Time-Dependent Alterations of VEGF and Its Signaling Molecules in Acute Lung Injury in a Rat Model of Sepsis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2012-04

AUTHORS

Subrina Jesmin, Sohel Zaedi, A. M. Shahidul Islam, S. Nusrat Sultana, Yoshio Iwashima, Takeshi Wada, Naoto Yamaguchi, Michiaki Hiroe, Satoshi Gando

ABSTRACT

Molecular mechanisms of sepsis-associated acute lung injury (ALI) are poorly defined. Since vascular endothelial growth factor (VEGF) is a potent vascular permeability and mitogenic factor, it might contribute to the development of ALI in sepsis. Thus, using lipopolysaccharide (LPS)-induced (15 mg/kg, intraperitoneal) endotoxemic rat model, we studied the timeline (1, 3, 6, and 10 h) of pulmonary VEGF expression and its signaling machinery. Levels of pulmonary VEGF and its angiogenic-mediating receptor, Flk-1, were downregulated by LPS in a time-dependent manner; levels of plasma VEGF and its permeability-mediating receptor, Flt-1, in contrast, was upregulated with time. In addition, blockade of Flt-1 could improve the downregulated pulmonary VEGF level and attenuate the elevated plasma and pulmonary levels of TNF-α, followed by improvement of arterial oxygenation and wet-to-dry weight ratio of the lung. Expression of signaling, pro- and or apoptotic factors after LPS administration were as follows: phosphorylated Akt, a downstream molecule was downregulated time dependently; endothelial nitric oxide synthase levels were significantly reduced; pro-apoptotic markers caspase 3 and Bax were upregulated whereas levels of Bcl-2 were downregulated. The present findings show that VEGF may play a role through the expression of Flt-1 in LPS-induced ALI. Moreover, downregulation of VEGF signaling cascade may account for LPS-induced apoptosis and impaired physiological angiogenesis in lung tissues, which in turn may contribute to the development of ALI induced by LPS. More... »

PAGES

484-500

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10753-011-9337-1

DOI

http://dx.doi.org/10.1007/s10753-011-9337-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041885771

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21528367


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