Cytoskeletal protein modulation in pulmonary alveolar myofibroblasts during idiopathic pulmonary fibrosis. Possible role of transforming growth factor beta and tumor necrosis factor alpha - PubMed (original) (raw)

Cytoskeletal protein modulation in pulmonary alveolar myofibroblasts during idiopathic pulmonary fibrosis. Possible role of transforming growth factor beta and tumor necrosis factor alpha

Y Kapanci et al. Am J Respir Crit Care Med. 1995 Dec.

Abstract

Pulmonary biopsy specimens from ten cases of idiopathic pulmonary fibrosis (IPF) were examined using routine histological stains, including toluidine blue, and immunohistochemistry by means of specific antibodies against alpha-smooth muscle (alpha-SM) actin, desmin, keratin, TGF beta 1, and TNF alpha. The sections were compared with two cases of normal lung. As shown previously, normal alveolar interstitium did not contain alpha-SM actin positive myofibroblasts nor did the alveolar lining contain any significant number of TGF beta 1 or TNF alpha laden epithelial cells. In IPF, during the inflammatory stage, the alveolar myofibroblasts expressed alpha-SM actin and the regenerating type II alveolar epithelium staining strongly with TGF beta 1 and TNF alpha antibodies. The former cytokine was also detected in the interstitial matrix and fibroblastic cells as well as in the wall of vessels. At this stage, a manifest mast cell infiltration was noted. In very fibrotic and cystic alveolar tissue, i.e., at end stage fibrosis, the number of alpha-SM actin positive myofibroblasts as well as that of TNF alpha laden type II epithelial cells diminished, while TGF beta 1 positive cells persisted. Our findings demonstrate that during IPF alveolar type II epithelium constitutes, if not the site of synthesis, at least the main reservoir for TGF beta 1 and TNF alpha. These cytokines, besides their involvement in fibrogenesis, play probably an important role in the expression of alpha-SM actin by alveolar myofibroblasts. Our study suggests the possibility of an interaction between interstitial cells and alveolar epithelium, during IPF.

PubMed Disclaimer

Cited by

Current and novel drug therapies for idiopathic pulmonary fibrosis.
Adamali HI, Maher TM. Adamali HI, et al. Drug Des Devel Ther. 2012;6:261-72. doi: 10.2147/DDDT.S29928. Epub 2012 Sep 26. Drug Des Devel Ther. 2012. PMID: 23055696 Free PMC article. Review.
Epithelial origin of myofibroblasts during fibrosis in the lung.
Willis BC, duBois RM, Borok Z. Willis BC, et al. Proc Am Thorac Soc. 2006 Jun;3(4):377-82. doi: 10.1513/pats.200601-004TK. Proc Am Thorac Soc. 2006. PMID: 16738204 Free PMC article. Review.
Bone marrow-derived progenitor cells in pulmonary fibrosis.
Hashimoto N, Jin H, Liu T, Chensue SW, Phan SH. Hashimoto N, et al. J Clin Invest. 2004 Jan;113(2):243-52. doi: 10.1172/JCI18847. J Clin Invest. 2004. PMID: 14722616 Free PMC article.
Mesenchymal Stem Cell-Derived Extracellular Vesicles as Idiopathic Pulmonary Fibrosis Microenvironment Targeted Delivery.
Sang L, Guo X, Fan H, Shi J, Hou S, Lv Q. Sang L, et al. Cells. 2022 Jul 28;11(15):2322. doi: 10.3390/cells11152322. Cells. 2022. PMID: 35954166 Free PMC article. Review.

Cytoskeletal protein modulation in pulmonary alveolar myofibroblasts during idiopathic pulmonary fibrosis. Possible role of transforming growth factor beta and tumor necrosis factor alpha - PubMed (original) (raw)