Asbestos-induced Disruption of Calcium Homeostasis Induces Endoplasmic Reticulum Stress in Macrophages

Ryan, Alan J.; Larson‐Casey, Jennifer L.; He, Chao; Murthy, Shuhba; Carter, A.Brent

doi:10.1074/jbc.m114.579870

Cited by 37 publications

(28 citation statements)

References 52 publications

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“…Ox-LDL caused significant SR-A1 upregulation with concomitant activation of ERS as assessed by upregulation of GRP78. Ryan et al [85] also detected an increased level of ERS in macrophages. ERS induced by asbestos caused disruption of calcium homeostasis.…”

Section: Endoplasmic Reticulum Stress Regulates Cardiovascular Physiomentioning

confidence: 89%

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

2016

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Endoplasmic reticulum is a principal organelle responsible for folding, post-translational modifications and transport of secretory, luminal and membrane proteins, thus palys an important rale in maintaining cellular homeostasis. Endoplasmic reticulum stress (ERS) is a condition that is accelerated by accumulation of unfolded/misfolded proteins after endoplasmic reticulum environment disturbance, triggered by a variety of physiological and pathological factors, such as nutrient deprivation, altered glycosylation, calcium depletion, oxidative stress, DNA damage and energy disturbance, etc. ERS may initiate the unfolded protein response (UPR) to restore cellular homeostasis or lead to apoptosis. Numerous studies have clarified the link between ERS and cardiovascular diseases. This review focuses on ERS-associated molecular mechanisms that participate in physiological and pathophysiological processes of heart and blood vessels. In addition, a number of drugs that regulate ERS was introduced, which may be used to treat cardiovascular diseases. This review may open new avenues for studying the pathogenesis of cardiovascular diseases and discovering novel drugs targeting ERS.

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Section: Endoplasmic Reticulum Stress Regulates Cardiovascular Physiomentioning

confidence: 89%

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

2016

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“…Several factors linked with an increased likelihood of pulmonary fibrosis, e.g. viral infection, asbestos, amiodarone and old age, each activate the UPR in the lung, which is consistent with a potential role for ER stress in the pathogenesis of pulmonary fibrosis [10][11][12][13][14]60]. However, the link between ER stress and interstitial lung disease appears to be complex.…”

Section: Pulmonary Fibrosismentioning

confidence: 92%

Endoplasmic reticulum stress in lung disease

Marciniak

2017

Eur Respir Rev

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Exposure to inhaled pollutants, including fine particulates and cigarette smoke is a major cause of lung disease in Europe. While it is established that inhaled pollutants have devastating effects on the genome, it is now recognised that additional effects on protein folding also drive the development of lung disease. Protein misfolding in the endoplasmic reticulum affects the pathogenesis of many diseases, ranging from pulmonary fibrosis to cancer. It is therefore important to understand how cells respond to endoplasmic reticulum stress and how this affects pulmonary tissues in disease. These insights may offer opportunities to manipulate such endoplasmic reticulum stress pathways and thereby cure lung disease.

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“…Asbestos-induced ER-Ca 2+ release and proapoptotic ER stress in AECII could also be prevented by overexpression of the antiapoptotic protein Bcl-X L , but not with the chemical chaperone 4-PBA [226]. Similarly, Ryan and coworkers observed rapid and sustained increases in cytosolic Ca 2+ -levels in macrophagelike THP-1 cell lines in response to crysotile-exposure, with concomitant activation of ATF6α-and XBP1-pathways [228]. Anisomycin, an inhibitor of translocon Ca 2+ leak, inhibited induction of ER stress markers suggesting that ER Ca 2+ depletion may be the major cause of ER stressactivation in macrophages exposed to chrysotile [228].…”

Section: Er Stress In Drug-induced Interstitial Lung Disease (Ild)mentioning

confidence: 88%

“…Of note, no significant apoptosis was observed in macrophages of chrysotile-exposed C57Bl/6 mice, and active TGF-β levels were increased in BALF of such mice. The authors then concluded, that bronchoalveolar macrophages undergo adaptive/protective ER stress for cell survival in response to chrysotile exposure, and that this is an important contributory factor for development of asbestos-induced lung fibrosis [228]. However, the authors did not analyse by means of immunohistochemistry the expression patterns of ER stress-markers in fibrotic lungs of chrysotile exposured mice, and the putative involvement of AECII in disease pathogenesis was also not addressed in this study [228].…”

Section: Er Stress In Drug-induced Interstitial Lung Disease (Ild)mentioning

confidence: 90%

“…Similarly, Ryan and coworkers observed rapid and sustained increases in cytosolic Ca 2+ -levels in macrophagelike THP-1 cell lines in response to crysotile-exposure, with concomitant activation of ATF6α-and XBP1-pathways [228]. Anisomycin, an inhibitor of translocon Ca 2+ leak, inhibited induction of ER stress markers suggesting that ER Ca 2+ depletion may be the major cause of ER stressactivation in macrophages exposed to chrysotile [228]. Moreover, BALF cells of asbestosis patients indicated significantly increased expression of ER stress-markers GRP78, ATF6, ERO1A and CHOP.…”

Section: Er Stress In Drug-induced Interstitial Lung Disease (Ild)mentioning

confidence: 92%

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The role of Endoplasmic Reticulum (ER) stress in pulmonary fibrosis

Korfei

Ruppert

Loeh

et al. 2016

Endoplasmic Reticulum Stress in Diseases

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The activation of Endoplasmic Reticulum (ER) stress and Unfolded Protein Response (UPR) was first observed in patients with familial interstitial pneumonia (FIP) carrying mutations in the C-terminal BRICHOS domain of surfactant protein C (SFTPC). Here, aggresome formation and severe ER stress was demonstrated in type-II alveolar epithelial cells (AECII), which specifically express this very hydrophobic surfactant protein. In subsequent studies, FIP-patients with mutations in the gene encoding surfactant protein A2 (SFTPA2) were discovered, whose overexpression in epithelial cells in vitro also resulted in significant induction of ER stress. Moreover, prominent ER stress in AECII was also observed in FIP-patients not carrying the SFTPC/SFTPA2 mutations, as well as in patients with the more common sporadic forms of IP. Additionally, cases of adult-onset FIP with mutations in Telomerase genes and other telomereassociated components were reported. These mutations were associated with telomere shortening, which is a potential cause for triggering a persistent DNA damage response and replicative senescence in affected cells. Moreover, shortened telomeres were observed directly in the AECII of FIP-patients, and even sporadic IP cases, in the absence of any gene mutations. Here, we try to figure out the possible origins of ER stress in sporadic IP cases and non-SFTPC/SFTPA2-associated FIP.

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Asbestos-induced Disruption of Calcium Homeostasis Induces Endoplasmic Reticulum Stress in Macrophages

Cited by 37 publications

References 52 publications

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

Endoplasmic reticulum stress in lung disease

The role of Endoplasmic Reticulum (ER) stress in pulmonary fibrosis

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