scholarly journals Essential role of stem cell factor-c-Kit signalling pathway in bleomycin-induced pulmonary fibrosis

2013 ◽  
Vol 230 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Lin Ding ◽  
Vladilsav Dolgachev ◽  
Zhuang Wu ◽  
Tianju Liu ◽  
Taku Nakashima ◽  
...  
Keyword(s):  
Stem Cell ◽  
Pulmonary Fibrosis ◽  
Stem Cell Factor ◽  
Essential Role ◽  
Signalling Pathway ◽  
Factor C

Essential Role Of Stem Cell Factor In Bleomycin-Induced Pulmonary Fibrosis

2011 ◽  
Author(s):  
Lin Ding ◽  
Vladilsav Dolgachev ◽  
Zhuang Wu ◽  
Tianju Liu ◽  
Zhe Wu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Pulmonary Fibrosis ◽  
Stem Cell Factor ◽  
Essential Role

scholarly journals The Paracrine Role of Stem Cell Factor/c-kit Signaling in the Activation of Human Melanocytes in Ultraviolet-B-Induced Pigmentation

2001 ◽  
Vol 116 (4) ◽  
pp. 578-586 ◽  
Author(s):  
Akira Hachiya ◽  
Akemi Kobayashi ◽  
Atsushi Ohuchi ◽  
Yoshinori Takema ◽  
Genji Imokawa
Keyword(s):  
Stem Cell ◽  
Stem Cell Factor ◽  
Ultraviolet B ◽  
Human Melanocytes ◽  
Factor C

Activation Of Stem Cell Factor/c-Kit Signaling Pathway In Pulmonary Fibrosis

2010 ◽  
Author(s):  
Lin Ding ◽  
Zhuang Wu ◽  
Tianju Liu ◽  
Matthew Ullenbruch ◽  
Jianhua Liu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Pulmonary Fibrosis ◽  
Signaling Pathway ◽  
Stem Cell Factor ◽  
Factor C

scholarly journals Endothelial cell-fatty acid binding protein 4 promotes angiogenesis: role of stem cell factor/c-kit pathway

Angiogenesis ◽  
2012 ◽  
Vol 15 (3) ◽  
pp. 457-468 ◽  
Author(s):  
Harun Elmasri ◽  
Elisa Ghelfi ◽  
Chen-wei Yu ◽  
Samantha Traphagen ◽  
Manuela Cernadas ◽  
...  
Keyword(s):  
Stem Cell ◽  
Fatty Acid ◽  
Endothelial Cell ◽  
Stem Cell Factor ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
Factor C

Mast cells and fibroblasts work in concert to aggravate pulmonary fibrosis: role of transmembrane stem cell factor (SCF) and PAR-2/PKCalpha/Raf-1/p44/42 signaling pathway

Pneumologie ◽  
2013 ◽  
Vol 67 (S 01) ◽  
Author(s):  
M Wygrecka ◽  
B Dahal ◽  
D Kosanovic ◽  
F Petersen ◽  
B Taborski ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mast Cells ◽  
Pulmonary Fibrosis ◽  
Signaling Pathway ◽  
Stem Cell Factor

The Essential Role of Stem Cell Factor/KIT Signaling in the Proliferation and Survival of Blast Cells from Transient Leukemia in Neonates with Down Syndrome.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1807-1807
Author(s):  
Tsutomu Toki ◽  
Rika Kanezaki ◽  
Souichi Adachi ◽  
Hisanori Fujino ◽  
Gang Xu ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Stem Cell ◽  
Tyrosine Kinase ◽  
Stem Cell Factor ◽  
Myeloid Leukemia ◽  
Essential Role ◽  
Therapeutic Benefits ◽  
Significant Difference ◽  
Transient Leukemia

Abstract Children with Down syndrome (DS) are predisposed to developing leukemia. A leukemoid reaction occurring uniquely in approximately 10% of newborn infants with DS referred to as transient leukemia (TL). This disorder, in most cases, resolves spontaneously within three months after birth. Of all TL patients approximately 20–30% develop myeloid leukemia (ML-DS) within four years. Although treatment with low dose cytarabine is effective in high-risk TL cases, about 20% of severe patients still suffer early death. Improved treatments for TL are necessary for a better long-term prognosis of DS patients. In this study, we demonstrate abundant KIT expression in all 13 TL patients examined, although no significant difference in expression levels was observed between TL and acute myeloid leukemia (AML). Stem cell factor (SCF) mRNA was expressed at extremely low levels in TL cells and there were no significant differences in SCF expression between TL and AML. SCF stimulated the proliferation of the TL cells from all five patients examined and treatment with the tyrosine kinase inhibitor imatinib suppressed the proliferation and KIT phosphorylation effectively in vitro. To investigate the signal cascade, we established the first SCF-dependent, ML-DS cell line, KPAM1. Withdrawal of SCF or treatment with imatinib induced apoptosis of KPAM1 cells. SCF activated the RAS/MAPK and PI3K/AKT pathways, followed by downregulation of the pro-apoptotic factor BIM and upregulation of the anti-apoptotic factor MCL1. Although we found novel missense mutations of KIT in two of 14 TL patients, functional analysis using KPAM1 cells showed that neither mutation led to KIT activation and neither reduced the cytotoxic effects of imatinib. These results suggest the essential role of SCF/KIT signaling in the proliferation of DS-related leukemia and the possibility of therapeutic benefits of KIT-targeting tyrosine kinase inhibitors for TL patients.

Presence of c-KIT–Positive Mast Cells in Obliterative Bronchiolitis From Diverse Causes

2009 ◽  
Vol 133 (9) ◽  
pp. 1420-1425
Author(s):  
Neil E. Fuehrer ◽  
Alberto M. Marchevsky ◽  
Jaishree Jagirdar
Keyword(s):  
Stem Cell ◽  
Mast Cells ◽  
Stem Cell Factor ◽  
Obliterative Bronchiolitis ◽  
Small Airways ◽  
Kit Ligand ◽  
Immune Mediated ◽  
Large Airways ◽  
Factor C

Abstract Context.—The mechanism of fibrosis is not clear in patients with obliterative bronchiolitis after a remote injury. Immune-mediated progression may be a reason. c-KIT (CD117)–positive mast cells have been associated with chronic fibrosing diseases and may potentially be treated with imatinib (Gleevec), a c-KIT blocker. Objective.—To evaluate the role of mast cells in fibrosis associated with obliterative bronchiolitis. Design.—Four cases of obliterative bronchiolitis (household cleaner exposure, ammonia exposure, idiopathic, and posttransplantation) were compared with asthma/emphysema. Small and large airways were stained for CD20, CD3, CD4, CD8, CD117, CD34, CD25, stem cell factor (c-KIT ligand) and with toluidine blue, hematoxylin-eosin, and trichrome. c-KIT (CD117)–stained slides were digitally scanned with Aperio ScanScope and stained cells within the epithelium and subepithelium of small and large airways were counted (per millimeter of basement membrane). Results.—Mast cells were concentrated within the involved subepithelium of small airways in obliterative bronchiolitis (122 cells/mm), unlike asthma/emphysema (25 cells/mm). Conversely, there were more mast cells in the epithelium in cases of asthma/emphysema than in obliterative bronchiolitis (7 cells/mm and 2 cells/mm, respectively). Mast cells were significantly increased around involved airways versus uninvolved airways (52 cells/mm vs 14 cells/mm). Large airways in either group had similar c-KIT (CD117) expression. Stem cell factor was not increased. Conclusions.—Mast cells appear to be concentrated in the lesional small-airway subepithelium in obliterative bronchiolitis. The possible role of c-KIT inhibitors such as imatinib (Gleevec) in the progression of fibrosis preceding the development of obliterative bronchiolitis is discussed.

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