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2015 ; 10
(12
): e0143961
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The Role of M2 Macrophages in the Progression of Chronic Kidney Disease following
Acute Kidney Injury
#MMPMID26630505
Kim MG
; Kim SC
; Ko YS
; Lee HY
; Jo SK
; Cho W
PLoS One
2015[]; 10
(12
): e0143961
PMID26630505
show ga
INTRODUCTION: Acute kidney injury (AKI) is a major risk factor in the development
of chronic kidney disease (CKD). However, the mechanisms linking AKI to CKD
remain unclear. We examined the alteration of macrophage phenotypes during an
extended recovery period following ischemia/reperfusion injury (IRI) and
determine their roles in the development of fibrosis. METHODS: The left renal
pedicle of mice was clamped for 40 min. To deplete monocyte/macrophage, liposome
clodronate was injected or CD11b-DTR and CD11c-DTR transgenic mice were used.
RESULTS: Throughout the phase of IRI recovery, M2-phenotype macrophages made up
the predominant macrophage subset. On day 28, renal fibrosis was clearly shown
with increased type IV collagen and TGF-?. The depletion of macrophages induced
by the liposome clodronate injection improved renal fibrosis with a reduction of
kidney IL-6, type IV collagen, and TGF-? levels. Additionally, the adoptive
transfer of the M2c macrophages partially reversed the beneficial effect of
macrophage depletion, whereas the adoptive transfer of the M1 macrophages did
not. M2 macrophages isolated from the kidneys during the recovery phase expressed
2.5 fold higher levels of TGF-? than the M1 macrophages. The injection of the
diphtheria toxin into CD11b or CD11c-DTR transgenic mice resulted in lesser
depletion or no change in M2 macrophages and had little impact on renal fibrosis.
CONCLUSION: Although M2 macrophages are known to be indispensible for short-term
recovery, they are thought to be main culprit in the development of renal
fibrosis following IRI.