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. 2022 Apr 14;17(1):238.
doi: 10.1186/s13018-022-03035-2.

Long non-coding PRNCR1 regulates the proliferation and apoptosis of synoviocytes in osteoarthritis by sponging miR-377-3p

Guan Wang  1 , Chunhong Li  2 , Xihai Zhang  1 , Lian Tang  1 , Yao Li  3
Affiliations

Long non-coding PRNCR1 regulates the proliferation and apoptosis of synoviocytes in osteoarthritis by sponging miR-377-3p

Guan Wang et al. J Orthop Surg Res. .

Abstract

Background: LncRNA PRNCR1 has been reported to be involved in LPS-induced inflammation, which contributes to osteoarthritis (OA). We predicted that miR-377-3p could bind to PRNCR1.MiR-377-3p can suppress OA development. We therefore analyzed the potential interaction between them in OA.

Methods: Expression of miR-377-3p and PRNCR1 in both OA (n = 40) and control (n = 40) samples were analyzed by RT-qPCR. MiR-377-3p or PRNCR1 were overexpressed in synoviocytes to explore their potential interaction. The subcellular location of PRNCR1 was analyzed by nuclear fractionation assay. The direct interaction between miR-377-3p and PRNCR1 was analyzed by RNA-pull down assay. The proliferation and apoptosis of synoviocytes were analyzed by BrdU and apoptosis assay, respectively.

Results: PRNCR1 was overexpressed in OA, while miR-377-3p was downexpressed in OA. PRNCR1 was detected in the cytoplasm and directly interacted with miR-377-3p. Interestingly, overexpression of PRNCR1 and miR-377-3p showed no regulatory role in each other's expression. LPS treatment increased PRNCR1 expression and decreased miR-377-3p expression. PRNCR1 overexpression decreased LPS-induced synoviocyte proliferation and increased LPS-induced synoviocyte apoptosis. MiR-377-3p played opposite roles in cell proliferation and apoptosis. Moreover, PRNCR1 suppressed the role of miR-377-3p.

Conclusions: Therefore, PRNCR1 is was detected in cytoplasm and regulates synoviocyte proliferation and apoptosis in OA by sponging miR-377-3p.

Keywords: Apoptosis; Osteoarthritis; PRNCR1; Proliferation; miR-377-3p.

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Conflict of interest statement

All other authors declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted.

Figures

Fig. 1
Fig. 1
PRNCR1 and miR-377-3p expression in OA and their correlations. PRNCR1 (A) and miR-377-3p (B) expression in both 40 OA and normal articular cartilage tissues were analyzed by RT-qPCR. The correlations between PRNCR1 and miR-377-3p across OA (C) and normal (D) samples were analyzed using Pearson’s correlation coefficient. **p < 0.01
Fig. 2
Fig. 2
Subcellular location of PRNCR1 in OA synoviocytes and its interaction with miR-377-3p. The subcellular location of PRNCR1 in the nuclear (N) and cytoplasm (C) fractions from OA synoviocytes was analyzed using nuclear fractionation assay (A). The binding of miR-377-3p to PRNCR1 was predicted using IntaRNA 2.0 (B) and confirmed using RNA pull-down assays using biotin-ligated miR-377-3p (Bio-miR-377-3p) or negative control (NC) miRNA (Bio-NC) (C). **p < 0.01
Fig. 3
Fig. 3
Regulatory role of PRNCR1 and miR-377-3p in each other’s expression. PRNCR1 was overexpressed in OA synoviocytes, and PRNCR1 overexpression was confirmed by RT-qPCR every 24 h until 72 h (A). MiR-377-3p was overexpressed in OA synoviocytes, and miR-377-3p overexpression was confirmed by RT-qPCR every 24 h until 72 h (B). The role of PRNCR1 in regulating miR-377-3p expression (C) and the role of miR-377-3p in regulating PRNCR1 expression (D) were analyzed using RT-qPCR. *p < 0.05
Fig. 4
Fig. 4
Role of PRNCR1 and miR-377-3p in the proliferation and apoptosis of OA synoviocytes. OA synoviocytes were treated with 0, 3, 9, 12, and 15 μg/ml LPS (Sigma-Aldrich) for 48 h, and PRNCR1 expression (A) and miR-377-3p expression (B) was analyzed using RT-qPCR after RNA isolation. The role of PRNCR1 and miR-377-3p in regulating the proliferation (C) and apoptosis of synoviocytes induced by LPS (D) were analyzed using cell proliferation and apoptosis analyses. IL-1β expression level was analyzed using qRT-PCR (E). *p < 0.05
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References

    1. Glyn-Jones S, Palmer AJ, Agricola R, Price AJ, Vincent TL, Weinans H, et al. Osteoarthritis. Lancet. 2015;386(9991):376–387. doi: 10.1016/S0140-6736(14)60802-3. - DOI - PubMed
    1. Vina ER, Kwoh CK. Epidemiology of osteoarthritis: literature update. Curr Opin Rheumatol. 2018;30(2):160–167. doi: 10.1097/BOR.0000000000000479. - DOI - PMC - PubMed
    1. Prieto-Alhambra D, Judge A, Javaid MK, Cooper C, Diez-Perez A, Arden NK. Incidence and risk factors for clinically diagnosed knee, hip and hand osteoarthritis: influences of age, gender and osteoarthritis affecting other joints. Ann Rheum Dis. 2014;73(9):1659–1664. doi: 10.1136/annrheumdis-2013-203355. - DOI - PMC - PubMed
    1. Rahmati M, Mobasheri A, Mozafari M. Inflammatory mediators in osteoarthritis: a critical review of the state-of-the-art, current prospects, and future challenges. Bone. 2016;85:81–90. doi: 10.1016/j.bone.2016.01.019. - DOI - PubMed
    1. Bay-Jensen AC, Slagboom E, Chen-An P, Alexandersen P, Qvist P, Christiansen C, et al. Role of hormones in cartilage and joint metabolism: understanding an unhealthy metabolic phenotype in osteoarthritis. Menopause. 2013;20(5):578–586. doi: 10.1097/gme.0b013e3182745993. - DOI - PubMed