Cyclosporine-A induces endoplasmic reticulum stress in human gingival fibroblasts – An in vitro study

Rao, Suresh Ranga; Ajitkumar, Supraja; Rajasekaran, Subbiah; Girija, Dinesh Murugan

doi:10.1016/j.jobcr.2016.11.002

Cited by 6 publications

(9 citation statements)

References 14 publications

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“…Treatment of cyclosporine could induce the ER stress level and secretion of ECM in HGFs, with the up-regulation of ER stress markers (GRP78 and CHOP) and fibrosis markers (α smooth muscle actin (αSMA), transforming growth factor β (TGFβ), and connective tissue growth factor (CTGF)) expression. [35][36][37][38] The expression of XBP1 and XBP1s was increased by cyclosporine as well, furthermore, XBP1s expression was comparatively higher than XBP1. 35,38 4-PBA reversed the effect of cyclosporine on ER stress and reduced the ECM.…”

Section: Effec T Of Er S Tre Ss On Periodontal Sof T Tissue Remodelingmentioning

confidence: 99%

“…[35][36][37][38] The expression of XBP1 and XBP1s was increased by cyclosporine as well, furthermore, XBP1s expression was comparatively higher than XBP1. 35,38 4-PBA reversed the effect of cyclosporine on ER stress and reduced the ECM. 35 The periodontal inflammatory environment caused by P. gingivalis lipopolysaccharide (LPS) induced the ER stress in human periodontal ligament cells (hPDLCs).…”

Section: Effec T Of Er S Tre Ss On Periodontal Sof T Tissue Remodelingmentioning

confidence: 99%

“…Up‐regulation of GRP78 (Ref. [34–38,40,41,51–53,55,59,61,65,67–69]), ATF6 (Ref. [67,69]), PERK/p‐PERK (Ref.…”

Section: Introductionmentioning

confidence: 99%

“…[34,55,59,61,64,65,69,71]), CHOP (Ref. [34–38,40,51,53,55; 59,61,63,67–70]), IRE1/p‐IRE1 (Ref. [34,53,54,69,76]), XBP1 (Ref.…”

Section: Introductionmentioning

confidence: 99%

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The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

Jiang

Zhu

2022

J of Periodontal Research

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The endoplasmic reticulum (ER) is a principal organelle for folding, post‐translational modifications and transport of secretory, luminal, and membrane proteins. ER stress is a condition induced by the accumulation of unfolded or misfolded proteins owing to a variety of physiological and pathological phenomena. To overcome the deleterious effects of ER stress, unfolded protein response (UPR) is initiated to translocate and remove the misfolded and accumulated proteins. Plenty of evidence shows the correlation between ER stress/UPR and the pathology of inflammatory disease. Periodontal disease is a chronic inflammatory disease characterized by the irreversible destruction of periodontal tissues, which associates with the onset and progress of several systemic diseases. Periodontopathic bacterium and pro‐inflammatory mediators play a pivotal role in the progress of periodontal disease. Besides, cigarette smoke has long been associated with periodontal disease. As an inflammatory disorder of the periodontium, periodontal disease is highly related to ER stress. In this review, we provide an overview of the pathophysiological effect of ER stress on periodontal disease through five aspects as follow: ER stress and periodontal tissue remodeling, including both soft tissue and hard tissue; ER stress and the inflammation; ER stress and systematic effect during the periodontal disease; last but not least, ER stress and the autophagic apoptosis in cells.

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Section: Effec T Of Er S Tre Ss On Periodontal Sof T Tissue Remodelingmentioning

confidence: 99%

Section: Effec T Of Er S Tre Ss On Periodontal Sof T Tissue Remodelingmentioning

confidence: 99%

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The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

Jiang

Zhu

2022

J of Periodontal Research

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“…This can cause cellular dysfunction and even the onset of a disease [13]. Such diseases may be the result of the cells' decreased ability to fold secreted membrane proteins, or a low ability to recognize or respond to misfolded protein and/or increased secretion of abnormally folded proteins [25].…”

Section: Figurementioning

confidence: 99%

Endoplasmic Reticulum Involvement in Drug-Induced Gingival Overgrowth

GORIUC¹

2021

FARMACIA

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Gingival overgrowth is an undesirable and well-recognized side effect following the use of various drugs, such as phenytoin, nifedipine and cyclosporine A (CsA). Apoptosis constitutes a necessary process for constant tissue remodelling, its absence playing a critical role in gingival overgrowth. The aim of this study was to evaluate the effects of THP (thapsigargin), brefeldin A, cyclopiazonic acid, and capsaicin on the endoplasmic reticulum (ER) and their involvement in apoptosis of normal fibroblasts compared with those treated with drugs. These substances are well known for inducing stress in the ER through different mechanisms, thus leading to the induction of apoptosis. In conclusion, ER stress induction in normal fibroblasts using cyclopiazonic acid, THP, brefeldin A and capsaicin had no significant effects on mitochondrial permeability transition pore opening. In the case of CsA or nifedipine pre-treatment, cyclopiazonic acid, capsaicin and THP decreased mitochondrial calcein, suggesting that the opening of mitochondrial permeability transition pore (MPTP) is due to ER stress. For the phenytoin pre-treatment case, only cyclopiazonic acid, and capsaicin have induced significant effects on MPTP. RezumatHipercreșterea gingivală reprezintă un efect secundar ce apare la administrarea mai multor substanțe medicamentoase, precum fenitoină, nifedipină și ciclosporină. Apoptoza constituie un proces indispensabil pentru remodelarea tisulară continuă, iar absența acesteia joacă un rol important în hipercreșterea gingivală. Scopul prezentului studiu a fost evaluarea efectelor thapsigargin (THP), brefeldin A, acidului ciclopiazonic și a capsaicinei asupra reticulului endoplasmic (RE) și implicarea în apoptoza fibroblastelor tratate cu substanțele menționate. În concluzie, inducerea stresului la nivelul RE în culturile de fibroblaste normale tratate cu THP, brefeldin A, acid ciclopiazonic și capsaicină nu a influențat semnificativ deschiderea porului de permeabilitate tranzitorie mitocondrială (MPTP). În cazul tratamentului prealabil cu ciclosporină A sau cu nifedipină, acidul ciclopiazonic, capsaicina și THP au determinat scăderea încărcării mitocondriale cu calceină, sugerând că deschiderea MPTP se datorează stresului RE. În cazul pre-tratamentului cu fenitoină, doar acidul ciclopiazonic și capsaicina au indus modificări semnificative asupra MPTP.

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Radioprotective effect of Hohenbuehelia serotina polysaccharides through mediation of ER apoptosis pathway in vivo

Wang

2019

International Journal of Biological Macromolecules

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Cyclosporine-A induces endoplasmic reticulum stress in human gingival fibroblasts – An in vitro study

Cited by 6 publications

References 14 publications

The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

Endoplasmic Reticulum Involvement in Drug-Induced Gingival Overgrowth

Radioprotective effect of Hohenbuehelia serotina polysaccharides through mediation of ER apoptosis pathway in vivo

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