Detection of apoptosis in pemphigus vulgaris by TUNEL technique

Cuevas-González, Juan Carlos; Vega‐Memije, María Elisa; García-Vázquez, Francisco; Aguilar-Urbano, Marco António

doi:10.1590/abd1806-4841.20164598

Cited by 9 publications

(6 citation statements)

References 8 publications

(8 reference statements)

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“…Previously, many studies have demonstrated that cellular apoptosis participates in disc degeneration [25–28]. In most cases, apoptosis is identified by the method of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining [29–31]. Moreover, a previous study has reported that the IVDs from patients have considerably more TUNEL-positive cells than the healthy control discs [15].…”

Section: Discussionmentioning

confidence: 99%

Mechano growth factor attenuates mechanical overload-induced nucleus pulposus cell apoptosis through inhibiting the p38 MAPK pathway

Fang

Zhao

et al. 2019

Bioscience Reports

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Mechanical overload is a risk factor of disc degeneration. It can induce disc degeneration through mediating cell apoptosis. Mechano growth factor (MGF) has been reported to inhibit mechanical overload-induced apoptosis of chondrocytes. The present study is aimed to investigate whether MGF can attenuate mechanical overload-induced nucleus pulposus (NP) cell apoptosis and the possible signaling transduction pathway. Rat NP cells were cultured and subjected to mechanical overload for 7 days. The control NP cells did not experience mechanical load. The exogenous MGF peptide was added into the culture medium to investigate its protective effects. NP cell apoptosis ratio, caspase-3 activity, gene expression of Bcl-2, Bax and caspase-3, protein expression of cleaved caspase-3, cleaved PARP, Bax and Bcl-2 were analyzed to evaluate NP cell apoptosis. In addition, activity of the p38 MAPK pathway was also detected. Compared with the control NP cells, mechanical overload significantly increased NP cell apoptosis and caspase-3 activity, up-regulated gene/protein expression of pro-apoptosis molecules (i.e. Bax, caspase-3, cleaved caspase-3 and cleaved PARP) whereas down-regulated gene/protein expression of anti-apoptosis molecule (i.e. Bcl-2). However, exogenous MGF partly reversed these effects of mechanical overload on NP cell apoptosis. Further results showed that activity of the p38 MAPK pathway of NP cells cultured under mechanical overload was decreased by addition of MGF peptide. In conclusion, MGF is able to attenuate mechanical overload-induced NP cell apoptosis, and the p38 MAPK signaling pathway may be involved in this process. The present study provides that MGF supplementation may be a promising strategy to retard mechanical overload-induced disc degeneration.

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Section: Discussionmentioning

confidence: 99%

Mechano growth factor attenuates mechanical overload-induced nucleus pulposus cell apoptosis through inhibiting the p38 MAPK pathway

Fang

Zhao

et al. 2019

Bioscience Reports

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“…The possibility that these apoptotic pathways can be active in pemphigus was demonstrated in several studies ( 79 , 154 , 302 , 306 – 310 ). Apoptosis can occur in the skin ( 307 , 309 , 311 , 312 ) as well as the mucosa ( 308 ) of pemphigus patients. However, in acantholytic areas apoptotic cell death is not typically observed ( 154 , 177 , 178 ).…”

Section: Pre-apoptotic Caspase Signalling Reducing Dsg1 and Dsg3 In Pemphigusmentioning

confidence: 99%

Autoantibody-Specific Signalling in Pemphigus

Schmitt

Waschke

2021

Front. Med.

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Pemphigus is a severe autoimmune disease impairing barrier functions of epidermis and mucosa. Autoantibodies primarily target the desmosomal adhesion molecules desmoglein (Dsg) 1 and Dsg 3 and induce loss of desmosomal adhesion. Strikingly, autoantibody profiles in pemphigus correlate with clinical phenotypes. Mucosal-dominant pemphigus vulgaris (PV) is characterised by autoantibodies (PV-IgG) against Dsg3 whereas epidermal blistering in PV and pemphigus foliaceus (PF) is associated with autoantibodies against Dsg1. Therapy in pemphigus is evolving towards specific suppression of autoantibody formation and autoantibody depletion. Nevertheless, during the acute phase and relapses of the disease additional treatment options to stabilise desmosomes and thereby rescue keratinocyte adhesion would be beneficial. Therefore, the mechanisms by which autoantibodies interfere with adhesion of desmosomes need to be characterised in detail. Besides direct inhibition of Dsg adhesion, autoantibodies engage signalling pathways interfering with different steps of desmosome turn-over. With this respect, recent data indicate that autoantibodies induce separate signalling responses in keratinocytes via specific signalling complexes organised by Dsg1 and Dsg3 which transfer the signal of autoantibody binding into the cell. This hypothesis may also explain the different clinical pemphigus phenotypes.

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“…Specifically, auto-antibody binding to a myriads of pemphigus autoantigens leads to initiation of apoptotic enzyme cascades in keratinocytes, resulting in basal cell shrinkage and supra-basal acantholysis [ 4 ]. Studies show that there is a notable increase in the expression of both caspases and apoptotic cells in PV patients [ 5 , 6 , 7 , 8 , 9 ], and that apoptosis in PV takes place via both intrinsic and extrinsic pathways. The extrinsic apoptotic pathway in PV includes the Fas receptor (FasR) which is located at the cell surface of keratinocytes [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Caspase Inhibition as a Possible Therapeutic Strategy for Pemphigus Vulgaris: A Systematic Review of Current Evidence

HudaSanna

Chau

Chen

et al. 2022

Biology

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Background: Pemphigus vulgaris (PV) is an IgG-mediated autoimmune disease characterised by epithelial cell–cell detachment (acantholysis) resulting in mucocutaneous blistering. The exact pathogenesis of blister formation is unknown and this has hampered the development of non-steroidal, mechanism-based treatments for this autoimmune disease. This systematic review aims to investigate the role of caspases in the pathogenesis of PV to inform the choice of more targeted therapeutic agents. Methods: A systematic search of MEDLINE/PubMed and Scopus databases was conducted to identify eligible studies. Multiple phases of inclusion and exclusion of the primary articles were conducted in pairs, and studies were recorded and analysed according to the latest version of the preferred reporting items for systematic reviews and meta-analyses (PRISMA). Risk of bias assessment was conducted for extracted in vivo animal intervention studies using SYRCLE’s risk of bias tool. Results: Eight articles from a total of 2338 in vitro, in vivo, and human studies met the inclusion criteria, with a high degree of inter-rater reliability. By and large, the results show that caspase activation was pathogenic in experimental PV because pan-caspase inhibitors could block or reduce PV acantholysis and blistering in vitro and in vivo, respectively. The pathogenic pathways identified involved caspase-1 and caspase-3. One study failed to show any improvement in the PV model with a caspase inhibitor. The majority of animal studies had high or unclear risk of bias. Conclusion: There are consistent data pointing towards a pathogenic role of caspase activation in PV acantholysis. However, high-quality evidence to confirm that caspase inhibition can prevent PV-induced blistering in vivo is limited. Therefore, further research is required to test the preclinical efficacy of caspase inhibitors in PV.

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Detection of apoptosis in pemphigus vulgaris by TUNEL technique

Cited by 9 publications

References 8 publications

Mechano growth factor attenuates mechanical overload-induced nucleus pulposus cell apoptosis through inhibiting the p38 MAPK pathway

Mechano growth factor attenuates mechanical overload-induced nucleus pulposus cell apoptosis through inhibiting the p38 MAPK pathway

Autoantibody-Specific Signalling in Pemphigus

Caspase Inhibition as a Possible Therapeutic Strategy for Pemphigus Vulgaris: A Systematic Review of Current Evidence

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