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MiR-29b expression is altered in crescent formation of HSPN and accelerates Ang II-induced mesangial cell activation
Shan Cheng1, Chun-Hua Zhu2, Ai-Hua Zhang2
1Department of Infectious Disease, Children's Hospital of Nanjing Medical University, 72 Guangzhou Road, Nanjing, 210008, China.
Background:
MicroRNA-29b (miR-29b) has been suggested to possess pro-inflammatory activity, which can partially be explained by the repression of tumor necrosis factor alpha protein three antibody (TNFAIP3). Meanwhile, it also promotes thyroid cell proliferation via Smad signaling pathways. The present study aimed to elucidate the role of miR-29b in Henoch Schönlein purpura nephritis (HSPN) and its underlying molecular mechanism in angiotensin II (Ang II)-induced human glomerular mesangial cell (HGMC) activation.
Methods:
We evaluated miR-29b expression in 35 HSPN renal tissues based on crescent formation, glomerular sclerosis, interstitial fibrosis, thrombosis formation and capillary loop necrosis. Meanwhile, HGMCs were cultured, treated with Ang II and then transfected with LV-hsa-miR-29b-1 to induce miR-29b overexpression or LV-hsa-miR-29b-3p-inhibition to inhibit miR-29b expression. Finally, we examined the effects of miR-29b on cell proliferation and release of inflammatory mediators.
Results:
We observed that miR-29b expression was significantly higher in the crescent group than in the no crescent group. MiR-29b overexpression induced the release of intercellular adhesion molecule-1, interleukin-1β (IL-1β), IL-6, IL-8, the increase of CyclinA2, CyclinD1, and cell proliferation. It also could inhibit the expressions of TNFAIP3 and NF-kappa-B-repressing factor (NKRF). Correspondingly, miR-29b inhibition produced the opposite effects and increased the expression of TNFAIP3 and NKRF.
Conclusion:
MiR-29b expression is altered in crescent formation of HSPN and accelerates Ang II-induced mesangial cell proliferation and release of inflammatory mediators.
Insights
MicroRNA-29b (miR-29b) is elevated in Henoch Schönlein purpura nephritis (HSPN) with crescents. It drives mesangial cell proliferation and inflammation by inhibiting TNFAIP3 and NKRF, contributing to HSPN progression.
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- MicroRNA-29b (miR-29b) exhibits pro-inflammatory properties by repressing TNFAIP3.
- miR-29b promotes cell proliferation via Smad signaling pathways.
- The role of miR-29b in Henoch Schönlein purpura nephritis (HSPN) and its mechanism in angiotensin II (Ang II)-induced human glomerular mesangial cell (HGMC) activation requires elucidation.
Purpose of the Study:
- To investigate the role of miR-29b in HSPN.
- To elucidate the molecular mechanism of miR-29b in Ang II-induced HGMC activation.
Main Methods:
- miR-29b expression was assessed in 35 HSPN renal tissues.
- HGMCs were treated with Ang II and transfected for miR-29b overexpression or inhibition.
- Effects on cell proliferation and inflammatory mediator release were examined.
Main Results:
- miR-29b expression was significantly higher in HSPN renal tissues with crescents.
- miR-29b overexpression increased HGMC proliferation, inflammatory mediator release (ICAM-1, IL-1β, IL-6, IL-8), and inhibited TNFAIP3/NKRF.
- miR-29b inhibition reversed these effects, increasing TNFAIP3/NKRF expression.
Conclusions:
- miR-29b expression is altered in HSPN crescent formation.
- miR-29b accelerates Ang II-induced mesangial cell proliferation and inflammatory mediator release in HSPN.
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