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MiR-29b expression is altered in crescent formation of HSPN and accelerates Ang II-induced mesangial cell activation

  • Shan Cheng
  • Chun-Hua Zhu
  • Ai-Hua Zhang
  • Song-Ming HuangEmail author
Original Article
  • 87 Downloads

Abstract

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.

Keywords

Cell proliferation Crescent Inflammation MiR-29b 

Notes

Author contribution

SC participated in the study design, collection of clinical data, performed experiments analysis and results interpretation, and drafted the paper. CHZ participated in the study design and revised the manuscript. AHZ participated in the study design and revised the manuscript. SMH participated in the study design, performed genotyping and statistical analysis and revised the manuscript. All authors approved the final version of the manuscript.

Funding

This study was supported by Clinical Medicine Science and Technology Project of Jiangsu Province (BL2014007).

Compliance with ethical standards

Ethical approval

All procedures performed in studies involving human participants were approved by the Ethics Committee of Nanjing Medical University. Parents of study participants were given oral informed consent.

Conflict of interest

No financial or nonfinancial benefits have been received or will be received from any party related directly or indirectly to the subject of this article.

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Copyright information

© Children's Hospital, Zhejiang University School of Medicine 2019

Authors and Affiliations

  • Shan Cheng
    • 1
  • Chun-Hua Zhu
    • 2
  • Ai-Hua Zhang
    • 2
  • Song-Ming Huang
    • 2
    Email author
  1. 1.Department of Infectious DiseaseChildren’s Hospital of Nanjing Medical UniversityNanjingChina
  2. 2.Department of NephrologyChildren’s Hospital of Nanjing Medical UniversityNanjingChina

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