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Connective tissue growth factor stimulates the proliferation, migration and
differentiation of lung fibroblasts during paraquat-induced pulmonary fibrosis
#MMPMID25815693
Yang Z
; Sun Z
; Liu H
; Ren Y
; Shao D
; Zhang W
; Lin J
; Wolfram J
; Wang F
; Nie S
Mol Med Rep
2015[Jul]; 12
(1
): 1091-7
PMID25815693
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It is well established that paraquat (PQ) poisoning can cause severe lung injury
during the early stages of exposure, finally leading to irreversible pulmonary
fibrosis. Connective tissue growth factor (CTGF) is an essential growth factor
that is involved in tissue repair and pulmonary fibrogenesis. In the present
study, the role of CTGF was examined in a rat model of pulmonary fibrosis induced
by PQ poisoning. Histological examination revealed interstitial edema and
extensive cellular thickening of interalveolar septa at the early stages of
poisoning. At 2 weeks after PQ administration, lung tissue sections exhibited a
marked thickening of the alveolar walls with an accumulation of interstitial
cells with a fibroblastic appearance. Masson's trichrome staining revealed a
patchy distribution of collagen deposition, indicating pulmonary fibrogenesis.
Western blot analysis and immunohistochemical staining of tissue samples
demonstrated that CTGF expression was significantly upregulated in the PQ-treated
group. Similarly, PQ treatment of MRC-5 human lung fibroblast cells caused an
increase in CTGF in a dose-dependent manner. Furthermore, the addition of CTGF to
MRC-5 cells triggered cellular proliferation and migration. In addition, CTGF
induced the differentiation of fibroblasts to myofibroblasts, as was evident from
increased expression of ?-smooth muscle actin (?-SMA) and collagen. These
findings demonstrate that PQ causes increased CTGF expression, which triggers
proliferation, migration and differentiation of lung fibroblasts. Therefore, CTGF
may be important in PQ-induced pulmonary fibrogenesis, rendering this growth
factor a potential pharmacological target for reducing lung injury.
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