal opening of the mitochondrial permeability transition pore (mPTP), which were finally restored by the ROS scavenger NAC. Conclusions: Accumulation of ROS can induce mitochondria-dependent apoptosis and likely to play a key role in DB-induced hepatocellular injury. Activation of autophagy may inhibit apoptosis, but also reduces antioxidant capacity.

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“…Mammalian target of rapamycin (mTOR) is universally acknowledged as an inhibitor of autophagy, so that autophagy will occur after mTOR is inactivated 8 . Our previous studies found that MA‐induced inactivation of mTOR promoted autophagy‐mediated alveolar epithelial injury 9 …”

Section: Introductionmentioning

confidence: 99%

“…8 Our previous studies found that MA-induced inactivation of mTOR promoted autophagy-mediated alveolar epithelial injury. 9 Senescence is the complex process of deterioration that occurs over the lifetime of an organism, resulting in progressive functional decline and eventual death. 10 Cellular senescence is a phenomenon that the cells lose the ability of self-proliferation.…”

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confidence: 99%

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mTOR‐autophagy promotes pulmonary senescence through IMP1 in chronic toxicity of methamphetamine

Zhu

Liu

Shi

et al. 2020

J Cellular Molecular Medi

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Methamphetamine (MA) abuse has been a growing global health problem. 1,2 The highest absorption and distribution of MA in the lungs are extremely vulnerable to pulmonary infections, pulmonary hypertension and oedema. 3 Lung toxicity by long-term exposure to MA is very harmful to health. 4 Alveolar epithelial cells in defence against infections and toxins are the key barriers to maintain the pulmonary homeostasis. 5,6 Therefore, alveolar epithelial injury is an important pathological change of MA-induced lung toxicity. Autophagy refers to a process by which cellular components are degraded by lysosomes or vacuoles. 7 Mammalian target of rapamycin (mTOR) is universally acknowledged as an inhibitor of autophagy,

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Concurrence of autophagy with apoptosis in alveolar epithelial cells contributes to chronic pulmonary toxicity induced by methamphetamine

Abstract: Concurrence of autophagy with apoptosis in alveolar epithelial cells contributes to chronic pulmonary toxicity induced by MA.

Cited by 17 publications

References 46 publications

Methamphetamine facilitates pulmonary and splenic tissue injury and reduces T cell infiltration in C57BL/6 mice after antigenic challenge

Methamphetamine facilitates pulmonary and splenic tissue injury and reduces T cell infiltration in C57BL/6 mice after antigenic challenge

Diosbulbin B-Induced Mitochondria-Dependent Apoptosis in L-02 Hepatocytes is Regulated by Reactive Oxygen Species-Mediated Autophagy

mTOR‐autophagy promotes pulmonary senescence through IMP1 in chronic toxicity of methamphetamine

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