Cigarette Smoke Condensate Exposure Induces Receptor for Advanced Glycation End-Products (RAGE)-Dependent Sterile Inflammation in Amniotic Epithelial Cells
"> Figure 1
<p>CSC treatment induces a cell danger response into amnion. (<b>A</b>) Cell toxicity was evaluated by measuring LDH release in a supernatant culture after a 24 h treatment with CSC in amnion and choriodecidua (<span class="html-italic">n</span> = 6). (<b>B</b>) HMGB1 release in a supernatant culture after a 48 h treatment with CSC was quantified by the western blot method in amnion and chori-odecidua; the results are reported in the histogram (<span class="html-italic">n</span> = 5). (<b>C</b>) Toxicity was evaluated by LDH release measurement in primary amniocytes (pAECs) cell-culture supernatants after a 48 h treatment with CSC (100 µg/mL) (<span class="html-italic">n</span> = 6). (<b>D</b>) HMGB1 nuclear toward cytosolic translocation was investigated by immunocytochemistry on pAECs after 7 h treatment with CSC (yellow staining; Alexa488). Nuclei were counterstained with Hoechst (red). Scales bars: 50 µM (magnification ×200). Negative control was realized without primary antibody hybridization. White arrows indicate the cytosolic cloud of HMGB1. Comparison with the control (DMSO) was realized by a Mann-Whitney <span class="html-italic">t</span>-test. *** means <span class="html-italic">p</span> < 0.001, and “ns” means “not significant”. Results are presented in Tukey boxes; means are indicated by “+”.</p> "> Figure 2
<p>Amniotic epithelial cells expressed a functional RAGE axis. (<b>A</b>) RNA expressions of RAGE, TIRAP, Myd88, and Diaphanous-1 were detected by RT-PCR in pAECS. Negative controls were performed in the absence of a cDNA template. (<b>B</b>) The RAGE receptor and its adaptors, Diaphanous-1, MyD88, and TIRAP (green staining, Alexa488), were detected by immunocytochemistry on primary amniocytes (pAECs). Nuclei were counterstained with Hoechst (blue). Scales bars: 50 µM (magnification ×200). Negative control was realized without primary antibody hybridization.</p> "> Figure 3
<p>Activation of RAGE axis by CSC-response in pAECs. (<b>A</b>) Quantification of RAGE and its signaling adaptors (Diapahnous-1, Myd88, and TIRAP) transcription by RT-qPCR following 48 h of CSC (100 µg/mL) +/− RAP (12.7 µg/mL) treatment of pAECs (<span class="html-italic">n</span> = 7). (<b>B</b>) NFκB luciferase reporter assay was performed after 48 h of CSC treatment (100 µg/mL), whether combined or not with RAP (12.7 µg/mL) (<span class="html-italic">n</span> = 4). (<b>C</b>) p65-NFκB relocalization was investigated by immunocytochemistry on pAECs, whether treated or not with CSC for 48 h (yellow staining; Alexa488). Nuclei were counterstained with Hoechst (red). Scales bars: 50 µM (magnification ×200). Negative controls were realized without primary antibody hybridization. White arrows indicate perinuclear/nuclear relocalization of the p65 protein. A comparison of conditions was realized by a Kruskal–Wallis one-way ANOVA test, followed by a Dunn’s post-test. ** means <span class="html-italic">p</span> < 0.01, *** means <span class="html-italic">p</span> < 0.001, and “ns” means “not significant”. Results are presented in Tukey boxes, and means are indicated by “+”.</p> "> Figure 4
<p>RAGE is implicated in CSC-induced pro-inflammatory cytokine production in pAECs. (<b>A</b>) Quantification of cytokine mRNA expression by RT-qPCR following 48 h of CSC (100 µg/mL) +/− RAP (12.7 µg/mL) treatment of pAECs (<span class="html-italic">n</span> = 6). (<b>B</b>) Pro-inflammatory cytokine (IL8, IL6, IL1β) secretion was quantified by ELLA technology after 48 and 72 h (with 48 h re-treatment) of CSC treatment (<span class="html-italic">n</span> = 4). A comparison of conditions was realized by a Kruskal–Wallis one-way ANOVA test, followed by a Dunn’s post-test. * means <span class="html-italic">p</span> < 0.05, ** means <span class="html-italic">p</span> < 0.01, *** means <span class="html-italic">p</span> < 0.001, and “ns” means “not significant”. Cigarette Smoke Condensate Enhances Gelatinase Activity in pAECs through the RAGE Pathway.</p> "> Figure 5
<p>CSC exposure stimulates gelatinase activity in pAECs through the RAGE pathway. (<b>A</b>) Transcription of MMP2 and MMP9 gelatinases were measured by RT-qPCR into pAECS after 48 h of CSC treatment (100 µg/mL), whether combined or not with RAP (12.7 µg/mL) (<span class="html-italic">n</span> = 8). (<b>B</b>) Gelatinase activity was studied by a zymography kit assay on pAECs cell media after 48 and 72 h (with 48 h re-treatment) of CSC treatment (<span class="html-italic">n</span> = 5). Statistical analysis was performed using a Kruskal–Wallis one-way ANOVA test, followed by a Dunn’s post-test. * means <span class="html-italic">p</span> < 0.05, ** means <span class="html-italic">p</span> < 0.01, *** means <span class="html-italic">p</span> < 0.001, and “ns” means “not significant”. Results are presented in Tukey boxes, and means are indicated by “+”. Black dots indicate values outside of the Tukey boxes.</p> "> Figure 6
<p>Maternal tabagism model of negative consequences on amniotic cells by the induction of RAGE-dependent sterile inflammation and gelatinase activity. Sterile inflammation is a key phenomenon of FM weakening, not only in physiological rupture, but also in pPROM. Exposure to tobacco during pregnancy is a well-known risk factor of pPROM. We demonstrated here that CSC induces an in vitro HMGB1 release by the amnion, a well-known danger signal. Then, this alarmin, a major ligand of RAGE, can induce a pro-inflammatory response (NF-κB activation and cytokine production) through the RAGE pathway in amniotic epithelial cells, which suggests the essential role of RAGE in FM rupture and pPROM. smart.servier.com was used to create the figure.</p> ">
Abstract
:1. Introduction
2. Results
2.1. Cigarette-Smoke Condensate Induces a Danger Response in the Fetal Amnion and Its Cells
2.2. RAGE Axis Actors Are Expressed in Primary Amniotic Epithelial Cells (pAECS)
2.3. Cigarette Smoke Condensate Induces RAGE Signaling Cascade in pAECs
2.4. Cigarette Smoke Condensate Induces Pro-Inflammatory Response in pAECs
3. Discussion
4. Materials and Methods
4.1. Chemicals
4.2. Tissue Collection
4.3. Tissue and Cell Culture
4.4. Tissue and Cell Treatment
4.5. Global Cellular Distress Determination
4.6. Western Blot Analysis of HMGB1 Release
4.7. RT-PCR and Quantitative RT-PCR on Explants and Cells
4.8. Cytokine Release Assay
4.9. Immunofluorescence
4.10. NFκB Gene Reporter Luciferase Assay
4.11. Gelatinase Activity Measurement
4.12. Statistical Analysis
Supplementary Materials
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Conflicts of Interest
References
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Gene | Sequence 5′-3′ (F: Forward, r: Reverse) | Product Size (bp) | Annealing Temperature (°C) |
---|---|---|---|
hsRAGE | F: TGTGCTGATCCTCCCTGAGA | 139 | 61 |
R: TGCAGTTGGCCCCTCCTCG | |||
hs36B4 | F: AGGCTTTAGGTATCACCACT | 219 | 61 |
R: GCAGAGTTTCCTCTGTGATA | |||
hsRSP17 | F: TGCGAGGAGATCGCCATTATC | 169 | 61 |
R: AAGGCTGAGACCTCAGGAAC | |||
hsMyD88 | F: GCAGGAGGAGGCTGAGAAGC | 177 | 66 |
R: CGGATCATCTCCTGCACAAACT | |||
hsTIRAP | F: AAGTACCAGATGCTGCAGGCC | 200 | 66 |
R: AGTGTCAACTGAGTGTCTGCAG | |||
hsDia-1 | F: AGAGCCACACTTCCTTTCCATC | 167 | 66 |
R: TCAATCTCAATCTGGAGGTGCC | |||
hsIL6 | F: AATGAGGAGACTTGCCTGGTG | 143 | 61 |
R: AGGAACTGGATCAGGACTTTTG | |||
hsIL8 | F: TGATTTCTGCAGCTCTGTGTG | 154 | 61 |
R: TCTGTGTTGGCGCAGTGTGG | |||
hsIL1β | F: AATCTCCGACCACCACTACAG | 174 | 62 |
R: TCCCATGTGTCGAAGAAGATAG | |||
hsMMP9 | F: ATTGACGACGCCTTTGCCCG | 201 | 61 |
R: ATGGGCGTCTCCCTGAATGC | |||
hsMMP2 | F: AGCTCATCGCAGATGCCTGG | 199 | 61 |
R: AAGGGCCTGTGGGAGCCAG |
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Choltus, H.; Minet-Quinard, R.; Belville, C.; Durif, J.; Gallot, D.; Blanchon, L.; Sapin, V. Cigarette Smoke Condensate Exposure Induces Receptor for Advanced Glycation End-Products (RAGE)-Dependent Sterile Inflammation in Amniotic Epithelial Cells. Int. J. Mol. Sci. 2021, 22, 8345. https://doi.org/10.3390/ijms22158345
Choltus H, Minet-Quinard R, Belville C, Durif J, Gallot D, Blanchon L, Sapin V. Cigarette Smoke Condensate Exposure Induces Receptor for Advanced Glycation End-Products (RAGE)-Dependent Sterile Inflammation in Amniotic Epithelial Cells. International Journal of Molecular Sciences. 2021; 22(15):8345. https://doi.org/10.3390/ijms22158345
Chicago/Turabian StyleCholtus, Helena, Régine Minet-Quinard, Corinne Belville, Julie Durif, Denis Gallot, Loic Blanchon, and Vincent Sapin. 2021. "Cigarette Smoke Condensate Exposure Induces Receptor for Advanced Glycation End-Products (RAGE)-Dependent Sterile Inflammation in Amniotic Epithelial Cells" International Journal of Molecular Sciences 22, no. 15: 8345. https://doi.org/10.3390/ijms22158345