Published online Jun 26, 2020. doi: 10.12998/wjcc.v8.i12.2530
Peer-review started: February 24, 2020
First decision: March 27, 2020
Revised: May 9, 2020
Accepted: May 19, 2020
Article in press: May 19, 2020
Published online: June 26, 2020
Processing time: 120 Days and 21.7 Hours
Previous publications indicated that genetic predisposition might play important roles in the onset of osteonecrosis of the femoral head (ONFH) in systemic lupus erythematosus (SLE).
Complement C3d receptor 2 (CR2), nitric oxide synthase 3 (NOS3), collagen type II alpha 1 chain (COL2A1), protein tyrosine phosphatase non-receptor type 22 (PTPN22), and transient receptor potential cation channel subfamily V member 4 (TRPV4) were reported to be involved in the onset of ONFH in SLE.
To investigate whether the risk of ONFH in SLE is associated with single nucleotide variations (SNVs) in CR2, NOS3, COL2A1, PTPN22, and TRPV4.
SNVs in the CR2, NOS3, COL2A1, PTPN22, and TRPV4 genes were examined by using FastTarget and Illumina Miseq sequencing technologies in 49 cases of SLE with ONFH. Burrows–wheeler aligner was used to align the sequencing reads to hg19, and GATK and Varscan programs were used to perform SNV calling. PolyPhen-2, SIFT, and MutationTaster were used to assess the functional effects of non-synonymous SNVs.
Six patients were confirmed to have low frequency SNVs, including one patient with SNVs in NOS3 (exon 6: c.814G>A: p.E272K and exon 7: c.814G>A: p.E272K.), four in COL2A1 (rs41263847: exon 29: c.1913C>T: p.T638I, exon 28: c.1706C>T: p.T569I, and rs371445823: exon 8: c.580G>A: p.A194T, exon 7: c.373G>A: p.A125T), and one in CR2 (rs45573035: exon 2: c.200C>G: p.T67S).
The onset of ONFH in SLE might be associated with the identified SNVs in NOS3, COL2A1, and CR2. And the low frequency functional mutations in NOS3 had never been reported previously.
These findings may have important pharmacogenetic implications. But the detailed mechanisms of the associations need to be determined in further studies.