Investigation of bone marrow mesenchymal stem cells (BM MSCs) involvement in idiopathic pulmonary fibrosis (IPF)

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• 作者：Katerina M. Antoniou ; Helen A. Papadaki ; Giannoula Soufla ; Maria Christina Kastrinaki ; Athina Damianaki ; Helen Koutala ; Demetrios A. Sp ; idos ; Nikolaos M. Siafakas
• 关键词：Mesenchymal stem cells ; CXCR4 ; Angiogenesis ; SDF-1a
• 刊名：Respiratory Medicine
• 出版年：2010
• 出版时间：October 2010
• 年：2010
• 卷：104
• 期：10
• 页码：1535-1542
• 全文大小：517 K

文摘

Summary

Background

Experimental data have provided evidence that progenitor cells of bone marrow (BM) origin may play a role in the fibrogenic process of the lung.

Objective

To probe the possible involvement of BM mesenchymal stem cells (MSCs) in the pathophysiology of Idiopathic Pulmonary Fibrosis (IPF) by investigating the molecular profile of these cells.

Design

BM MSCs were studied in 10 IPF patients and 10 healthy controls. MSCs were identified by their immunophenotypic characteristics and their potential to differentiate towards adipocytes/osteocytes/chondrocytes. We evaluated the mRNA expression of genes involved in the lung injury of IPF, namely the vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), transforming growth factor beta-1 (TGF-β1) and the axis stromal-cell-derived factor-1 (SDF-1)/CXCR4 in BM MSCs using quantitative RT-PCR.

Results

The BM MSCs of IPF patients displayed normal immunophenotypic characteristics and differentiation potential. No statistically significant difference was found between patients and controls in VEGF and FGF mRNA expression. TGF-β1 was not expressed in either patients or controls. A significant increase in SDF-1-TR1 and CXCR4 mRNA expression was detected in IPF patients (1.6 × 10²⁵ ± 1.2 × 10²⁵ and 3.1 × 10⁷ ± 3.1 × 10⁷, respectively) compared to controls (0.32 × 10²⁵ ± 0.07 × 10²⁵ and 1.67 × 10⁷ ± 0.30 × 10⁷, respectively) (p = 0.001 and p = 0.001, respectively) whereas SDF-1 levels in MSC supernatants were similar in patients and controls.

Conclusions

The increased CXCR4 expression by patient MSCs suggests that the BM is probably implicated in the pathophysiology of IPF by mobilizing MSCs in response to or preceding lung injury. The potential role of BM MSCs in IPF is another interesting field for further investigation.