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X Demographics
Mendeley readers
Attention Score in Context
| Title |
Crosstalk between TGF‐β1 and complement activation augments epithelial injury in pulmonary fibrosis
|
|---|---|
| Published in |
FASEB Journal, June 2014
|
| DOI | 10.1096/fj.13-247650 |
| Pubmed ID | |
| Authors |
Hongmei Gu, Elizabeth A. Mickler, Oscar W. Cummings, George E. Sandusky, Daniel J. Weber, Adam Gracon, Trent Woodruff, David S. Wilkes, Ragini Vittal |
| Abstract |
The epithelial complement inhibitory proteins (CIPs) cluster of differentiation 46 and 55 (CD46 and CD55) regulate circulating immune complex-mediated complement activation in idiopathic pulmonary fibrosis (IPF). Our previous studies demonstrated that IL-17A mediates epithelial injury via transforming growth factor β1 (TGF-β1) and down-regulates CIPs. In the current study, we examined the mechanistic role of TGF-β1 in complement activation-mediated airway epithelial injury in IPF pathogenesis. We observed lower epithelial CIP expression in IPF lungs compared to normal lungs, associated with elevated levels of complement component 3a and 5a (C3a and C5a), locally and systemically. In normal primary human small airway epithelial cells (SAECs) treated with TGF-β1 (10 ng/ml), C3a, or C5a (100 nM), we observed loss of CIPs and increased poly(ADP-ribose) polymerase (PARP) activation [also observed with RNA interference (RNAi) of CD46/CD55]. TGF-β1-mediated loss of CIPs and Snail induction [SNAI1; a transcriptional repressor of E-cadherin (E-CAD)] was blocked by inhibiting mitogen-activated protein kinase (p38MAPK; SB203580) and RNAi silencing of SNAI1. C3a- and C5a-mediated loss of CIPs was also blocked by p38MAPK inhibition. While C3a upregulated TGFb transcripts, both C3a and C5a down-regulated SMAD7 (negative regulator of TGF-β), and whereas TGF-β1 induced C3a/C5a receptor (C3aR/C5aR) expression, pharmacologic C3aR/C5aR inhibition protected against C3a-/C5a-mediated loss of CIPs. Taken together, our results suggest that epithelial injury in IPF can be collectively amplified as a result of TGF-β1-induced loss of CIPs leading to complement activation that down-regulates CIPs and induces TGF-β1 expression.-Gu, H., Mickler, E. A., Cummings, O. W, Sandusky, G. E., Weber, D. J., Gracon, A., Woodruff, T., Wilkes, D. S., Vittal, R. Crosstalk between TGF-β1 and complement activation augments epithelial injury in pulmonary fibrosis. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Israel | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Practitioners (doctors, other healthcare professionals) | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 62 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| South Africa | 1 | 2% |
| Unknown | 61 | 98% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 12 | 19% |
| Student > Master | 9 | 15% |
| Student > Ph. D. Student | 8 | 13% |
| Student > Bachelor | 5 | 8% |
| Student > Doctoral Student | 5 | 8% |
| Other | 7 | 11% |
| Unknown | 16 | 26% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 14 | 23% |
| Agricultural and Biological Sciences | 14 | 23% |
| Biochemistry, Genetics and Molecular Biology | 9 | 15% |
| Immunology and Microbiology | 6 | 10% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 2% |
| Other | 1 | 2% |
| Unknown | 17 | 27% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 04 July 2014.
All research outputs
#20,674,485
of 25,394,764 outputs
Outputs from FASEB Journal
#9,067
of 11,453 outputs
Outputs of similar age
#178,783
of 243,427 outputs
Outputs of similar age from FASEB Journal
#47
of 62 outputs
Altmetric has tracked 25,394,764 research outputs across all sources so far. This one is in the 10th percentile – i.e., 10% of other outputs scored the same or lower than it.
So far Altmetric has tracked 11,453 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.5. This one is in the 12th percentile – i.e., 12% of its peers scored the same or lower than it.
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