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2011 ; 18
(3
): 128-35
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Dysregulation of miRNAs in AL amyloidosis
#MMPMID21834602
Weng L
; Spencer BH
; SoohHoo PT
; Connors LH
; O'Hara CJ
; Seldin DC
Amyloid
2011[Sep]; 18
(3
): 128-35
PMID21834602
show ga
Bone marrow plasma cells (BMPCs) were purified using anti-CD138 immunomagnetic
beads, from aspirates obtained with permission of the Boston University Medical
Campus Institutional Review Board, from patients with immunoglobulin light chain
(AL) amyloidosis and from controls. Expression levels of MicroRNAs (miRNAs) were
compared by microarray; 10 were found to be increased more than 1.5-fold. These
results were confirmed using stem-loop RT-qPCR for the most highly upregulated
miRNAs, miR-148a, miR-26a, and miR-16. miR-16, a micro-RNA linked to other
hematopoietic diseases, was significantly increased in the AL group at diagnosis,
and also in treated patients with persistent monoclonal plasma cells in the bone
marrow, but not in patients who achieved a hematologic remission after therapy.
miR-16 can be derived from the miR-16-1/mirR-15, a cluster on chromosome 13 or
the miR-16-2/miR-15b cluster on chromosome 3. The expression of miR-15b was much
higher than miR-15a in both AL and control BMPC, suggesting that miR-16 in plasma
cells is mainly derived from miR-16-2/miR-15b. The anti-apoptosis gene BCL-2, a
putative target mRNA that can be downregulated by miR-16, was expressed in BMPCs
from AL patients, despite elevated levels of miR-16. Our data suggests that
miRNAs are dysregulated in clonal plasma cells in AL amyloidosis and may be
potentially useful as biomarkers of disease.
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